Endo & Repro 1 Flashcards
(174 cards)
1
Q
What is metabolism?
A
The sum of all chemical reactions in the body
2
Q
What are anabolic and catabolic processes?
A
- Anabolic: builds large molecules from smaller ones
- Catabolic: breaks large molecules into smaller ones
3
Q
What controls energy balance and what is Basal Metabolic Rate (BMR)?
A
- Caloric intake and exercise
- Energy expended at rest, comfortable temperature, and fasted
4
Q
What is the fed state and when does it occur?
A
- The absorptive state
- Right after a meal
- Glucose is the primary energy source
5
Q
What is the fasted state and when does it occur?
A
- The postabsorptive state
- After 3–4 hours of fasting
- Energy comes from glucose and fat
6
Q
What happens to plasma levels after a meal and what happens ~4 hours after a meal?
A
- Glucose and insulin rise
- Glucagon drops
- 4 hours: Glucagon starts to rise again
7
Q
What is the goal of glucose homeostasis?
A
Maintain stable blood glucose
8
Q
What hormone dominates the fed state?
A
Insulin
9
Q
In the fasted state, are insulin and glucagon high or low?
A
- Insulin: low
- Glucagon: high
10
Q
What is glycolysis?
A
- Along with the TCA cycle and oxidative phosphorylation, it breaks down glucose to produce ATP
11
Q
What is glycogenesis vs glycogenolysis vs gluconeogenesis?
A
- Glycogenesis: makes glycogen from glucose
- Glycogenolysis: breaks down glycogen into glucose
- Gluconeogenesis: synthesis of glucose from non-carb sources
12
Q
What is lipogenesis vs lipolysis?
A
- Lipogenesis makes fat (triglycerides) from fatty acids and glycerol
- Lipolysis breaks triglycerides into fatty acids and glycerol
13
Q
What is beta-oxidation?
A
The breakdown of fatty acids to produce ATP
14
Q
What is the primary substrate for regulating blood sugar?
A
Glucose
15
Q
Where is the pancreas?
A
- Below the stomach
- Near the small intestine and liver
16
Q
What does the exocrine pancreas do?
A
Produces bicarbonate and proenzymes for digestion, releasing them into ducts
17
Q
What does the endocrine pancreas do?
A
Releases hormones directly into the bloodstream via Islets of Langerhans
18
Q
What do alpha, beta, and delta cells secrete?
A
- Alpha: glucagon
- Beta: insulin
- Delta: somatostatin
19
Q
What is proinsulin?
A
- Precursor made by beta cells
- Cleaved to insulin
20
Q
How are insulin and glucagon related?
A
They are antagonistic hormones
21
Q
What receptors do insulin and glucagon bind to?
A
- Insulin: receptor tyrosine kinase
- Glucagon: G protein-coupled receptor (7 transmembrane regions)
22
Q
Do insulin and glucagon use the same intracellular pathway and do they act on the same target cells?
A
- No, they initiate different cascades
- Yes, they often do
23
Q
What is the ultimate goal of insulin and glucagon?
A
Switch between feeding and fasting metabolism
24
Q
What happens after binding to their receptors?
A
Intracellular signaling begins, changing metabolism
25
Is insulin anabolic or catabolic, how is it synthesized, and what does it do to blood glucose levels?
- Anabolic
- As a typical peptide
- Lowers it by increasing glucose uptake into cells
26
What processes does insulin promote and inhibit?
- Promotes: Glycogenesis, lipogenesis, protein synthesis
- Inhibits: Glycogenolysis, lipolysis, protein breakdown
27
How does insulin affect muscles and what is the insulin:glucagon ratio important for?
- Increases amino acid uptake and protein synthesis
- Controls organ responses and overall metabolism
28
What are insulin’s metabolic effects on glucose, fat, and protein?
- Inhibits gluconeogenesis, lipolysis, and beta oxidation
- Promotes the formation of glycogen, fat, and protein
- Increases amino acid uptake in muscle cells
- Enhances cell proliferation
29
How does insulin signaling promote glucose uptake in muscle and fat cells?
- Binds to a receptor tyrosine kinase
- Phosphorylates IRS to activate second messengers that alter protein synthesis and function
- This increases GLUT4 transporter movement to the membrane
- Enhancing glucose entry into cells
30
How does insulin regulate GLUT4 transporters in fed vs. fasted states?
- In the fed state (high insulin/low glucagon): insulin triggers GLUT4 exocytosis in muscle and adipose tissue to allow glucose uptake
- In the fasted state (low insulin/high glucagon): GLUT4 remains inside the cell and glucose storage is limited
31
What experiment demonstrated insulin’s effect on GLUT4 location?
- In muscle and adipose tissue, GFP-tagged GLUT4 was shown via microscopy to move from inside the cell to the membrane during the fed state
- Insulin triggered exocytosis to increase glucose uptake
32
How does insulin promote liver glucose uptake and storage?
- In the fed state, insulin stimulates GLUT2-mediated glucose entry and activates hexokinase to convert glucose to glucose-6-phosphate
- This maintains the concentration gradient to increase uptake and store glucose
33
How is insulin secreted from pancreatic beta cells?
- Increased plasma glucose causes glycolysis and the Citric Acid Cycle to raise ATP
- Closing K+ channels
- Causing membrane depolarization which opens Ca2+ channels
- Ca2+ influx triggers insulin release from vesicles
34
What is the Incretin effect and how does oral glucose affect insulin release?
- Compared to IV glucose, intrajujunal (intestinal) glucose triggers a higher insulin spike due to gastrointestinal hormones like GIP and GLP-1
- This enhanced oral response is called the Incretin effect
- This shows the intestine’s strong role in stimulating insulin
35
How do glucose and insulin levels change after a meal?
- Plasma glucose rises initially then falls
- Insulin spikes after glucose increases
- Then drops as glucose levels decline
36
What stimulates the release of GIP and GLP-1?
- GIP: stimulated by glucose, fatty acids, and amino acids
- GLP-1: stimulated by nutrients and parasympathetic activity
37
What are the effects of GIP and GLP-1 on insulin and gastric activity?
- Both increase insulin secretion
- GIP decreases gastric emptying/acid
- GLP-1 also decreases glucagon, increases beta cell growth, slows gastric emptying/acid, and promotes satiety
38
Do GLP-1 and GIP support insulin action, and what type of regulation do they demonstrate?
Yes, they support insulin action and represent feedforward regulation in response to nutrient ingestion
39
What stimulates insulin secretion, and what nervous systems regulate it?
- Insulin is stimulated by increased plasma glucose and amino acids
- The parasympathetic system stimulates it
- The sympathetic system inhibits it to mobilize fuel for fight or flight
40
What cells secrete glucagon and what organ does it target?
- Alpha cells secrete glucagon
- Mainly targets the liver
41
How does glucagon oppose insulin and in which metabolic state?
- Glucagon antagonizes insulin and dominates in the fasted state
42
What metabolic processes does glucagon increase and why?
- Increases glycogenolysis
- Gluconeogenesis
- Ketogenesis
- All of these release glucose and prevent hypoglycemia
43
What signaling pathway does glucagon use in the liver?
1. Glucagon binds to a Gs protein-coupled receptor
2. Activates adenylyl cyclase
3. Produces cAMP
4. Activates protein kinase A
44
How does glucagon increase glucose export from liver cells?
- It indirectly increases intracellular glucose, which is transported out via GLUT2 transporters.
45
How do cortisol and glucagon interact to affect glucose levels?
- Glucagon needs cortisol to build up glucose
- With epinephrine, they raise blood glucose significantly in 2–3 hours
46
What stimulates and inhibits glucagon secretion?
Stimulated by:
- ↓ plasma glucose
- ↑ amino acids
- Sympathetic activity
Inhibited by:
- GLP-1
47
What is proglucagon and where is it expressed?
- A large gene with multiple hormones
- Expressed in alpha cells, intestinal L cells, and the brain
48
What are the products of proglucagon in different tissues and why?
- In alpha cells: glucagon
- In L cells/brain: GLP-1 and GLP-2
- Tissue-specific enzymes cleave proglucagon differently
49
What metabolic pathways does glucagon promote?
Glucagon promotes catabolic pathways like gluconeogenesis and glycogenolysis
50
Where is GLP-1 released from and what effect does it have on insulin and glucagon?
- Intestine
- Stimulates insulin
- Decreases glucagon
51
What is Type 1 diabetes also known as, what percentage of diabetics have it, what causes it, and how is it typically treated?
- Also called insulin-dependent or juvenile diabetes
- ~10% of diabetics have it
- Caused by autoimmune destruction of beta cells, leading to reduced or absent insulin secretion
- Insulin injections or pumps
52
What happens to plasma glucose in uncontrolled T1DM and why?
- Without insulin, GLUT4 transporters don’t move to the membrane, so glucose can’t enter muscle/fat cells
- This decreases glucose uptake and utilization
- Leading to hyperglycemia
- The brain thinks it’s starving, causing polyphagia
53
What happens to protein and fat in uncontrolled T1DM?
With no insulin, the body breaks down protein and fat for energy, causing tissue and weight loss
54
What alternative fuels are used without insulin, and what does this cause?
- Fat and protein are used
- Fat metabolism produces ketones, which cause acidosis
55
How does the body respond to acidosis?
It hyperventilates to expel CO₂ and reduce acidity
56
What happens when high blood glucose is filtered by the kidneys?
The kidneys can't reabsorb all the glucose, leading to glucosuria
57
How does glucosuria lead to polyuria and its consequences?
- Water follows glucose into the urine, causing polyuria
- This reduces blood volume
58
How does low blood volume affect ADH and osmolarity?
- It activates carotid baroreceptors, increasing ADH secretion
- Despite water loss, total sodium remains, increasing osmolarity
59
What is Type 2 diabetes also known as, what percentage of diabetics have it, what are the main issues, and how is it treated?
- Non-insulin-dependent or mature onset diabetes
- ~90% of diabetics have it
- A defect in insulin secretion and reduced target cell responsiveness
- Treatment: diet, exercise, oral hypoglycemics, and sometimes insulin
60
What effect does exercise have on GLUT4 transporters in Type 2 diabetes?
It causes translocation of GLUT4 to the membrane, improving glucose uptake
61
What is a common feature of both types of uncontrolled diabetes?
High blood glucose (hyperglycemia)
62
What type of diabetes are Sulfonylureas used to treat, and how do they work?
- Used for Type 2 diabetes
- They close KATP channels in beta cells
- Leading to cell depolarization
- Ca²⁺ entry
- Insulin release
63
What type of hormone is GLP-1, where is it released from, and how is it relate to insulin, glucagon, and gastric emptying?
- An incretin hormone
- Released from the intestine
- Increases insulin secretion
- Decreases glucagon
- Delays gastric emptying
64
What are GLP-1's effects on the pancreas, liver, brain, and heart?
- Pancreas: ↑ insulin biosynthesis, ↑ beta cell proliferation, ↓ beta cell apoptosis
- Liver: ↓ glucose production
- Brain: ↑ neuroprotection, ↓ appetite
- Heart: ↑ cardioprotection, ↑ cardiac output
65
What two structures work together to regulate hormone secretion and what are they made of?
- The hypothalamus and pituitary gland regulate bodily functions
- The pituitary is two fused glands: the anterior (endocrine tissue) and posterior (neural tissue)
66
Where are posterior pituitary hormones made and how are they released?
- Made and packaged in hypothalamic neurons
- Transported down axons
- Stored in vesicles
- Released into the bloodstream
67
What neurohormones are secreted by the posterior pituitary and what do they do?
- Vasopressin (ADH): regulates fluid balance
- Oxytocin: targets the mammary glands and uterus
68
What is the physical connection between the hypothalamus and posterior pituitary, and how do neurohormones travel there?
- They are connected by the stalk (infundibulum)
- Neurohormones travel down axons, not through a portal system
69
How is the anterior pituitary controlled and how do its hormones act?
- Tropic hormones from the hypothalamus travel via a portal system to stimulate anterior pituitary hormone release
- Then acts on target organs to stimulate further hormone release
70
Which hormones are secreted by the anterior pituitary and what are their targets?
- Prolactin – mammary glands
- TSH – thyroid
- ACTH – adrenal cortex
- GH – musculoskeletal system & liver
- FSH & LH – reproductive organs
71
What do anterior pituitary hormones do at their target organs?
- They stimulate those organs to secrete more hormones
Examples:
- Testis/Ovary – sex hormones
- Adrenal cortex – cortisol
- Thyroid – thyroid hormones
- Liver – IGF-1
72
What are common endings for hypothalamic and anterior pituitary hormones?
- Hypothalamic releasing hormones end in -RH (e.g., GHRH)
- Anterior pituitary stimulating hormones end in -SH (e.g., TSH)
73
What type of hormone is Growth Hormone (GH), and how is it regulated?
- A peptide hormone from the anterior pituitary
- GHRH stimulates GH
- Somatostatin (GHIH) inhibits GH
- GH acts on the liver to release IGF-1, which:
1. Promotes cartilage, bone, and tissue growth
2. Increases blood glucose
3, Negatively feeds back on GH
74
What else does GH do besides promoting growth?
- GH also has catabolic actions
- Bone and tissue growth
- Increased blood glucose
75
How and when do bones grow longer?
- Long bones grow at each end at the epiphyseal growth plate (a zone of cartilage between bone ends)
- Cartilage (laid down first by chondrocytes) is replaced by bone from osteoblasts
76
How do epiphyseal plates function and when do they close?
- Chondrocytes divide and produce new cartilage
- Old ones die and are replaced by bone via osteoblasts
- This causes bone to lengthen
- Plates close around puberty
- This ends bone growth
77
What causes female bone mass to decrease faster after a certain age?
Due to menopause and the role of sex hormones
78
When does bone mass increase and peak?
It increases from birth to ~10 years, and peaks in the 20s
79
What do the X-rays show the difference between a child’s and adult’s hand?
- A child's hand shows epiphyseal cartilage (growth plates), which appear as dark lines because cartilage is not detected by X-rays
- An adult hand shows epiphyseal lines where bones have fused after cartilage is replaced by bone
80
What happens to the cartilage in growth plates after puberty and what type of bones are finger bones in terms of growth?
- It is replaced by bone, forming epiphyseal lines
- After this fusion, bone growth in length ceases
- Long bones, which grow lengthwise
81
Where is GHRH released from and what does it do?
- GHRH is released from the hypothalamus
- Stimulates GH release from the anterior pituitary via the portal bloodstream
82
What is a main target of GH and what does it stimulate there?
- The liver
- GH stimulates the liver to secrete IGF-1
83
What tissues do GH and IGF-1 affect and what do they do?
- They target bone and soft tissues for growth and have anabolic effects
- IGF-1 promotes growth in almost every cell and is structurally similar to insulin
84
Which cells in cartilage are stimulated by GH and IGF-1 and what is the effect?
- Chondrocytes
- GH and IGF-1 promote their recruitment, proliferation (more cells), and cartilage matrix buildup
85
What are catabolic actions of GH?
- Lipolysis in fat tissue
- Increased amino acid uptake for tissue synthesis
- Glycogenolysis, and gluconeogenesis in the liver to increase energy availability
86
What other factors influence growth besides GH and IGF-1?
- Diet
- Genetics
- Hormones like thyroid hormones (important in childhood)
- Sex steroids (important during puberty)
- Insulin (helps glucose uptake)
- Cortisol (releases energy by catabolizing tissues)
87
What is gigantism and acromegaly and what causes them?
- Gigantism: Excessive height from too much GH in childhood when growth plates are still open
- Acromegaly: Abnormal bone thickening from too much GH in adulthood
88
What hormones are needed for normal growth?
- GH
- Thyroid hormones
- Insulin
- Sex hormones
- Plus adequate nutrition and absence of chronic stress
89
Is GH secretion constant across life?
- No
- Follows a circadian rhythm
- Higher in childhood and adolescence
90
Where is the thyroid gland located and what is its shape?
- At the base of the neck
- Butterfly-shaped with two lobes
91
What are the functional units of the thyroid gland?
- Thyroid follicles
- Composed of follicular cells and protein-rich colloid
92
What do follicular cells and C cells do?
- Follicular cells synthesize thyroid hormones
- C cells secrete calcitonin
93
Are thyroid follicles well-supplied with blood and what surrounds them?
Yes, they are heavily capillarized and surrounded by connective tissue
94
What is the large protein precursor to thyroid hormones synthesized in follicular cells?
Thyroglobulin
95
What essential element is needed for thyroid hormone synthesis? Can the body produce it?
- Iodine
- No, comes from the diet
96
Which transporter brings iodide into the follicular cell and which moves it into the colloid?
- Na⁺-I⁻ symporter (NIS) brings it into the cell
- Pendrin moves it into the colloid
97
What enzyme adds iodine to tyrosine residues on thyroglobulin? What are MIT and DIT?
- Thyroid peroxidase
- MIT is monoiodotyrosine (1 iodine)
- DIT is diiodotyrosine (2 iodines)
98
How many iodine atoms are in T3 and T4? Where are they cleaved before release?
- T3 has 3 iodines
- T4 has 4
- They’re cleaved in vesicles inside the follicular cell before release
99
What hormones regulate the thyroid and where are they released from?
- TRH (hypothalamus) stimulates TSH (anterior pituitary), which stimulates the thyroid gland
100
How do T3 and T4 regulate TRH and TSH? What happens when T3/T4 are high or low?
- Negative feedback:
- High T3/T4: ↓ TRH & TSH
- Low T3/T4: ↑ TRH & TSH
101
Is TRH released constantly? What type of hormone is TSH and where is it released from?
- Yes, TRH has a tonic rhythm
- TSH is a peptide hormone from the anterior pituitary
102
What kind of receptors does TSH bind to? What pathway and transcription factors are activated?
- TSH binds to GPCRs on the thyroid membrane
- Activates adenylate cyclase
- Activates c-fos & c-myc
103
What does TSH stimulate besides hormone synthesis? Why is this important?
- It stimulates thyroid growth to sustain hormone production and gland health
104
Does TSH directly cause TRH release? Are TSH receptors inside or on the membrane?
- No, TSH is downstream of TRH
- TSH receptors are on the membrane
105
How do T3 and T4 circulate in blood? Which is more potent? Where is T4 converted to T3?
- They circulate bound to plasma proteins
- T3 is 3–5x more potent
- T4 is converted to T3 in target tissues
106
Where are thyroid hormone receptors located and what do they bind to?
- Inside the cell (usually in the nucleus)
- Bind to nuclear thyroid receptors
107
What do thyroid receptors form with retinoic acid receptors? What is their action on genes?
- Form homodimers or heterodimers
- Alter gene transcription
108
Are thyroid hormones lipophilic? What is their main function?
- Yes
- They regulate metabolism
109
How do thyroid hormones affect metabolism, growth, nervous, muscular, and cardiovascular systems?
1. ↑ Metabolic rate, oxygen use, heat, protein degradation, lipolysis
2. ↑ Speech, thinking, reflexes (nervous system)
3. ↑ Heart rate, contractility, blood flow (↑ β-adrenergic receptors)
4. Support growth with GH
5. Too much → muscle weakness
110
What is hyperthyroidism and what are common causes?
- Excess thyroid hormone
- Caused by tumors or thyroid-stimulating immunoglobulins (Graves' disease)
111
What is goiter and what are symptoms of hyperthyroidism?
- Goiter = thyroid enlargement
- Symptoms:
1. Goiter
2. Nervousness
3. Insomnia
4. Anxiety
5. ↑ HR
6. Exophthalmos
7. Weight loss
112
What is exophthalmos? How does hyperthyroidism affect metabolism?
- Bulging eyes
- It increases metabolism
113
What are treatments for hyperthyroidism?
- Surgical thyroid removal
- Drugs that block T4/T3 synthesis/conversion
114
What type of disease is Graves’? What is produced and what does it mimic?
- Autoimmune
- Abnormal antibodies mimic TSH and bind to its receptor
115
What happens when antibodies bind the TSH receptor? What is the result?
- It mimics TSH
- Activates the receptor
- Increasing thyroid hormone release
116
Is the cause of Graves’ disease known? What is it the most common cause of?
- No, it’s unknown
- Most common cause of hyperthyroidism and thyroid enlargement in developed countries
117
What is hypothyroidism, its causes, and treatment?
- Thyroid hormone deficiency
- Caused by underactive thyroid or iodine deficiency
- Taking exogenous T4 (thyroxine)
118
How does hypothyroidism affect metabolism and what are the symptoms?
- ↓ Metabolism
- Symptoms:
1. Goiter
2. Slow HR/speech
3. Fatigue
4. Cold intolerance
5. Cretinism
6. Stunted growth
7. Weight gain
119
What happens to thyroid hormone secretion in iodine deficiency? What compensatory mechanisms occur?
- ↓ T3/T4 secretion
1. ↑ TRH & TSH due to low feedback
2. Thyroid grows to compensate
3. Goiter
120
What are severe, semi-severe, and mild effects of iodine deficiency?
- Severe: mental retardation, cretinism, stunting
- Semi-severe: ↑ infant mortality, hypothyroidism, goiter
- Mild: nodular goiter, hyperthyroidism, reduced intelligence
121
How many people are iodine deficient or show symptoms? How is it prevented?
- 2 billion deficient
- 50 million symptomatic
- Iodized salt is an effective prevention
122
In an iodine-deficient man, what happens to T3/T4, TRH, and TSH? Why?
- T3/T4 ↓
- ↑ TRH
- ↑ TSH due to lack of negative feedback
123
What are two commonalities in reproduction between sexes?
1. Formation of gametes
2. Hypothalamic/pituitary control
124
What are gametes? Where are they formed and how many chromosomes do they have?
- Gametes are sex cells (sperm and egg)
- Formed in the gonads, with 23 chromosomes
125
How many chromosomes do gonadal cells have before meiosis, and what process forms gametes?
- 46 chromosomes before meiosis
- Meiosis produces gametes
126
How does meiosis differ from mitosis?
- Meiosis has 2 cell divisions after 1 DNA replication, cutting chromosome numbers in half
- Mitosis has 1 division after 1 replication
127
Are gametes haploid or diploid? Are most somatic cells haploid or diploid?
- Gametes are haploid
- Most somatic cells are diploid
128
What happens in meiosis II?
Genetic material is further divided
129
Does meiosis increase genetic diversity and how?
Yes, through random assortment and non-homologous recombination
130
What axis controls reproduction and what hormone starts the process?
- The hypothalamic-pituitary axis
- GnRH is released from the hypothalamus
131
Where does GnRH travel and what does it stimulate?
- Travels to the anterior pituitary to stimulate LH and FSH release
132
What are the target organs for LH and FSH, and how is this axis regulated?
- Target organs are the gonads
- Regulated by both negative and positive feedback
133
How is GnRH secreted and why is its pulsatility important?
- GnRH is secreted in pulses
- Pulsatility is critical for reproductive function.
134
What hormone is released at different GnRH pulse frequencies?
- Low frequency = FSH
- High frequency = LH
135
What regulates GnRH pulse frequency and amplitude?
Hormonal feedback and higher brain centers
136
What is the primary reproductive organ in males and where is it located?
The testes, located in the scrotum
137
What helps keep the testes cool and why is this important?
- The scrotum and a complex capillary network keep testes 2–3ºC below body temp (~35ºC)
- Optimal for sperm production
138
Where are sperm produced and what is this process called?
- In seminiferous tubules of the testes
- The process is spermatogenesis
139
How long does spermatogenesis take and how many sperm are produced daily?
- Around 64 days
- ~200 million sperm/day
140
Where do sperm mature after production?
In the epididymis
141
What is the vas deferens and what does it do?
A duct that transports sperm
142
What structures transport sperm and what is shared with the urinary system?
Ducts like the vas deferens and urethra (shared structure)
143
Name one accessory gland and its function.
- Seminal vesicles
- Prostate gland
- Bulbourethral glands
- Secrete fluids for semen
144
What are Sertoli cells (sustentacular cells) and their function?
- Supporting cells in seminiferous tubules that aid sperm development
145
What structure do Sertoli cells form and what is its role?
- The blood-testis barrier
- Protects developing sperm from the immune system
146
Why would the immune system attack developing sperm?
They have half the genetic material and novel proteins seen as foreign
147
Do capillaries enter the lumen of the seminiferous tubule?
- No; immune cells circulate in the bloodstream
- Could destroy sperm if they reach them
148
What are Leydig cells (interstitial cells) and what do they secrete?
Cells between seminiferous tubules that secrete testosterone
149
What are precursor sperm cells called and where do they develop in the tubule?
- Spermatogonia
- Development starts toward the outside corners
150
What part of mature sperm is visible in later stages of development?
Tails
151
Where are spermatogonia located, what division do they undergo, and when are they first formed?
- They are located near the basement membrane of the seminiferous tubule
- Undergo mitosis
- Are formed during fetal development
152
What happens when a spermatogonium divides and what is its ploidy?
- One stays behind to make more spermatogonia
- They are diploid (2n)
153
What cells support and surround developing sperm cells and what do they form?
- Sertoli cells (sustentacular cells) support and surround developing sperm cells
- They form tight junctions crucial for protection
154
What cell begins meiosis and where is it located in relation to the basement membrane and tight junctions?
- The primary spermatocyte begins meiosis
- Located further inward under tight junctions, behind the blood-testis barrier
155
What is the ploidy of a primary spermatocyte, and what is the outcome of meiosis?
- Primary spermatocytes are diploid (2n)
- Meiosis produces haploid sperm (spermatids)
156
What happens during Meiosis I and II, and what cells result?
- Meiosis II follows Meiosis I
- Four haploid spermatids are produced per primary spermatocyte
- DNA replicates before Meiosis I, not Meiosis II
157
What is spermiogenesis and what changes occur?
- It's the process where spermatids differentiate into spermatozoa
- They lose cytoplasm
- Gain a tail for motility
- Take on sperm appearance
- No cell division occurs
158
Where are spermatozoa released, and what is their ploidy?
- They are released into the lumen of the seminiferous tubules
- Haploid
159
What part of sperm contains enzymes and where do they come from?
- The acrosome, which comes from the Golgi apparatus
- Contains enzymes like hyaluronidase/acrosin to break down the zona pellucida
160
Where is genetic material in sperm and where are mitochondria located?
- Genetic material is in the nucleus
- Mitochondria are at the base of the tail and provide energy for swimming
161
What is the composition of semen and what are its functions?
1. 1% spermatozoa
2. 99% accessory gland secretions
- Water
- Mucus
- Buffers: neutralize acidity
- Zinc
- Enzymes
- Nutrients like fructose, citric acid, vitamin C, carnitine
- Prostaglandins: aid smooth muscle contraction
162
What is the path and control of hormone regulation in male reproduction?
1. Hypothalamus
2. GnRH
3. Anterior pituitary
4. LH (stimulates Leydig cells → testosterone)
4. FSH (stimulates Sertoli cells → support spermatogenesis, secrete inhibin and ABP)
5. Inhibin inhibits FSH
163
What are the testosterone level changes across life stages and their effects?
- High in fetal life
- Spike at birth (neonatal)
- Low during childhood
- Rise at puberty (develops reproductive tract)
- Stay high in adulthood
- Decline with age
164
What hormones are involved in testicular descent and male sex differentiation?
- Testosterone and INSL3 are involved in descent
- AMH in sex differentiation
165
How does testicular volume change and what cell types dominate?
- Constant in childhood
- Increases at puberty
- Sertoli cells dominate before puberty
- Germ cells dominate during
166
What is hypogonadism, its causes, and hormone effects?
- It's reduced testicular function
- Causing ↓ androgens, inhibin B, AMH, and sperm
1. Primary: Testicular defect; ↑ LH/FSH due to no negative feedback.
2. Secondary: Hypothalamus/pituitary defect; ↓ GnRH, LH, FSH
167
How is testosterone synthesized and what are its effects?
- Testosterone (a steroid hormone) is derived from cholesterol
- Progesterone
- Testosterone (via enzymes in testes)
- Converts to DHT by 5α-reductase
168
What are the functions of testosterone in sex-specific tissues?
- Promotes spermatogenesis
- Maintains and stimulates secretion from prostate and seminal vesicles
- Maintains reproductive tract
169
What other reproductive effects does testosterone have?
- It increases sex drive
- Has negative feedback effects on GnRH, LH (and FSH) secretion
170
What are the non-reproductive effects of testosterone?
- Promotes protein synthesis
- Increases aggression
- Stimulates erythropoiesis
171
What secondary sex characteristic are influenced by testosterone?
- Male pattern of hair growth (including baldness)
- Promotes muscle growth
- Increases sebaceous gland secretion (odors)
172
What is the overall purpose of using 5α-reductase inhibitors clinically? What condition do they treat?
- To treat conditions caused by DHT
- Benign prostate enlargement
- Male pattern baldness
173
What is the direct result of blocking the enzyme 5α-reductase and what drug can do this?
- No more DHT is converted from testosterone
- Propecia (Finasteride) is a drug that blocks 5α-reductase
174
What are some potential side effects of blocking 5α-reductase?
- Depression
- Loss of libido
- Fatigue
