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Block 4: Endocrinology > Block 4 general > Flashcards

Block 4 general Flashcards

1
Q

female genital ducts and glands derive from

A

UG sinus, paramesonephric ducts

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2
Q

what kind of process is sexual determination of female?

A

active

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3
Q

what supports persistence and devel of paramesonephric ducts?

A

estrogens

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4
Q

what does the unfused portion of the paramesonephric duct become?

A

uterine tubes

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5
Q

what does the fused portions of the paramesonephric duct become?

A

uterus and superior vagina

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6
Q

what develops from the UG sinus?

A

inferior vagina bladder, urethra, paraurethral glands, greater vestibular glands

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7
Q

bicornate uterus

A

incomplete fusion of the paramesonephric ducts

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8
Q

what happens to primitive sex cords in females?

A

primitive sex cords dissociate in females and second generation of cortical cords develop

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9
Q

where do the gonadal ridges appear?

A

gonadal (or “genital”) ridges appear on the medial surface of the urogenital ridges

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10
Q

what does the genital system consist of

A

gonads genital ducts and glands external genitalia

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11
Q

what are the three events initiating puberty

A

1) proper nutrition 2) gene activation 3) development of limbic system

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12
Q

A 15 year-old male does not demonstrate any signs of puberty. He is short for his age, his testicles show no evidence of enlargement, his testosterone levels are low, and he has a reduced ability to smell.

A

Kallmann syndrome

  • KAL1 gene deficiency
    • KAL1 induces migration of nerves from olfactory placode to olfactory bulb
    • responsible for differentation and migration of GnRH secreting nerves
  • Lack of GnRH results in ↓ LH, FSH, testosterone, sperm count
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13
Q

IGF-3

A
  • allows descent of testes
  • under influence of gene HOXA10
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14
Q

precocious puberty

A

premature development of genital organs and secondary sexual characteristics

  • can be due to GnRH secreting tumor (optic glioma or hypothalmic astrocytoma)
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15
Q

chromophils

A
  • acidophils (40%)
  • basophils (10%)
  • part of pars distalis of the anterior pituitary
    • ​ectoderm origin
  • synthesize and secrete a variety of hormones
    • each type generally secretes a single hormone
  • arranged in cords; envolped by a delicate covering of connective tissue
  • large cells, alot of RER, well developed Golgi complex, many secretion granules
  • become chromophobes when they dump their hormones
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16
Q

chromophobe

A

chlorophils that have released their specific hormones and are “degranulated” and thus stain poorly

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17
Q

Identify

A

Chromophils

  • large cells, much RER,well developed Golgi complex, many secretion granules (contain hormone)
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18
Q

Idenitfy circled structure

A

Chromophobe

  • chromophils that have released their specific hormones and are “degranulated”
    • therefore, stain poorly
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19
Q

Steroidogenic TF

A

promotes gonadotroph lineage

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20
Q

T-box TF (“Tpit”)

A

promotes the corticotroph lineage

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21
Q

POU1F1

A
  • encodes a POU domain
    • this domain is essential for differentiation and expansion of somatotrophs, lactotrophs and thyrotrophs
  • transcription factor
  • mutations - responsbile for GH, PRL and TSH deficiencies
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22
Q

supraoptic nuclei

A

ADH

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23
Q

Paraventricular nuclei

A

oxytocin

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24
Q

hypothalamic nuclei

A

cell bodies of neurosecretory neurons that releasing or release-inhibiting hormones are synthesized

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25
Q

how do release/release-inhibiting hormones reach their target cells in the pars distalis?

A

hypophyseal portal system

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26
Q

Hypophyseal Portal System

A

primary capillary plexus, portal venules and secondary capillary plexus

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27
Q

colloid cysts

A

found in pars intermedia

  • colloid = viscous material within
  • cyst = encapsulated structure
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28
Q

Identify

A

Pars nervosa (of the posterior pituitary)

  • dots are nuclei of glial cells
  • axons are the stringy lines throughout (where the lines are pointing)
  • stores neuroendocrine secretions made by the neurons of the hypothalamus
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29
Q

Identify

A

Herring bodies

  • found in the pars nervosa of the posterior pituitary
  • large swellings formed by ends of axons
  • stores oxytocin (from paraventricular nuclei) and ADH (from supraoptic nuclei)
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30
Q

Identify

A

Pars nervosa of the posterior pituitary

  • can visualize axons (arrows pointing to them) and lots of secretory vesicles that are storing hormones
    • Oxytocin (from paraventricular nuclei of hypothalamus)
    • ADH (from supraoptic nuclei of hypothalamus)
  • axon terminals end near fenestrated capillary
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31
Q

Diabetes insipidus

A

excessive thrist and urination due to inadequate secretion or utilization of vasopressin / ADH

  • could be caused by damage to hypothalamus, damage to pituitary stalk, brain tumors
  • neurogenic
    • mutations in neurophysin II
  • nephrogenic
    • mutation in V2 receptor, aquaporin channel
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32
Q

What do corticotropes express?

A

express ACTH, contains alpha MSH

therefore, stimulates cortisol synthesis in adrenal gland but IN EXCESS, will stimulate melanin produciton in melanocytes (recall that hyperpigmentation allows differentiation between primary and secondary adrenal insufficiency)

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33
Q

A 15-year-old male presents to his pediatrician with complaints of fatigue, weight loss, and recurrent nausea and vomitting. On physical exam he appears weak and has skin that appears abnormally tan. A basic metabolic panel reveals hyponatremia and hyperkalemia.

A

Addison disease / Primary adrenal insufficiency

  • elevated plasma ACTH
    • low cortisol levels in response to ACTH stim test
  • decreased aldosterone, therefore
    • hyponatremia
    • hyperkalemia
    • hypoglycemia
    • increased BUN & Cr
    • metabolic acidosis
    • eosinophilia
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34
Q

secondary adrenal insufficency

A

no hyperpigmentation and overall decreased ACTH

due to: isolated failure of ACTH production

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35
Q

JAK tyrosine kinase

A
  • the type of tyrosine kinases that GH and prolactin receptors associate with
  • activate STAT
    • which regulates transcription
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36
Q

STAT

A
  • activated by JAK tyrosine kinase (which is activated by association with GH and prolactin receptors)
  • regulates transcription
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37
Q

GH release type

A

GH is a peptide hormone and therefore release is exocytosis

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38
Q

mucosa

A

epithelium

lmaina propria

muscularis mucosae

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39
Q

serosa

A

epithelium and CT

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40
Q

muscularis externa

A

longitudinal muscle and circular muscle

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41
Q

isthmus of gastric mucosa

A

parietal cells

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42
Q

neck of gastric mucosa

A

neck mucous cells

stem cells

parietal cells

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43
Q

base of gastric gland

A
  • peptic cells
  • parietal cells
  • mucous cells
  • neuroendocrine cells
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44
Q

What kind of cells in the stomach make histamine

A

ECL

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45
Q

What kind of cells make gastrin?

A

G cells in the pylorus of the stomach

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46
Q

Gastrin

A
  • made by G cells of the pylorus
  • peptide
  • increases secretion of HCL, pepsionogen
  • Increases motility
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47
Q

What are the direct ways of promoting HCl release from the parietal cells?

A

ACh acts on muscarinic reeptor

Gastrin acts on CCK receptor

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48
Q

Whats an indirect ways of promoting HCl release from the parietal cells?

A

Acetylcholine and gastrin can work to stimulate the ECL cell, which causes the ECL cell to release histamine

  • histamine will then act on H2 receptor to directly stimulate parietal cell to release H
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49
Q

enteroendocrine cells

A
  • “neuroendocrine cells”
  • must be stained with certain antibodies
  • involved in coordination of GI funciton
  • anatomically dispersed throughout GI tract
  • Receive and send signals
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50
Q

three phases of bacteria in stomach

A

1. Active phase -produce ammonia to increase pH through “urase”

2. Stationary phase - attach to a receptor on cell; make proteases, get nutrients from cell, attract leukocytes

3. Colonization phahse - detach from receptor, replicate and then attach to sialic and acid cotaining proteins in mucus blanket

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51
Q

Hormones made in pylorus of the stomach

A

gastrin

somatostatin

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52
Q

histological features of pyloric stomach

A

deep pits and short, coiled glands

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53
Q

histological features of the cardiac stomach

A

equal lengh pits and glands

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54
Q

histological features of the fundic stomach

A

short pits with long glands

55
Q

Identify

A

Microvilli

  • actin filaments extend down where they attach to termianl web
  • core of actin filaments are crosslinked by several actin binding proteins
  • number and shape associate with absorptive capacity
  • glycocalyx is an amorphous coat of glycoprotein
  • have plasmalemma
  • found at apical surface of enterocytes
    • ​have lactase, maltase and sucrase
56
Q

Three places enzymes in duodenum come from

A
  1. liver/gall baldder
  2. microvillus brushboarder of enterocytes
  3. pancreas
57
Q

cholecystokinin

A
  • from intestine
  • slows down emptying of stomach by acting on pyloric sphincter
  • stimulates bile release from gallbladder and secretion of pancreatic enzymes
    *
58
Q

Secretin

A
  • stimulates pancreatic bicarbonate secretin
  • enhances insulin secretion by B cells of the islet of Langerhans
59
Q

Gastrin

A
  • stimulates HCl secretion from parietal cells
  • stimulates insulin secretion from B cells on islet of langerhans
  • stimulates gastric motility and growth of mucosal cells
60
Q

Teniae coli

A

equally spaced bands of outer longitudinal layer of muscularis externa

61
Q

haustra coli

A

sacculations between teniae coli; parts of colon contract independently

62
Q

funcitons of the colon

A
  • recovery of water, salt and fat soluble vitamins
  • Na/K ATPase driven system
  • get fat soluble vitamins derived from bacetrial activity
63
Q

What are some histological features that can help you identify the large intestine?

A

you will not see any villi or plicae

the mucosa has straight, tubular glands that are arranged like testubes

64
Q

Crypts of Liberkuhn

A
  • found in both small and large intestine
  • simple columnar epithelium
  • glands
65
Q

Four cell types of the large intestine epithelium

A
  1. mucus producing goblet cells
  2. absorptive cells
  3. regenerative cells
  4. enteroendocrine cells - release paracrine hormones
66
Q

Hirschprung’s disease

A
  • agangionosis - arrest in migration of neural crest cell (precursor cells for ganglion cell)
  • permanently contracted distal segment - no entry of contents
  • “megacolon” = congenital malformation
  • mutuation in four different genes which regulate differntiation and migration of neural crest cells that form enteric nervous system
67
Q

what does a deficiency of AVP cause?

A
  • recall AVP = arginine vasopressin = ADH
  • an ADH deficiency prevents sodium and water reuptake
  • therefore, deficiency in ADH means the patient cannot concentrate urine, resulting in production of large quantities of dilute urine

note: release of AVP is more sensitive to small changes in plasma osmolarity than to small changes in blood volume

68
Q

what is the most important factor regulating ADH secretion

A

increased plasma osmolarity

69
Q

prolactin inhibits

A

GnRH release (thereby decreasing FSH and LH)

70
Q

menopause

A

permanent cessation of menstruation resulting from loss of ovarian follicular activity

71
Q

where is thyroid hormone metabolized

A
  • IN THE PERIPHERY
  • aka mainly the liver
  • therefore, in graves disease, youre going to have increased cAMP in the THYROID
72
Q

How does estrogen inhibit differentiation and activation of osteoclasts

A

estrogens suppress activation by inhibiting M-CSF and RANK-ligand from the osteoblast

recall: the osteoblast secretes M-CSF , which causes the monocyte precursor to express a RANK receptor, which then binds the RANK-ligand which is secreted from the osteoblast

THIS HELPS EXPLAIN OSTEOPOROOSIS!!! because in menopause, ovaries not producing estrogen, thus estrogen can’t inhibit bone resorption

73
Q

osteoprotegin

A
  • binds to RANK-L and prevents it from causing osteoclast differntiation and activity
  • osteoprotegin is stimulated by estrogen
  • osteoPROTEC(T)gin - it protects against osteoporsis
  • when no more estrogen (menopause), no more osteoprotecgin, therefore, can get osteoporosis
74
Q

hepatic failure effect on TBG

A
  • TBG = thyroxine-binding globulin
  • this is what T3 and T4 bind to in circulation
  • TBG DECREASES in hepatic failure (unlike pregnancy where it increases)
    • this decrease causes
      • decrease in total thyroid hormone levels
      • normal levels of free hormone
75
Q

TBG in pregnancy

A
  • TBG = thyroxine-binding globulin
  • this is what T3 and T4 bind to in circulation
  • TBG INCREASES in pregnancy (unlike hepatic failure where it decreases
  • this increase causes
    • increase in total thyroid hormone levels
    • normal levels of free hormone
76
Q

what enzyme converts T4 to T3

A

5’-iodinase

77
Q

Result of dexamethasone suppression test in patient with Adrenal Cushings Syndrome

A
  • in adrenal cushings syndrome the adrenal gland is just making its own cortisol for no reason
  • therefore, the levels of ACTH are low (its not that the pituitary is secreting too much ACTH)
  • the cortisol secretion will NOT be suppressed by dexamethasone because its not the pituitary’s problem
    • the adrenal gland is just over secreting tumor without the message from the pituitary (ACTH)
78
Q

Result of the dexamethasone supppression test in a patient with an ectopic ACTH secreting tumor (ex: NSCLC)

A
  • with an ectopic ACTH secreting tumor levels of ACTH are high
    • as a result, will have excess cortisol secretion
  • however, because the tumor is ectopic the ACTH is not coming from the anterior pituitary
    • therefore, a dexamethasone suppression test will result in NO suppression
79
Q

Result of the dexamethasone suppression test in a patient with pituitary adenoma?

A
  • pituitary tumor causes increased secretion of ACTH therefore ACTH levels are high
    • high levels of ACTH cause high levels of cortisol
  • using the dexamethasone suppression test WILL result in suppression because the dexamethasone at such a high does will cause the pituitary to get some negative feedback and then should get decr in ACTH and the cortisol prod should decr
80
Q

What conditions can the dexamethasone suppression test be used to differnetiate between?

A
  • cushings syndrome tumor (normal ACTH, adrenal gland secreting excess cortisol)
  • ectopic ACTH secreting tumor (NSCLC)
  • pituitary adenoma (excess ACTH secretion from anterior pituitary)
81
Q

what makes and secretes PTH

A

chief cells of the parathyroid glands

82
Q

what makes calcitonin

A

parafollicular cells of the thyroid gland (“C-cells”)

83
Q

spironolactone

A

potassium sparing diuretic; aldosterone antagonist

used to treat Conn’s syndrome - which is an aldosterone secreting tumor

84
Q

what factors increase 1 alpha hydroxylase activity

A

1 alpha hydroxylase makes active form of vitamine D in the kidney!!!

decr serum calcium

incr PTH

decr serum phosphate

85
Q

decreased Ca

increased PO4

response to PTH administration

A

hypoparathyroidism

(note: increase in PO4 is incr in blood PO4 , while the urinary phospahte is decraesed (becasuse more is reabsorbed into systemic circ))

86
Q

decr Ca

decr PO4

A

vit D deficiency

87
Q
A
88
Q

onset of menopause is indicated by

A

onset of irregular menses

89
Q

what causes contractions in early labor

A

estrogen induction of PROSTAGLANDIN!!!!

90
Q

placental hPL

A

increases diabetogenicity in pregnancy; glucose is major energy source for the fetus; therefore hPL (which is similar to prolacitn) inhibits maternal glucose uptake in order to provide more avaliable glucose for baby

91
Q
A
92
Q
A
93
Q
A
94
Q
A
95
Q

What delays puberty in boys?

A
  • decreased leptin
  • obesity
96
Q

What does elevated leptin do to puberty in females?

A

causes precocious puberty

97
Q

What does definitive zone give rise to?

A

zona glomerulosa

98
Q

what does the transitional zone give rise to?

A

zona fasiculata

99
Q

3rd pharyngeal pouch

A

thymus and the inferior part of the parathyroid gland

100
Q

cleft

A

outside

101
Q

pouch

A

inside

102
Q

arch

A

cleft outside and pouch inside; the arch is the whole thing

103
Q

what does the arch come from

A

mesenchyme

104
Q

when do pharyngeal arches go to develope face, palate, ears

A

wk 4

105
Q

how does the external auditory meatus form?

A

when the cleft meets up with pouch

pharyngeal arch 1

106
Q

what does #2,3,4 form?

A

cervical sinus

107
Q

what nerves do the pharyngeal pouches correspond to

A

Mandibular (V)

Facial (VII)

Glossopharyngeal (IX)

Vagus (X)

108
Q

what are the three parts of the intermaxillary segment

A

labial

jaw

palate

109
Q

What nerve comes from the midbrain

A

V3

110
Q

What nerves of the pharyngeal pouches come from the hindbrain

A

facial, glossopharyngeal, vagus

111
Q

location of the myoid cells (aka the myoepithelial cells)

A

between the basement membrane and the plasma membrane of the sertoli cells

112
Q

5 alpha reductase

A

causes the conversion of testosterone to DHT

113
Q

What information does the carotid sinus sense and how does it take that information to the brain?

A

the carotid sinus has baroreceptors therefore senses pressure; communicates informatino to brain via the glossopharyngeal nerve (IX)

114
Q

lactose

A

glucose + galactose

115
Q

what kind of cells predominate in the sublingual gland?

A

mucus secreting cells ; apical region is occupied by mucin-filled secretory vesicles

116
Q
A
117
Q

epithelium in stomach

A

simple columnar

118
Q
A
119
Q

gastrulation

A

week 3 - converts bilaminar embryo to trilaminar embryo

120
Q

intermediate mesoderm

A

part of mesoderm that gives rise to

  • UG system
    • ducts
    • seminal vesicle
    • upper vagina
121
Q

what gives rise to prostate

A

Endoderm

122
Q

what gives rise to urinary bladdar??

A

endoderm

123
Q

_____ is a longitudinal elevation of the intermediate mesoderm

A

urogenital ridge

  • recall gonadal/genital ridge appear on the midline of the urogenital ridge
124
Q

Describe the descent of the testes

A
  • reach inguinal region around 12 weeks
  • acutally migrate through the inguinal canal ~28 weeks
  • reach scrotum 33 weeks
125
Q

cryptorchidism

A
  • testes doesnt descend as they should
  • either remains in inguinal region, pelvic cavity or at top of scrotum, rather than descending to their normal location toward bottom of scrotum
126
Q

when is genetic sex determiend?

A

at fertilization

127
Q

secondary cortical cords

A

only develop in females; do not develop in males

128
Q

what do testes cords contain?

A

germ cells and sertoli cells

129
Q

what do leydig cells derive from?

A

mesenchyme

130
Q

in males, what do mesonephric ducts devleop into

A

the leydig cells make testosterone, which allow mesonephric ducts to develop into: epididymous, vas deferens , seminal vesicle, ejaculator duct

131
Q

what is the normal path of sperm

A

seminiferous tubules –> rete testes –> efferent tubules –> epididymus -> vas deferens

132
Q

cloaca

A

expanded caudal poriton of hindgut

133
Q

urorectal septum

A

divides the cloaca into the rectum and the urogenital sinus

134
Q

UG sinus in male becomes

A

bladder, bulbourethral glands, prostate, most of male urethra

Block 4: Endocrinology (4 decks)

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