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Unit 1 Flashcards

1
Q

Peds Os Coxa (Innominate) - what features ensure us that the os coxa is pediatric and when does it fuse

A

Triradiate cartilage

fuse by 25 yo

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2
Q

what makes up SI joint

A

auricular surface of os coxa articulates with sacrum

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3
Q

pubic symphysis: Why is it this kind of joint?

A

only want movement during child birth (flex and expand)

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4
Q

sacrospinous lig

A

ischial spin to sacral spine

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5
Q

between sacrotuberous lig and sacrospinous exiting greater sciatic foramen

A

pudendal n and int. pudendal art. and vein

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6
Q

through gap in obturator membrane

A

obturator n, a, v (L2-L4) -> med compartment of thigh

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7
Q

what forms Pudendal n.

A

S2-S4

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8
Q

weak spot of pelvis and what does it effect?

A

pubic rami
will effect pelvic stability
could have laceration or rupture of internal organs (bladder)

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9
Q

Through pelvic inlet:

S1 of sacrum to sup pubic symphysis anteriorly

A

true pelvis

reproductive organ

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10
Q

sup. to pelvic inlet is:

A

false pelvis: inf. abdominal viscera

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11
Q

most post. muscle

A

coccygeus and overlying sacrospinous lig

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12
Q

levator ani fxn

A

supports and elevates ligament, fecal continence
tonically contracted
all posterior to rectum

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13
Q

innervation for levator ani

A

pudendal n.

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14
Q

other attachment of levator ani

A

attachment to tendinous arch (central thickening of fascia of internal obturator)

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15
Q

what grades are stretching and tearing of pelvic floor during pregnancy?

A

skin, fascia (grade 1)

levator ani components (grade 2)

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16
Q

consequences of tearing levator ani?

A

incontinence

urinary stress incontinence (sneeze, cough, sudden laugh/intra-abd pressure)

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17
Q

rectovesical pouch - clinical relevance?

A

collects fluid if standing up - most inf point of abd cavity (blood internal hemorrhage, pus from infxn, ascites)

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18
Q

what is migration of testes?

A

start sup. lumbar region and migrate down, and is guided by gubernaculum (fibrous tract) and connected to deep inguinal ring

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19
Q

diverticulum of peritoneum/porcessus vaginalis and fxns to:

A

push it’s way through abd layers and forming inguinal canal and pulls along abd wall to cover spermatic cord and scrotum
creates serous potential space that covers testes and forms tunica vaginalis - covers testes

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20
Q

Crytorchidsm

A

when testes don’t descend - usu along their natural migration

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21
Q

dartos fascia fxn and make up:

A

dartos muscle is within = smooth muscle

will crincle up skin of testes to elevate if temp cools

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22
Q

epididymis parts and fxn:

A

head = receives form
body
tail = convuluted and straightens and becomes continuous with ductus/vas deferens

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23
Q

ductus deferens what’s inside?

A 
spermatic cord
testicular artery (from abd aorta because testes move down) 
pampiniform venous plexus
cremateric fascia and musc. 
internal and external spermatic fascia
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24
Q

drainage of testicular v

A

L testicular v = renal

R testicular v = IVC

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25
Q

testicular torsion causes and progression

A

usu. congenital abnl of processus vaginalis
twisting of spermatic cord
occlude pampiniform venous plexus -> back up of venous blood -> edema and swelling -> compress testicular artery
no anastomoses -> ischemia

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26
Q

variococele

A

more often on left side -> more acute angle, and more pressure -> valves may be more dysfxn
if pain -> could be cancer, tumor

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27
Q

ductus deferens, what does it join?

A

joins seminal gland/vesicles and secretes seminal fluid -> forms

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28
Q

trigone in bladder -> demarcated by?

A

openings of ureters and inf opening of urethra

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29
Q

male urethra - different parts?

A

intramural in neck of bladder
prostatic -> goes through prostate where it first receives semen, combines with seminal and prostatic fluid
short intermediate or membranous
penile or spongy urethra

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30
Q

prostatic urethra contains:

A

prostatic ducts + opening of ejaculatory duct

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31
Q

which ducts pass through perineal membrane?

A

bulbourethral glands

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32
Q

BPH (benign prostate hypertrophy)

A

central/middle part and impinges on prostatic urethra and can push up on neck of bladder and bladder

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33
Q

complications of BPH

A

dysuria

urgency

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34
Q

post and sup to bladder

A

uterus

anteverted (anteplex orientation) = most common

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35
Q

Female pouch/continuation of abd cavity

A 
vesicouterine pouch (ant and smaller)
rectouterine pouch (pouch of Douglas) -> lowest point
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36
Q

permetrium joins with

A

perineum

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37
Q

myometrium fxn:

A

contracts during childbirth
dilation of cervix
generate force to expel fetus

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38
Q

endometrium fxn:

A

grow new BV and where implantation occurs, and is shed during monthly cycle if no fetus

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39
Q

narrowing of uterus

A

isthmus

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40
Q

opening of uterus

A

internal os

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41
Q

what part of uterus atrophies post menopause

A

body of uterus

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42
Q

fxn of fimbrae

A

projects into ovary, guide egg as ovulated from ovary

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43
Q

fertilation usu in?

A

ampulla

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44
Q

where can ectopic pregnancy occur?

A

peritoneum cavity, uterine tube

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45
Q

Broad ligament

A

covering and surround uterine tube = mesosalpinx
mesentary = mesovarium
mesometrium = remaining

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46
Q

insertion of round ligament

A

labia majora (analagous to spermatic cord, remnant of gubernaculum also ligamen of ovary is remnant)

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47
Q

ligament of ovary fxn

A

tethers ovary

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48
Q

suspensory ligament

A

covers ovarian vessels (arteries and veins)

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49
Q

ovarian a. comes from?

A

abd aorta

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50
Q

ligaments

A

thickening of endopelvic fascia
tranverse cervical
uterosacral

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51
Q

primary support of uterus?

A

bladder

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52
Q

uterine artery relationship and where does it come from?

A

ant and sup to ureter
and from int iliac
so don’t clamp/cut ureter with historectomy

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53
Q

Uterine artery anastomoses

A

with ovarian

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54
Q

Vaginal artery anastomoses

A

with internal pudendal

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55
Q

Ischial tuberosity and pubic symphysis comprise what?

A

urogenital triangle

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56
Q

Ischial tuberosity and coccyx comprise what?

A

anal triangle (at an angle to urogeneital triangle, not flat)

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57
Q

contents of deep perineal pouch in females

A

urethra passes through

  1. urethral sphincter
  2. (transverse over sup. perineal memb) deep trans. perineal m.
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58
Q

Contents of Deep Perineal pouch in males

A
  1. bulbourethral gland
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59
Q

sup. pouch in females (DOUBLE CHEC?)

A
  1. bulbs of vestibule
  2. crus -> angle body and glans of clitoris
  3. ischiocavernosus
  4. bubospongiosus
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60
Q

sup. pouch in males

A
  1. crus of penis
  2. bulb of penis
  3. ischiocavernosus around the crus
  4. bulbospongiosus musc. around bulb of penis
  5. sup transverse per.
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61
Q

corpus spongiosum expands to form

A

glans penis

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62
Q

deep dorsal vein relationship

A

post to fascia and imp for erection

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63
Q

nerve blocks in female perineum

A

ilioinguinal n. block if still feeling pain

pudendal n. (esp. for tearing during childbirth -do near ischial spine for most prox)

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64
Q

what is Prader classification?

A

degrees of virilization where stage 0 is nl female and 5 is nl male

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65
Q

testing of virulization

A

FISH for Y (probes for SRY) and can get back within 48 hrs
karyotype and microarray takes a couple days
further work-up if SRY is present
imaging = US for presence of uterus
laparoscopy = best way to eval

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66
Q

46, XX DSD DDx?

A

95% CAH
46, XX sex reversal (SRY translocation onto X)
Ovotesticular DSD (both ovarian and testicular tissue) -> most have xx karyotype, mom exposed or has high androgens

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67
Q

what makes SRY so easy to translocate

A

proximal pseudoautosomal region of Y

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68
Q

46, XY DSD pure gonadal dysgenesis

A

present with lack of puberty - no breast development or menstrual cycle because internal and external is female but no ovaries

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69
Q

mixed gonadal dysgenesis (45x/46,xy)

A

mosaic -> different karyotype in different cells
usu testes on one side and streak gonad on other side
testes is usu abnl

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70
Q

testicular regression

A

usu within first year

present with cryptorchidism

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71
Q

46, xy WT-1 mutation

A

present with bilateral wilm’s tumor before they did lots of genetic testing
androgen insensitivity was initial dx

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72
Q

46, xy, der(9)t(2;9)(p22.2;p24.3) underexpression of DMRT2

A

gonadal dysgenesis
female genetalia
mental delays
orig. dx of androgen insensitivity

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73
Q

46, xy DSD

A

any of these, not enough testosterone
under virulized xy
- 5alpha reductase

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74
Q

5 alpha reductase deficiency

A

undervirulized but degree varies
testes usu in inguinal canal or labial-scrotal folds (should be able to palpate gonads)
wollfian ducts differentiated
make AMA so don’t have mullerian structures
at puberty, spontaneous virilization occurs (at puberty type 1 is expressed and test. can be converted to DHT
Type 2 in newborn is deficient

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75
Q

Androgen insensitivity syndrome

A

mut in androgen receptor gene

complete -> picked up in childhood (hernia) or puberty with primary menorrhea

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76
Q

CAIS

A

XY - testes develop, can’t respond to testosterone though they are making, wollfian ducts mostly regress, testes make normal AMA so mullerian structures go away -> no internal duct system

External - very female, no clitoral megaly, nl labia, separate urethra/vagina openings
vagina ends into a wall -> no cervix or uterus

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77
Q

CAIS

A

gonads intra-abdominal or inguinal canal because testost. needed for descent
bilateral inguinal hernias common
at puberty, spontaneous breast development because such high testosterone from testes that is converted to estrogen
little or no pubic/axillary hair
female gender identity

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78
Q

what is management of CAIS?

A

avoid gender assignment before expert evaluation (esp at birth or before thorough eval)
center with experienced interdisciplinary team -> endo, urologist, gyn, psych, geneticist
communicate with pt/families, respect concerns and address in confidence

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79
Q

DSD Outcomes

A

gender dysphoria underestimated in past and gender counseling as well as sexual counseling should be part of multi-disciplinary service available to pt with DSD
try not to encourage surgery

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80
Q

what is precursor to all steroid hormones?

A

cholesterol

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81
Q

3 B HSD converts what to what?

A

pregnenolone to progesterone
17OHpreg -> 17OHprogesterone
dehydroepiandrosterone -> androstenedione

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82
Q

what happens when cortisol goes down

A

increased CRH and ACTH

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83
Q

CAH pathophys?

A

one of many enzyme def that leads to decreased cortisol, and increased CRH/ACTH
drives adrenal gland to make more hormones in pathways that aren’t affected by def.

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84
Q

CAH enzyme def

A 
21-hydroxylase = 95%
11B-hydroxylase = ~5%
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85
Q

21 hydroxylase def hormone pattern?

A

decreased cort and aldo
increased androgens
most prominent feature = virilization

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86
Q

Clinical features of 21 OHase def?

A 
female = virilization of external genitalia - clit megaly, GU sinus aka one opening (mullerian develops fine and no wollfian ducts develop) 
males = nl external genitalia

hyperpigmentation
- MSH and ACTH from POMC (more MSH and ACTH can bind to MSH receptor)
hypoNA, hyperK due to aldo def.
mild forms - present later with early pubic hair, axillary hair, penile/cliterol enlargement

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87
Q

KNOW THIS: Dx of 21 OHase def?

A

dx suspected in virilized XX infant or XY with hypoNA and hyperK and vomiting
measure 17OH progesterone -> now on newborn screen

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88
Q

KNOW THIS: Tx of 21 OHase def?

A

surgery in females
replace def hormones and suppress ACTH overproduction
Glucocort (hydrocortisone and increased for illness/stress), mineralcort (florinef and salt supplements) , acute adrenal insufficiency - IM/IV solu-cortef

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89
Q

11BOHas def

A

virilization similar to 21-OHase def
no salt wasting
HTN frequent finding
more of late dx

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90
Q

StAR protein clinical features

A

rare

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91
Q

3B HDD

A

virilization in girls = similar to 21 OHase def

undervirilization in boys = difference between 21 OHase def

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92
Q

17alpha OHase, 17,20 Lyase Def

A

decr. androgens
but no def. of aldo
HTN secondary to incr 11-deoxycorticosterone
hypoK
female failure to develop 2ry sex characteristics at puberty
male = undervirilized

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93
Q

Which def are salt wasting and which one arent?

A 
Salt Wasting
- 3B HDD
- StAR protein Def
No Salt Wasting
11B-OHase Def
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94
Q

Pathophys of StAR protein Def

A

Cholesterol stays in cholesterol ester -> fatty adrenal gland = lipoid in adrenocortical tissue
StAR involved in transfer of cholesterol from outer to inner mito membrane

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95
Q

KNOW THIS: Monitoring Tx of 21-OHase Def?

A

Lab: 17OHP, androstenedione, testosterone
Growth
Skeletal Maturation

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96
Q

what gives rise embryologically to all GU system?

A

intermediate mesoderm

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97
Q

what are cardinal steps in mullerian dev?

A 
elongation 
fusion
canalization
septal resorption 
\+ union of mullerian (cephalad) with GU sinus (caudad)
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98
Q

cloaca divides into

A

anal and GU

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99
Q

sinovaginal bulbs

A

develop vagina from that

where mullerian system connects

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100
Q

upper vagina develops from?

A

paramesonephric duct (mullerian)

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101
Q

lower vagina develops from?

A

GU sinus (not skin) and migrates out

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102
Q

uterine tube migration

A

comes together to form fundus of uterus at top and bottom (septal/walls of tube) part has to resorb to form uterus

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103
Q

Obstructive lesions - sx depends on level of obstruction

Vagina obstruction

A
  • imperforate Hymen - failure of caudal end of sino-vagninal bulbs to canalize
  • transverse vaginal septum - Failed Canalization of the Vaginal Plate. this is where the Mullerian ducts meet Urogenital Sinus
  • Vaginal atresia
    Failure of Canalization of Urogenital Sinus Below Vaginal Plate
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104
Q

when is intervention probably not necessary?

A

If it doesn’t obstruct menstrual flow, affect fertility, or affect sexual function.

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105
Q

Imperforate Hymen Tx:

A

blue discoloration behind hymen - blood building up

- tx: surgery, very easily

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106
Q

transverse vaginal septum Tx:

A

more superior and thicker than hymen
excise
area is demuted and have to stitch close

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107
Q

Vaginal atresia Tx:

A

no vagina or uterus
incision posteriorly and skin graft is made and placed
bed rest so skin is re-vascularized

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108
Q

Failed cardinal steps of dev: elongation

A

mullerian agenesis

Unicornuate Uterus

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109
Q

Failed cardinal steps of dev: Fusion

A 
uterine didelphys 
(2 cervix)
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110
Q

Failed cardinal steps of dev: septal reabsorption

A

septate uterus

2 uterus, 1 cervix, 1 vagina

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111
Q

Which chromosome is androgen receptor gene on?

A

x chromosome

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112
Q

what is default pathway for genitalia dev?

A

female
wollfian ducts will involute and die
without AMH -> mullerian ducts differentiate
dev of female ducts and external genetale is indep of gonadal hormones
If no gonads, female format
results

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113
Q

Leydig cells fxn

A

make testosterone (95%) which move into sertoli cells
- spermatogenesis
make StAR and SCP (sterol-carrier protein)
- Transport cholesterol to mitochondrial side chain
cleavage enzyme
- Stimulate steroidogenesis

Respond to LH through a G-protein coupled
receptor (GPCR)

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114
Q

sertoli cells fxn

A

FSH - stim aromatase to make estrogen

form blood testes barrier
- AI response to own sperm (don’t want) and want to protect from pathogens/toxins

nurture developing sperm
APB - conc. locally so right level for spermatogenesis
secrete inhibin and other growth factors - in response to FSH
respond to FSH through GPCR

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115
Q

Cross-talk between Leydig and Sertoli cells via FSH

A
  • FSH also induces release of other Leydig cell growth factors from
    Sertoli cells (TGFa, TGFB, IGF-1, FGF-2)
  • FSH (acting on Sertoli cells) regulates proliferation and
    development of Leydig cells to provide adequate Testosterone for spermatogenesis
  • Testosterone from Leydig Cells synergizes with FSH to increase
    Androgen binding protein (ABP) production in Sertoli cells to
    maintain high local T concentrations
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116
Q

Hypothal-Pit-Testicular Axis

A

GnRH stimulates production of
FSH and LH from pituitary

LH acts on Leydig cells
 Increased Testosterone
 Increased StAR and SCP

FSH acts on Sertoli Cells
 Increased Androgen binding
protein (ABP)
 Increased Aromatase
 Increased growth factors
 Increased spermatogenesis
 Increased inhibin
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117
Q

H-P-T Axis: Neg. Feedback

A
  • Androgens (Testosterone) inhibit release of GnRH from
    hypothalamus
  • Androgens (and Estrogen) inhibit LH and FSH release from pituitary
  • Inhibin suppresses FSH production from pituitary gonadotrophs
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118
Q

hCG: role in doping in sports?

A

LH substitute -> stim testosterone release

  • would have to be pulsatile because these hormones are
  • stimulates fetal tissue to produce testosterone
  • hCG can be produced from some cancers
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119
Q

what happens with aging in males with FSH/LH if gonadal fxn is compromised?

A

in males pituitary fxn starts to decline -> produce less LH/FSH even with loss of neg feedback with steroid hormones

decr spermatogenesis => decr. inhibin -> elevated FSH

FSH is sensitive marker of fertility in males

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120
Q

Actions of Androgens?

A

 Differentiation and development of male internal and external
genitalia-T, DHT
 Initiation and maintenance of Spermatogenesis-T,DHT, E
 Development and maintenance of 2nd sex characteristics
 Anabolic

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121
Q

Actions of Androgens specifically with dev. and maintenance 2ry sex characteristics?

A

 Growth of external genitalia-T, DHT
 Male pattern of hair growth-DHT (baldness) also beard growth
 Sebaceous gland secretions-DHT
 Inhibition of breast growth (mammillary gland) -T
 Behavioral responses, Libido-T, E, DHT
 Negative feedback at hypothalamus, pituitary-E, T
 Stimulation of Androgen binding protein synthesis-T

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122
Q

Androgens action on Liver?

A

incr VLDL, LDL and decr HDL

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123
Q

Anabolic androgen action?

A

Muscle growth, strength
beer belly
bone growth - T -> E via aromatase

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124
Q

before puberty levels of LH/FSH?

A

FSH> LH

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125
Q

after puberty levels of LH/FSH?

A

LH> FSH

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126
Q

Male Pubertal Growth hormones?

A

 Increased Growth Hormone

 Increased Testosterone

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127
Q

growth spurt in females?

A

higher estrogen dampens growth and counters growth hormone

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128
Q

Male growth spurt?

A

Pubertal growth spurt
 Average 28cm (11”)
 Accounts for 10cm (4”) height disparity in males vs females

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129
Q

Post pubertal males comparison to females?

A

 150% of female muscle mass
 150% of female skeletal and lean body mass
 200% of female muscle cell number
 50% of female body fat

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130
Q

Effects of androgens mediated by?

A

ONE ANDROGEN Receptor
Hormone Dependent TF
- specific to organs or tissues though
-Effects mediated by same receptors and molecular
mechanisms
 Interactions with Insulin-like growth factor (IGF-1)/
Growth Hormone (GH) axis

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131
Q

Androgens and Growth Androgenic Effects

A

 Growth and development of male reproductive tract
 Secondary sexual characteristics
 Behavioural responses

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132
Q

Androgens and Growth

Anabolic Effects

A

 Growth of somatic tissue
 Linear body growth (long bones)
 Nitrogen retention, protein synthesis
 Muscle development

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133
Q

What happens with too much testosterone?

A
  • converted to estrogen

- so want to prevent, Aromatase inhibitors etc.

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134
Q

Interaction of the GH/IGF-1 and HPT axes

A 
 GH/IGF-1 stimulate
gonadal functional
 IGF-1 stimulates
GnRH secretion
 Testosterone and
Estrogen stimulate GH
secretion and growth
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135
Q

GH effect on long bone growth?

A 
GH causes balanced growth and
ossification; bones continue to
lengthen through childhood and
pubertal ages under its influence in the
absence of sex steroids.
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136
Q

sex steroids effect on long bone growth?

A 
promote ossification 
epiphyses narrows and eventually closes 
• Stimulates bone growth
• Accelerates bone maturation
• Promotes epiphyseal closure
• Dominant effect is to narrow growth window limiting
long-bone growth
• Growth ’levels off’ after puberty ( under control of
GH/IGF-1 axis)
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137
Q

how does pre-pubertal abuse of steroids look?

A

grow faster then end up shorter
rapid rate of growth but end up shorter
(could be using because congenital anomaly causes need for steroids)

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138
Q

Consequences of Steroid Abuse? GU

A

 Infertility-decreased sperm production
 Gynecomastia- breast development
 Testicular atrophy
 Fluid retention, Kidney failure

139
Q

Consequences of Steroid Abuse? CV

A

 Increase LDL decreased HDL-atherosclerosis
 High blood pressure
 Heart attack and stroke
 Enlargement of left ventricle

140
Q

Consequences of Steroid Abuse? Psych and Drugs

A

 Psychiatric disturbances- mania, delusions, rage & irritability -> anecdotal in humans and seen in animal models, insomnia
 Gateway drug b/c injectable -> Increased risk of HIV or hepatitis and other infections

141
Q

Consequences of Steroid Abuse? Hair/Bones/Liver/Skin

A

 Baldness and excessive body hair
 Short stature
 Tendon rupture - disproportionate musc. dev.
 Liver cancer, pelios hepatis (blood filled cysts)
 Severe acne, cysts, oily scalp

142
Q

hypogonadotropic hypogonadism

A

testes nl, baby is making plenty of testosterone in first trimester, penis is nl,
2nd phase of testicular dissent (b/c decr testosterone in 2nd and 3rd trimester)
- lack of puberty due to absence of GnRH and/or gonadotropin secretion from brain
- characterized by low gonadotropins
- complete or partial, temp. or permanent

143
Q

puberty in fetus/infancy?

A

not de novo event (reactivation because active from 2nd trimester on)

  • active in fetal development
  • continues to fxn in infancy “mini-puberty” (boys only until 6 mo, 18 mo in girls -> gives idea of what is developing)
  • after infancy, axis enters quiescent state, referred to as juvenile pause
144
Q

In juvenile pause what NT is higher?

A

Gabba, more inhib

keeps pre-pubertal

145
Q

indicator of puberty?

A

LH > FSH pulses at night

146
Q

HPG axis during puberty?

A

process is gradual

GnRH increasing first at night and increased LH

147
Q

pre-puberty hormones?

A

FSH> LH

148
Q

Lab evidence of Puberty?

A

Leuprolide = analoge of GnRH
look at response of LH
pubertal respons is > 5.6mlU/ml

if give and LH peaks at 2 or 3 -> pre-pubertal

149
Q

physical changes of Gonadarche (girls) -> due to estrogen

A 
breast dev. 
genital growth (labia minora) 
maturation of vaginal mucosa
uterine/endometrial growth
body comp changes (female fat distribution - hips) 
menarche (estrogen and progesterone)
150
Q

Only change early on in boys for gonadarche?

A

enlargement of testes (mediated by FSH and LH) - @ 4-5 ml of testes -> can happen 6mo to yr before pubic hair

151
Q

physical changes of Gonadarche (boys) -> due to testosterone from testes or adrenals

A 
scrotal changes (thins) 
sexual hair (upper lip, chin, sideburns, axilla, pubic area) 
penile growth 
prostatic/seminal vesicle growth 
deepening of voice (late) 
incr muscle mass (late)
152
Q

physical changes of Gonadarche (boys and girls)

A

linear growth acceleration
bone age advancement - mediate by estrogen in both boys and girls and testosterone is converted by aromatase enzyme in boys

153
Q

Aromatase inhibitor to pubertal boy?

A

slows skeletal maturation

testosterone goes through the roof

154
Q

Adrenarche what is it and what does it cause?

A

increased adrenal androgens (DHEA-S, androstenedione) which cause pubarche
girls - pubic hair, axillary hair, body odor, and acne -> because ovaries aren’t making
in boys - androgen is androgen
-> causes same changes but not specifically from adrenals

155
Q

Timing of Puberty Tanner 2 Breast development - Girls

A

early age, mean
white - 8 yrs, 10.4 years
black - 6.6, 9.5
Hispanic - 6.8, 9.8

156
Q

Menarche for caucasians?

A

between tanner 3 and 4 generally

157
Q

menarche for girls?

A

early age, mean
white - 10.65 yrs, 12.55 years
black - 9.7, 12.06
Hispanic - 10.05, 12.25

158
Q

Tanner stages- Breast

A 
1 = pre-pubertal
2 = breast bud, just under or extended from areola
159
Q

Tanner stages- Pubic

A

Stage 1: Prepubertal (can see velus hair similar to abdominal wall)
Stage 2: Sparse growth of long, slightly pigmented hair, straight or curled, at base of penis or along labia
Stage 3: Darker, coarser and more curled hair, spreading sparsely over junction of pubes
Stage 4: Hair adult in type, but covering smaller area than in adult; no spread to medial surface of thighs
Stage 5: Adult in type and quantity, with horizontal distribution (“feminine”)

160
Q

Timing of Puberty - boys

A

testes > 3 ml = 11.8 yo (9-14)
pubic hair = 12 y0
penile enlargement = 13 yo
peak height velocity = 14 yo (mid to late puberty = fast growth) w/ more musc mass and deepening of voice

161
Q

Tanner Stages boys

A

pubic hair and testicular volumes stages
genital stages- professor disregards

4 = triangular
5 = diamond shape
162
Q

delayed puberty criteria for dx?

A

no pubertal signs by 13 yrs in girls and 14 yrs in boys

or lack of progression

  • no menarche by 4 yrs after onset of breast development (puberty starts)
  • no completion of genital growth in boys after 5 years
163
Q

bone age and puberty?

A

onset of puberty is commensurate with child’s biologic age (bone age)
- girls start at bone age of 10.5 - 11
boys = 11.5-12

164
Q

delayed puberty and hormones

A
  • low gonadotropins = hypogonadotropic (or central hypogonadism)
  • elevated gonadotropins = hypergonadotropic (or primary) hypogonadism
165
Q

constitutional growth delay

A
  • onset and progression of puberty corresponds with bone age
  • growth continues later in life but reaches height potential
  • FH of “late bloomers”
  • decelaration of linear growth w/i first 2 yrs of life
  • normal linear growth after this with delayed bone age
166
Q

Tx of constitutional delay

A

reassurance

  • for boys sometimes short course testosterone, for girls, short course of estrogen
  • re-eval in 4-6 mo
167
Q

difference between constitutional delay and hypogonadotropic hypogonadism

A

bone age (if older and no puberty might be hormones)

  • presence/absence of adrenarche
  • HGHG = boys and girls -> gonadarche and adrenarche is delayed
  • adrenarche will start when it should
168
Q

unicoid body habitus

A

arms and legs are longer than should
not going through puberty at right time
low upper to lower ratio
arm span bigger than hight

169
Q

Congenital causes of HGHG

A

part of multiple hormone deficiencies - septo-optic dysplasia -> mult pit def from abnl brain development

  • genetic syndromes = prader-willi syndrome (most common)
  • hypotonia, wants to eat a lot
170
Q

IHH = idiopathic hypogonadotropic hypogonadism

A

absence of any structural abnormalities of hypothalamus or pituitary
isolated defect in GnRH or gonadotropins

171
Q

Kallman syndrome ?

A

IHH plus anosmia/hyposmia

  • agenesis of hypoplasia of olfactory sulci and/or lobes
  • association between from defect in shared developmental origins of GnRH and olfactory neurons -> migration of neurons
  • genes assoc with IHH = Kal-1, FGFR1 … -> only accounts for 30% of cases
172
Q

Fxn’l or revesible causes of HGHG

A

chronic illness, malnutrition
stress, excessive exercise (even in absence of low body wt)
anorexia, hyperprolactinemia(oma), hypothyroidism

173
Q

Acquired Causes of HGHG?

A

pituitary or hypothalamic tumor, cranial irradiation, CNS infection, infiltrative diseases (histiocytosis, granulomatous disease, hemachromatosis), AI hypophysitis

174
Q

HGHG

A

primary gonadal failure leads to decr. neg feedback

high LH and FSH - most common in girls = Turner Syndrome

175
Q

Primary Ovarian Failure

A
  • Turner Syndrome
  • XX or XY complete gonadal dysgenesis (XY = SRY, no testes - not picked up until puberty because don’t start, will have adrenarche, nl internal and external genitalia, usu tall)
  • galactosemia
  • radiation
  • chemotherapy (alkylating agents)
  • AI
176
Q

Turner Syndrome

A
  • Frequent
  • 45, X karyotype in 50% with the rest being moasaics or structural abnormalities of X chromosome
  • may have no phenotypic characteristics except for short stature
177
Q

Turner Syndrome phenotype percentages

A

100% short stature
94% ovarian failure
CV, thyroiditis, hx of otitis, dysmorphic facies = common

178
Q

Primary Testicular Failure

A
  • Klinefelter’s Syndrome
  • cryptorchidism
  • testicular regression syndrome
  • radiation (usu ok testosterone but lower sperm)
  • chemotherapy
179
Q

Klinefelter’s Syndrome

A

most common, typically present with gynecomastia, smaller testes than expected for degree of virilization - tanner 4, usu don’t present with delayed puberty, miss because don’t check testes size
- 1/1000
47, xxy (or can have 3 or 4 x -> more X, more dev probs and behavioral probs)
- hyalinization and fibrosis of seminiferous tubules

180
Q

phenotype Klinefelter’s Syndrome?

A

microphallus, infertil, small testes, learning disabilities, eunochoid, delayed or arrested puberty, gynecomastia, infertility

181
Q

Eval of Delayed Puberty

A

bone age (growth delay, hypothyroid… why?

  • if bone age is older -> check labs
  • Labs: gonadotropins, test in boys and estradiol in girls, may consider TSH, T4, Prolactin, CBC, ESR, BMP
  • karyotype if elevated gonadotropins
182
Q

Tx of hypogonadism

A
  • Boys
    testosterone Q3-4 wks initially low dose to gradually incr (gels are annoying)
  • Girls
    estrogen alone followed by cyclic therapy with estrogen and progesterone (add if have uterus like in Turner)
183
Q

Complete Precocious Puberty Signs

A 
onset and progression of changes
- accel linear growth
- advancement of skeletal age
Can be:  
- Central (GnRH dependent) 
OR
- Peripheral (GnRH independent)
184
Q

Incomplete Precocious Puberty

A 
benign thelarche
benign adrenarche 
Defn: 
boys - dev prior to 9 yrs of age
girls - dev prior to 8 yr in caucasian, 6.5-7 in AA and hispanic
185
Q

Central Precocious Puberty

A

same physical ∆ and lab testing are consistent with progressive ∆ of HPG axis activation

  • 5% in girls = CNS abnormality
  • 50% of time in boys is caused by CNS abnormality - lower threshold to image boys because more common
186
Q

Central Precocious Puberty Causes

A
  • Hypothalamic Hamartoma (present in first 2-3 yrs of life)
  • treat medically

anything that disrupts inhibition of HPG axis

  • suprasellar tumor
  • hydrocephalus
  • previous CNS infection
  • major head trauma
  • cranial irradiation
187
Q

Causes of Peripheral Puberty

Girls: Estrogen mediated

A

Ovarian cysts
granulosa cell tumor
exogenous estrogens
lavender or tea tree oil products

188
Q

Ovarian cysts

A

ovarian follicles form cysts (prepubertal FSH stimulation, can secrete estrogen for breast development but usu present with vaginal bleeding)

  • areola gets dark as estrogen increases but as estrogen goes down - causes bleeding
  • trans-abdominal US to assess and do it at that time
  • assoc with McCune- Albright Syndrome
189
Q

McCune-Albright Syndrome

A

lethal if mutation in all cells

  • constituative activation in alpha subunit of stim G-protein
  • triad of precocious puberty, cafe-au-lait spots (doesn’t cross midline usu or follows dermatome), polyostotic fibrous dysplasia (MOST COMMON)
  • can also have GH excess, hyperthyroidism, Cushing’s syndrome
190
Q

Peripheral Precocious Puberty Boys

A

Adrenal tumor
Leydig cell tumor
hCG secreting tumor (LH like, stims Leydig cells to make testosterone)
McCune-Albright Syndrome (rare)
Late-onset congenital adrenal hyperplasia

191
Q

presentation of adrenal tumor and late-onset congenital adrenal hyperplasia

A 
pubic hair
maybe axillary hair
maybe some growth acceleration
testes = small (no LH/FSH)
bone age advancement

LABS differentiate between the two

192
Q

hCG secreting tumor

A
  • testes a little bit enlarged but not as large as central precocious puberty
  • more virilization compared to how big testes are
193
Q

Familial testotoxicosis

A

Periph precocious puberty in boys

  • testes somewhat enlarged from leydig hyperplasia
  • high testost from early on
  • sign. penile growth
  • mutation of LH receptor - activated
  • AD with only male penetrance
  • Autonomous Leydig cell activity
  • more virilization compared to how big testes are
194
Q

severe primary hypothyroidism

A

TSH > 500 and close to 1000

  • both sexes
  • mechanism may be hormonal overlap - TSH is like FSH
  • girls can present with ovarian cysts, high estrogen, vaginal bleeding
  • boys - stim of sertoli cells, no testosterone so no leg hair etc. don’t have stim of leydig cell = macro-orchidism
  • delayed bone age and poor linear growth
195
Q

Eval of precocious puberty

A

hx

  • growth pattern (nl or accel)
  • BONE AGE
  • tanner staging, size and symmetry of testes, cafe au lait, neuro findings
  • GnRH stim test or random gonadotropins
196
Q

NL ranges for LH for Tanner stages and labs values to test for puberty

A

tanner 1 = .02-.18
tanner 2 = .02-4.7

so if do random LH and is above .18 then it is dx of precocious puberty but if below then have to do GnRH stim and if LH is above 5 then diagnostic

197
Q

eval of precocious puberty in girls

A

estradiol and pelvic US

198
Q

eval of precocious puberty in boys

A

testosterone, androstenedione, DHEA-S, 17-OH progesterone, hCG
- adrenal/testicular US based on lab results -> not first line

199
Q

ovarian cyst eval

A

high estradiol but GnRH stim test is pre-pubertal -> do US

200
Q

Tx of precocious puberty Central

A 
GnRH analogue (Lupron/Supprelin) - down regulates pit GnRH receptors 
supprelin suppresses better and just have implant so easier
decr gonadotropin secretion
201
Q

Peripheral Precocious Puberty TX?

A

Cyst = watchful waiting
- If large enough, ovaries can have torsion around cyst -> monitor for pain
McCune - Aromatase inhibitor (letrozole)
Familial Testotoxicosis: aromatse inhibito to block bone age but then testoterone gets high -> androgen blocker OR ketoconazole (SE)
CAH - Glucocorticoids

202
Q

Incomplete Pubertal Development causes?

A

Premature Thelarche

203
Q

Premature Thelarche defn:

A
  • onset of breast development w/o other assoc pubertal ∆
  • no growth acceleration or bone age advancement
  • breast development progresses very slowly or waxes and wanes in size
204
Q

GnRH

A 
Continuous = suppression
Pulsatile = increased
205
Q

Exogenous Testosterone effects (Pharm)

A 
Positive peripheral aspects but shuts down axis
testicular atrophy (give hCG) and decr. spermatogenesis
206
Q

Testosterone most important androgen in?

A

muscle and liver

207
Q

what actions in males mediated by estrogen receptors?

A

Bone

- closure of epiphyseal plate, if doesn’t then long bone growth continues -> osteoporotic

208
Q

HRT used in aging men?

A

testosterone levels below normal (below 200-300) and with symptoms
- low libido - decreased morning erections - small testes
- low bone mineral density
- gynecomastia
FSH or gonadotropins for spermatogenesis
ONLY for testosterone def.
- inc inappropriate use b/c ads for non specific sx encouraging men

209
Q

Symptoms related specifically to androgen def in aging males

A

LOW LIBIDO and Low Bone mineral density

210
Q

Testosterone abuse in sports

A

all anabolic hormones (testost. analogs) also have androgenic SE

  • block of LH-FSH release
  • promotion of prostate growth
  • trying cycling and stacking to reduce androgenic SE
211
Q

Testosterone administration and most stable chemical form?

A

infrequent administration and most stable
make it ester and inject IM
half life clock doesn’t start until in plasma
so this formulation extends half life

212
Q

Oral testosterone = methyltestosterone pharmacokinetics and ADR:

A

alkylated to reduce first pass metabolism but has Hepatic side effects

213
Q

Transdermal ADR and reasons for:

A

severe skin rash
sustained delivery over 24 hr pd (normalizes T levels)
- has a peak

214
Q

Transdermal gel pros and cons:

A

$$, best at maintaining stable levels

215
Q

ADR of Testosterone

A 
AVOID androgens in infants and young 
- decr spermatogeneis (androgenic) 
reversible cholestatic jaundice  (hepatotoxicity)
- incr PLT aggregation, arterial thrombosis
- roid rage
- concerns of stroke, MI, mortality 
- no info on PSA, prostate enlargement
- gynecomastia
216
Q

USE of testosterone where benefits outweigh risks:

A

HYPOGONADAL MEN (not just low T men)

217
Q

pulsatile agonist

A

increases LH and FSH

218
Q

Continuous agonist

A

blocks release - prior to desensitization -> LH/FSH will transiently rise and exacerbate

219
Q

Finasteride = efficacy in prevention of male pattern baldness by virtue of its ability to:

A

reduce production of DHT

5 alpha reductase inhibitor

220
Q

anti androgens flare sx?

A

no flare symptoms with antagonists

221
Q

clinical uses of anti-androgens

A

BPH, Androgenetic alopecia (male pattern baldness), precocious puberty in boys, Hirsutism (PCOS)

222
Q

first choice in hirsutism

A

estrogen-progestin contraceptive

synth of androgens is not controlled -> increase binding globulin so free levels go down

223
Q

ADR of anti androgens

A 
leuprolide = hypogonadism
finasteride = decr libido
224
Q

what size of testes will you know the male has gone through puberty?

A

> 10-12 mls

225
Q

low testosterone with hypogonadism

A

if at hypothalamus LH and FSH = nl or low

if at testes LH and FSH is high and testosterone is low

226
Q

Acquired central hypogonadism

A

GnRH pulse generator defect
Narcotics
Glucocorticoids - usu steroid injections
Supplements

227
Q

what can cause GnRH pulse generators defects?

A

stress, severe illness, abnormal wt loss, low body fat

228
Q

what other meds besides narcotics can cause hypogonadism?

A

opioids, other pain meds, synthetic marijauna

229
Q

What supplements can cause central hypogonadism and what should you do about it?

A

prohormones, anabolic steroids - major cuase if undetectable LH, FSH
Take them all out since not FDA approved and then add them back one at a time

230
Q

what do you do to recover from exogenous androgen supppression of hpt

A

time, data is weak to show any faster recover with clomiphene, hCG

231
Q

how do we measure testosterone?

A

testosterone bound to protein, assays aren’t good for free testosterone

232
Q

why could total testosterone be incorrect?

A

because testosterone binding protein can change with age and reflect a false low

233
Q

cause of borderline low testosterone in colorado?

A

obstructive sleep apnea
- cortisol and catecholamines from hypoxia
- decreased NO in cavernosal musc, decrease in cGMP
slight impairment of GnRH pulse generator
tx sleep apnea

234
Q

low LH and FSH, low T, what is DDX? (pituitary hypogonadism)

A

prolactinoma, craniopharyngioma, rathke’s cleft cyst, pituitary tumor (GH, ACTH, some gonadotrope), metastasis, hemachromatosis, inflammatory: lymphocytic hypophysitis

headache and blurred vision might be clues

235
Q

hypogonadism (8ml bilateral), nl testosterone, high FSH and nl LH, no sperm

A

something went wrong with puberty (small testes)
LH and FSH shoul be equal and should be about 10-12
FSH higher than LH -> loss of inhibin which inhibits FSH

probably congenital due to no sperm and small testes -> hypergonadotropic hypogonadism (high FSHH +/- LH, low T)

236
Q

congenital causes of hypergonadotropic hypogonadism

A

congenital anorchia

klinefelter’s

237
Q

klinefelter’s syndrome

A

delayed puberty, low inhibin, azospermis, eventual need for T replacement, mammogram, progressive tubular fibrosis, gynecomastia, if prime testes with hCG and sometimes harvest sperm, don’t know if risk for DVT/PE

238
Q

acquired causes of hypergonadotropic hypogonadism:

A

trauma/torsion
mumps orchitis
etoh: direct testicular toxin
dm
radiation/chemo
AI testicular failure: check for others (TSH, glucose, B12, vit D)
pituitary tumor gonadotrope (secreting FSH, nl LH and nl T)

239
Q

late onset hypogonadism

A

Rare only 3-5% of men
seen with comorbidities (dz), incr wt, increase with age
and T levels increase with wt loss

240
Q

tx of late onset hypogonadism

A

diet, lifestyle, wt loss

- improve CV health, OSA, metabolic fitness, testosterone levels, sometimes improves ED

241
Q

CAD events with Testosterone?

A

risk of event correlated with higher testosterone levels

242
Q

potential mechanisms for cardiac risk?

A

induction or worsening of polycythemia
Worsening obstructive sleep apnea
Stimulation of platelet aggregation via Thromboxane A2 receptor density
Decrease in HDL levels
Salt and water retention
? Dose, type of T administration - high testosterones correlated with IM testosterone but too low is bad too

243
Q

potential risks of testosterone tx? everything but CV

A

CHECK PSA, if rises more than 1.5 in 1 yr -> work up
Stimulation of prostate growth in previously undiagnosed prostate cancer (PSA rise 1.5/12mo w/u)
Risk of bladder outlet symptoms due to increase in prostate volume
Gynecomastia
Precipitation or worsening of sleep apnea

244
Q

potential risks of testosterone tx? CV

A

Erythrocytosis, Edema in patients with pre-existing cardiac, renal, or hepatic disease, Increased cardiovascular events

245
Q

Real hypogonadism with low LH, FSH, testosterone

A

Low LH, FSH, testosterone

  • Genetic rare
  • Acquired: narcotics, glucocorticoids, hemochromatosis, tumor, XRT, stress, illness
246
Q

Not Real hypogonadism

A

OSA, T assay (effects of SHBG)

247
Q

Real hypogonadism with High FSH, LH, low testosterone

A

Primary testicular failure (XXY, trauma, other)

Gonadotrope pituitary tumor

248
Q

tx testosterone indicated for what?

A

chronic narcotics -> testosterone
pituitary tumors and radiation -> hypopit
GnRH def
Klinefelter’s
if want to try and figure it out but know at incr risk for CV

good at physiological levels but pharmacological levels is less good.

249
Q

as testes distends they:

A

pulls peritoneum with it -> peritoneal pouch goes into scrotum -> can become traumatized/infxn

250
Q

histology of testes: leydig cells, tunica albuguinea etc.

A

tunica albuguinea = white coat around outside - protect from abrasion
leydig cells -> testosterone -> driving force for spermatogenesis
blue elastic fibers of BM -> hold spermatogoonia

251
Q

development of sperm

A

spermatogonium -> primary spermatocyte -> secondary -> spermatids -> spermiogenesis -> late spermatids

252
Q

without BTB

A

made by: tight jxn between sertoli cells -> AI towards self (granulomatous inflam) -> can cause infertility

253
Q

Congenital abnormalities of testis

A

maldescent, absence, fusion, cysts

254
Q

maldescent of testis

A

cryptorchidism -> not found it’s way properly into scrotum
can be found: abdominal, superficial or deep inguinal canal, opposite thigh, perineum, root of penis

Most in superficial inguinal canal

255
Q

testes maldescent, reason why:

A

lots of ligamentous attachments (the one the doesn’t degrade becomes high that pulls testes along)

256
Q

cryptorchidism complications and facts:

A

easily traumatized
unilateral (75%) and mostly idiopathic
atrophy as early as 2 yo
contralateral testis may also regress
2 degrees cooler than body for optimal sperm development
5x increased risk of malignancy (in cryptorchid testis and contralateral testis)

257
Q

when you tx cryptorchidism

A

the earlier the better

reduce risk of malignancy and atrophy of contralateral testis

258
Q

cryptorchidism histology at 2 yrs

A

∆ within tubules themselves

leydig cells almost vanished

259
Q

cryptorchidism histology at puberty

A

disorganized

260
Q

cryptorchidism histology at adulthood

A

atrophy

anaplasia and dysplasia

261
Q

testicular atrophy

A 
cryptorchidism 
athersclerosis and DM - affect blood stream (big role in US) 
worldwide = inflam and malnutrition 
hypopit
hormone tx (prostate cancer) 
klinefelter's syndrome
262
Q

histology of testicular atrophy

A

layers of spermatocytes etc = thinner
can completely lose all germ cells - just sertoli cells are left (usu hard to see)
interstitium devoid of leydig

263
Q

klinfelter’s sclerosing tubular degeneration

A

tubular sclerosis
leydig cell hyperplasia (hormones) b/c elevated FSH/LH
decreased testosterone (no feedback on FSH/LH)
no elastic fibers

264
Q

atrophy loss of hypertrophy of leydig

A

depends on etiology

265
Q

varicocele anatomy and common causes

A

def abnormal dilatation of tortuosity of veins in pampiniform plexus

  • venous valve insufficiency
  • LS more common only 10% bilateral
266
Q

varicocele assoc with infertility when:

A

bilateral,
possible thermal effect
Maturation arrest, hypospermatogenesis, abnormal sperm morphology
Possible epiphenomenon

267
Q

twisting/ torsion -> infertility

how does this cause?

A

block venous first- engorges with blood

  • > hemorrhagic infarction because arterial pressure -> congestion of interstitium
  • > pressure necrosis of testes parenchyma
  • > PAINFUL (dramatic)
268
Q

infertility with sperm specifically

A

dynein arms needed

if missing -> infertility

269
Q

inflam dz of testis and epididymis

A 
Nonspecific epididymitis & orchitis
Mumps orchitis
Tuberculous orchitis
Syphilis
Granulomatous (autoimmune) orchitis
270
Q

Nonspecific Epididymitis/Orchitis - causes in children through elderly?

A

children - rare but use assoc with UT malformation (Gm neg rods)
Sexually active adults – C. trachomatis, N. gonorrhoeae
Elderly - Enterobacteria
Direct extension from urinary tract

271
Q

histology and pathogenesis of nonspecific epididymitis/orchitis

A

see pus

infxn in this area -> acts like abscess -> necrosis quickly because disturb vascular flow

272
Q

mumps orchitis

A

usu parotid infxn
1 - 2 wks after parotid involvement = mumps orchitis
painful/pressure
infertility uncommon because mumps is usu unilateral 70% of time
- shrunken and white scarring

273
Q

what two disease of testes mimic eachother

A

TB and syphilis

274
Q

TB orchitis

A

Epididymis → Testis
Usually part of systemic disease
Caseating granulomas- giant cells (look just like lung)

275
Q

syphilius orchitis

A 
gumma = coag necrosis that extend along blind ended arteries 
Testis → Epididymis
Congenital or acquired
Plasma cells, lymphs
Obliterative endarteritis
276
Q

Testicular Tumors

A

Germ cell tumors (95%)

  • Seminoma
  • Spermatocytic seminoma
  • Embryonal
  • Yolk sac
  • Choriocarcinoma
  • Teratoma
  • Mixed
277
Q

Germ cell tumors

A
  • most are pure or mixed
  • metastases can vary from primary
  • tend to occur in young men (15-30)
    Painless testicular enlargement
    Predisposing factors: cryptochidism (5X), genetic factors (family history-5X), dysgenesis (50X)
    Environmental factors?
    Chromosomal changes: +12p
278
Q

GERM CELL NEOPLASMS flow chart KNOW!

A

totipotential germ cell -> seminoma or can go to embryonal carcinoma

279
Q

totipotential germ cell -> most primitive form

A

seminoma

280
Q

embryonal carcinoma can go on to make what?

A 
extra embryonic (Yolk sac, choriocarcinoma)
or embryonic (teratoma)
281
Q

Testis seminoma

A 
Most common (50%)
Fourth decade
Radiosensitive and chemosensitive
Good prognosis
Serum markers often negative - so primitive don't really have
- late stage = efface the testis 
fish flesh tumor
282
Q

histology of seminoma

A
  • biphasic appearance = fried eggs

- benign lymphocytes that go along with BV

283
Q

Spermatocytic Seminoma

A

1-2% of GCT’s
Older age (>50 yrs)
Good prognosis - no report of metastasis
Serum markers negative

284
Q

Spermatocytic Seminoma histology

A

biphasic appearance
all different sized nuclei
some stuck in spermatid (phenotypically)
mixoid, gelatinous structure

285
Q

Embryonal Carcinoma

A

Pure – rare (3%)
Mixed – common (85%)
Third decade
Chemosensitive
Higher likelihood of extratesticular spread
Recurrences common
Markers variable: PLAP (placental alkaline phosphatase), placental lactogen, hCG

286
Q

Embryonal Carcinoma histology (immature phase carcinoma)

A 
destructive 
lots of areas of necrosis, hemorrhage 
cells = more anaplastic 
big dark nuclei 
more atypia
mitotic figures 
some structure - primitive tubular arrangements
287
Q

Teratoma

A

40% of testis tumors in infants
2-3% pure in adults
Mixed ~45%
Mature vs. Immature
Malignant transformation -> every part that is mature can undergo this
Chemoresistent – slow to progress but may undergo “malignant” change - surgically remove the rest

288
Q

Malignant transformation of teratoma

A

if mature sq cell can get squamous cell carcinoma

has seen pancreatic carcinoma from it

289
Q

histology of teratoma

A

cysts - lined by mature tissues

Elements -> can have cartilage, epithelial lined surface, can be epidermis, respiratory epithelium, colon epithelium, pancreas with acinar, skeletal muscle, nervous tissue

the more immature, the more likely to progrees to metastasis

290
Q

Yolk Sac Tumor

A

Pure common in children (80% of testicular tumors)
Part of mixed tumor in adults (40-50%)
Prognosis relatively good
Produces alpha-fetoprotein (AFP)

291
Q

histology of yolk sac tumor

A

AFP globules

AFP on IHC

292
Q

Choriocarcinoma

A 
Pure (0.3% of GCT’s)
Mixed (10%)
Aggressive – often metastasizes - often dx metastasis before finding primary tumor 
Chemosensitive, but worse prognosis
Produces hCG
functional- functions like placenta
293
Q

histology of choriocarcinoma

A

hemorrhagic
destructive
sinsitial trophoblast and cytotrophoblasts

294
Q

most common cancer in testes in adults?

A

mixed tumor

295
Q

Testis Cancer Staging

A

I - confined to testis
II - retroperitoneal nodes or below diaphragm
III - outside retroperitoneal nodes or above diaphragm

296
Q

Testis Cancer Serum Markers

A

AFP
hCG
Placental-like Alkaline Phosphatase (PLAP)
Human placental lactogen

297
Q

Testicular Tumors (5% that aren’t germ cell)

A 
Sex-cord/stromal tumors
Leydig cell
Sertoli cell
Granulosa cell
Mixed
Lymphoma
298
Q

Leydig Cell Tumors

A

2% of all testicular neoplasms
90% benign
10% malignant
Often masculinizing, some feminizing (because produce testosterone and sometimes can be converted via aromatase)

299
Q

sertoli cell tumor

A

more rare, more serious
very malignant
metastasize early
seminiferous tubules gone bad -> more sertoli, more invasive -> go into blood stream

300
Q

most common testicular tumor in men over age of 60

A

remember not GERM CELL

Lymphoma is answer!

301
Q

Penile Lesions

A 
Condyloma Acuminatum
Verrucous carcinoma
Carcinoma in situ
 - Bowen’s disease
 - Erythroplasia of Queyrat
Squamous cell carcinoma
Other malignancies
302
Q

Genital warts

A 
HPV- papillary outgrowths
atypia in squamous cells 
koilocytosis = big hollow cells (clear cytopasm) with wrinkled raison like nucleus 
virus filled cells 
16,18, 30-33 -> high risk
303
Q

limited lesions of penis

A

Verrucous carcinoma (wart like, large wart, keritinizing, local destruction without metastasizing)
Carcinoma in situ
- Bowen’s disease
- Erythroplasia of Queyrat (mucosa of uncircumsized male)

304
Q

Carcinoma in situ

A

full thickness dysplasia of squamous epithelium

305
Q

Penile malignancies epithelial

A 
Epithelial (95%)
Squamous cell carcinoma (95%)
Melanoma (1%)
Basal cell carcinoma (1%)
Urethral TCC (2%)
306
Q

Penile malignancies mesenchymal

A 
Mesenchymal (5%)
Leimyosarcoma
Fibrosarcoma
Rhabdomyosarcoma
Kaposi’s sarcoma
Angiosarcoma
Hemangioendothelioma
307
Q

Penile Squamous Carcinoma

A

0.3-0.6% of male cancers
0.5-1.0 per 100,000
60-80 years of age
African American:Caucasian 2:1
“Chimney sweeps disease”
Precursor lesion: carcinoma in situ

308
Q

Penile Squamous Carcinoma gross findings and histology

A

ulcerative lesions, destructive
pointlike downward lesions of skin -> then become glandlike
- invasion doesn’t have to be too far to get to blood -> dissemination

309
Q

most cancers effect what of prostate?

A

peripheral zone

310
Q

BPH effects what of prostate?

A

transitional zone

311
Q

cell layers of tubular alveolar gland

A

2 cell layers tall columnar = secretory
Basal or stem cell
Malignancies lose 2 cell morphology

312
Q

Prostatic Diseases

A

Inflammation
Hyperplasia
Neoplasia

313
Q

Prostatic dz: sx?

A

Can be asymptomatic until advanced

Symptoms, when present, are usually those of urethral obstruction or irritation while urinating

314
Q

inflammation of prostate

A 
Acute Prostatitis
Chronic Prostatitis
- Bacterial = rare
- “abacterial” = more common
- granulomatous
315
Q

Acute Prostatitis

A

Focal or diffuse polymorphonuclear inflammation
Enterobacter (E. coli), S. aureus most common, also think about STI bugs
Direct extension from urinary tract
Can be iatrogenic

316
Q

iatrogenic causes?

A

prostatitis

miss 45 degree angle and damage prostate

317
Q

Chronic Prostatitis

A

Mononuclear cell inflammation
Often associated with atrophy
Unclear etiology - ? Response to occult infection, dietary
Histologic chronic inflammation much more common than clinical prostatitis
Granulomatous form

318
Q

Granulomatous form of chronic prostatitis

A

Granulomatous form
Eroded corpora amylacea
Tuberculosis

319
Q

Chronic Prostatitis on histology

A

inflam infiltrate
around and into epithelium
atrophic changes
columnar cells have regressed

320
Q

BPH

A

Benign nodular enlargement of prostate
Most common proliferative disease of prostate
Blacks>Whites>Asians -> reflects same trend as cancer
Histologic BPH: Rule of “10’s”
Clinical BPH age 60
Lower urinary tract symptoms (LUTS)
NOT PREMALIGNANT

321
Q

LUTS voiding

A

voiding symptoms - hesitancy, poor urine flow, dribbling, incomplete bladder emptying

322
Q

LUTS storage

A

increased frequency >7x/day
nocturia
urgency
urge incontinence

323
Q

histology of BPH

A

transitional zone near urethra

large nodules confined to transitional zone

324
Q

classification of BPH nodules

A

3 major components that can be in any combo

epithelium, fibroblasts/stroma, smooth muscle

325
Q

BPH nodules - more stroma

A

worse it is symptomatically and more refractory to tx

326
Q

BPH natural hx complications:

A 
LUTS most common – quality of life impact
Complications:
Acute urinary retention
Recurrent UTI/ pyelonephritis
Renal failure
Incontinence
327
Q

BPH natural hx management

A

Management:
Medical - recently is main tx
Minimally invasive therapy (ex. Microwave thermotherapy)
Surgery (TURP) - lot of morbidity (incontinence)

328
Q

Prostatic Carcinoma

A

Most common non-skin cancer of adult males (~20% of all male cancers)
~200,000 new cases per year
Second leading cause of male cancer deaths (~27,000 per year)
More men die with PCa than of it
- US sees most because if you screen for it you’ll find it
- Asians = low risk

329
Q

Prostatic Cancer Risk Factors

A

Age - older, more likely
Race - AA more likely
Genetics - father had it, 4x more likely
Diet - thought to because asians living in Japan who move here adopt our risk of prostate cancer
DM - might effect mortality of prostate cancer

330
Q

Prostatic Carcinoma screening problems:

A

Effects peripheral zone > transition zone
Screening:
Serum prostate specific antigen (PSA) - not prostate or cancer specific
Digital rectal exam - only see posterior part of prostate 10% sensitive
Blind “random” biopsies still gold standard for diagnosis
- Only ~ 50% sensitive
- Many cancers detected will never be life threatening-

331
Q

grade progression of prostate carcinoma

A

thought prostate goes from low grade to high grade
can start as high grade -> this progression doesn’t always occur
- multifocal disease
multiple grades
2 tumors within prostate = different grades

332
Q

Relationship of PIN and PCa

A

Believed to represent noninvasive precursor to some prostate cancers
Genetic and molecular changes similar to PCa
Increases with age, peak prevalence 5-10 yrs before PCa [Sakr 1993]
30-50% of prostates with PIN harbor prostate cancer

333
Q

Prostatic adeno dx criteria

A 
Uniform round glands
Infiltrative pattern
Single cell layer (loss of basal cells)
Nuclear enlargement -prominent nucleoli
Perineural invasion
334
Q

Prognostic factors of prostate cancer

A

Grade most important
Stage
Tumor volume (PSA) - monitoring tool, larger = more likely to metastasize
Molecular markers – research in progress

335
Q

gleason grading of prostate

A

degree of invasiveness is in architecture = GLEASON SCORE
= ragged sheets vs. morphologic resemblance to nl prostate
Score = most + 2nd most
most informative about eventual mortality

336
Q

high grade malignancy in gleason score

A

lack of glandular formation

337
Q

metastasis of prostate cancer

A

lymph or hematologic spread of prostate cancer

can get into spain -> pathologic fracture and pain

338
Q

survival of prostate cancer

A 
Pelvic lymph nodes			  95%
Seminal vesicles				  85%
Established capsular penetration	  48%
Focal capsular penetration		  33%
Organ confined			          10%
organ confined doesn't mean you're out of woods
339
Q

random biopsy of prostate

A

might miss cancer or a high grade tumor because of multiple focality
combining epigenetic and genetic might be more

340
Q

genomics of prostate cancer

A

genes tell us more than grade - could determine prognosis by genes (deletions, amplifications)

341
Q

Prostate CancerTreatment Options

A 
Surgery – radical prostatectomy
External beam radiation
Brachytherapy (radioactive “seeds”)
Cryotherapy
Hormone ablation – mainline therapy for advanced metastatic PCa - eventually fails 
Chemotherapy
342
Q

new concept TX of prostate cancer

A

New concepts:
Expectant management
Targeted focal therapy

343
Q

BOTTOM LINE OF PROSTATE CANCER

A

~200,000 new cases expected
3/4 receive localized treatment (~150,000)
40% will experience PSA recurrence (60,000/yr)
~27,000 deaths expected
Autopsy: 30% of men > 50 years have PCa
SOOOOOO MANY MEN ARENT DYING OF PROSTATE CANCER THAT ARE BEING TREATED BUT WE’RE NOT CATCHING THE ONES THAT NEED TO BE TREATED

344
Q

new theories on how to tx/cure prostate cancer

A

need improved imaging and biomarkers to better assess tumor burden and aggressiveness

want to treat the people that will die of prostate cancer but not find and treat the ones that will die of other causes (not their prostate cancer)

haven’t done a good job of separating sleeping giants and mean mice

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