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Block 7 > Week 4 > Flashcards

Week 4 Flashcards

1
Q

Sacro-Iliac Joint
1. Where is it?
2. What tye of joint is this?

A
  1. where pelvis is joined with sacrum
  2. synovial joint but limited movement- weight bearing
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2
Q
  1. Lumbosacral joints - What does this join?
  2. Sacro-coccygeal joint- what does this join?
A
  1. Joins L5 and S1
  2. joins the sacrum and the coccyx
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3
Q
  1. What three bones make up the pelvis (one one side)
  2. Where do they all connect?
A
  1. ilium
  2. ischium
  3. pubis
  4. all connected at region of acetabulum (where femur inserts)
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4
Q
  1. What ligament connects the sacrum/coccyx to the spine of the ischium?
  2. what ligament connects the sacrum/coccyx to the ischial tuberosity
  3. What muscles are found in the plevic walls (between the three pieces)
A
  1. sacrospinous ligament (green)
  2. sacrotuberous ligament (white part)
  3. obturator internus and piriformis muscles
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5
Q
  1. Where is the greater sciatic foramen?
  2. What passes through here?
A
  1. where piriformis muscle passes. (image)
  2. The sciatic nerve passes through here
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6
Q
  1. What are the 3 parts of the levator ani muscle?
A
  1. iliococcygeus part (ilium to the coccyx)
  2. pubococcygeus (pubis to coccyx)
  3. puborectalis (pubis to rectum)
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7
Q
  1. What is the greater (false) pelvis?
  2. What is the lesser (true) pelvis?
A
  1. The greater (false) pelvis is located superiorly to the pelvic inlet and contains the distal part of the intestines.
  2. Below the pelvic inlet - contains parts of the urinary, GI, and reproductive system
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8
Q

Male vs Female
1. difference in pelvic inlent shape
2. difference in pubic arch

A
  1. male is more heart shaped vs female is more circular
  2. female have larger pubic arch - adapted for chidlbirth
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9
Q

SACRAL PLEXUS

  1. what parts of the spinal cord make up the saccral plexus?
  2. Where is it located?
  3. Important branches of this?
A
  1. S1-S4 and L4-L5
  2. located anterior to the piriformis muscle on the posterolateral pelvic wall
  3. Pudendal branch
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10
Q
  1. the internal iliac vessels supply what?
  2. What about the external iliac vessel?
A
  1. the pelvic viscera
  2. the lower extremity. Passes deep to the inguinal ligament to continue as femoral artery
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11
Q

Testes
1. what are the two coverings on testes

A
  1. Tunica abluginea (this is a fibrous capsule on top of the testes)
  2. On top of this, is the tunica vaginalis which is two layers since it folds on itself. It has parietal and visceral layer - this allows for movement of testes in scrotum
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12
Q

Testes
1. blood supply
2. lympathic drainage
3. innervation

A
  1. testicular artery
  2. lateral aortic (lumbar) nodes
  3. Testicular plexus (sympathetic fibers from T10/11 and parasympathetic fibers from vagus)
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13
Q

Spermatic cord
1. What are the three layers of fascia on the spermatic cord?
2. What are some major contents of the spermatic cord?

A
  1. External spermatic fascia, cremasteric fascia, internal spermatic fascia
  2. ductus deferens, cremasteric muscle, artery of ductus deferens, testicular artery and veins and LN, nerves
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14
Q

Epididymis
1. What does it connect?
2. what is its purpose?
3. parts?

A
  1. connects the testis to ductus deferens
  2. stores sperm until ejaculation
  3. head, body, and tail
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15
Q

What is the purpose of the retes testes?

A
  1. A network of small tubes in the testicle that helps move sperm cells (male reproductive cells) from the testicle to the epididymis
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16
Q

Ductus Deferens
1. What is its purpose? / What does it connect?
2. Where is it found/location/anatomy?

A
  1. Ductus deferens is a muscular duct that transports sperm from epididymis towards ejaculatory duct. Ductus deferens has to join seminal vesicles to form ejaculatory duct.
  2. Starts in scrotum in spermatic cord - then moves towards superficial inguinal ring, into inguinal canal, into deep inguinal ring, turns toward pelvic inlet, drops down and behind bladder until it meets the seminal vesicle. (image)
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17
Q

Seminal Vesicles
1. Where is found?
2. what is its purpose?
3. What does it join to form ejaculatory duct?

A
  1. Found behind the bladder at the base.
  2. Paired accessory glands that produces secretions contributing to semen
  3. Joins the ductus deferens (AKA vas deferens)
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18
Q

Prostate
1. Where is the prostate found?
2. What is its purpose?

A
  1. inferior to the bladder, posterior to the pubic symphysis, anterior to the rectum
  2. Makes secretions that empty into prostatic urethra. This makes up more of the semen contents.
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19
Q

Prostatic Zones
1. What are the four zones
2. What are they known for or important details of each

A
  1. anterior - it has non-glandular tissue
  2. central - around ejaculatory duct and involved in BPH
  3. peripheral - behind ejaculatory duct and involved in carcinoma of prostate (can find mass here via rectal exam)
  4. transitional - around the urethra and can also be involved in BPH
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20
Q

Prostate
1. Blood supply
2. LN drainage
3. innervation

A
  1. prostatic arteries
  2. internal iliac nodes
  3. prostatic nerve plexus
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21
Q

Penis
1. What are the two pairs of muscles that make up the root of the penis?
2. What are their purpose?

A
  1. Ischiocavernosus - forces blood distally during erection
  2. Bulbospongiosus - covers bulbe of penis. Forces blood distally during erection and empties erethra to emit semen.
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22
Q

Penis
1. What are the two types of tissue in the body of the penis
2. What are their functions?

A
  1. Corpora cavernosa - on dorsal side of penis (closer to abdomen when erect) - contains blood vessels that fill with blood to help make an erection.
  2. Corpus spongiosum - on ventral side of penis - this contains the urethra and in erection it prevents the urethra from pinching closed, thereby maintaining the urethra as a viable channel for ejaculation.
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23
Q

Penis
1. Blood supply
2. LN drainage
3. Innervation

A
  1. Branches of internal and external pudendal artery
  2. Internal iliac nodes (deep tissue), deep inguinal nodes (glans penis), superficial inguinal nodes (skin)
  3. Pudendal nerve (S2-S4)
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24
Q

Male Urethra
1. what are the 4 parts of the male urethra
2. What are important things to know of each section?

A
  1. preprostatic - surrounded by internal urethral sphincter (leaving bladder)
  2. prostatic - has openings for ejaculatory ducts and prostate glands
  3. membranous - surrounded by external urethral sphincter
  4. spongy (penile/bulbar) - contains opening for bulbourethral glands (cowpers glands)
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25
Q

Straddle Injury
1. What is it?/What can cause it?
2. What sx can occur?

A
  1. A forceful blow to perineum causes damage to corpus spongiosum (surrounds urethra) and Buck’s fascia (surrounding whole penis) - This leads to leaking of urine from urethra and into space between superficial fascia and deep fascia (Buck’s fascia) in scrotum, penis, and anterior abdominal wall
  2. Unable to excrete urine or pain when passing urine
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26
Q
  1. What are copwer’s glands/bulbourethral glands?
  2. What part of urethra do they empty into?
A
  1. pea shaped accessory glands that give secretions to lubricate urethral (the pre-ejaculatory emissions)
  2. Spongy part of the urethra
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27
Q

Gestational HTN
1. How is this different from pre-existing/chronic HTN?

A
  1. elevated BP develops after 20 weeks of pregnancy
  2. No proteinuria - so it is not as severe as preeclampsia
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28
Q

Pre-eclampsia
1. Sx
2. Pathogenesis
3. Risk factors

A
  1. HTN, proteinuria, end organ dysfunction, edema, headache, blurred vision, etc
  2. This develops due to initial formation of the placenta. When there is abnormal transformation of the spiral arteries then there is underperfusion of the placenta which becomes more troublesome as the pregnancy develops.
  3. First pregnancy, prior preeclampsia, family history, 40 years and older or younger than 18, multiple gestations (like twins), maternal conditions like DM/HTN/obesity/lupus, etc
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29
Q

Preeclampasia
1. What trimester does this present?
2. What is the dx criteria preeclampsia?
3. What is definite tx of this?

A
  1. 3rd trimetester
  2. new onset of HTN (over 140/90) with proteinuria OR end organ dysfunction after 20 weeks gestation
  3. delivery of fetus
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30
Q

Preeclampsia
1. what lab findings can indicate preeclampsia?

A
  1. ALT/AST twice as normal values (this indicates liver dysfunction - issues with liver are common)
  2. Kidneys show Cr > 1.1 or 2 fold rise
  3. Thrombocytopenia (<100 k)
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31
Q

Eclampsia
1. Signs and symptoms
2. Tx options
3. Complications

A
  1. seizures that occur in mother with preeclampsia. Can happen before, during, or after labor
  2. Magnesium sufate (can also be used if there is severe preeclampsia - for prevention), delivery of baby, antihypertensive therapy to prevent stroke (controling BP)
  3. coma, death, DIC, respiratory failure
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32
Q

Abruptio Placentae
1. When in pregnancy does this occur?
2. sx?
3. What is wrong in this situation?
4. What causes this/pathophysiology?

A
  1. 3rd trimester
  2. abrupt onset of PAINFUL vaginal bleeding, abdominal or back pain, uterine contractions
  3. this is premature separation of the placenta from the wall of the uterus.
  4. Abruption is thought to occur following a rupture of the maternal vessels within the basal layer of the endometrium. Blood accumulates and splits the placental attachment from the basal layer of endometrium.
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33
Q

Placenta abruptae
1. What are some risk factors for this?

A
  1. previous abruption, preeclampsia, smoking, cocaine, abnormal uterus, trauma
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34
Q

Placenta Previa
1. Sx
2. What is this?
3. Risk factors?

A
  1. PAINLESS bleeding. May lead to preterm birth and may require a c section
  2. Placenta is attached to lower uterus or close to cerivcal os.
  3. Prior placenta previa, prior c section, multiple prior pregnancies
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35
Q

Vasa previa
1. What is this?
2. How does this affect delivery?

A
  1. this is when the fetal blood vessels are near cerival os
  2. This can lead to rupture of membranes at birth and can cause bleeding. Usually require a C section
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36
Q

Placenta Accreta
1. what is this?
2. predisposing risk factors
3. Complications

A
  1. placenta attaches to the myometrium but does not penetrate the myometrium
  2. prior c section bc it leave behind scar tissue which make the decidua (part of endometrium) not form correctly
  3. maternal hemorrhage, Shock, DIC, often requires hysterectomy
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37
Q

Placenta Increta
1. what is this?
2. What is the purpose of the placenta?

A
  1. placenta penetrates myometrium
  2. This structure provides oxygen and nutrients to a growing baby. It also removes waste products from the baby’s blood.
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38
Q

Placenta Percreta (most dangerous)
1. what is this?

A
  1. placenta penetrates through myometrium and into uterine serosa meaning it can attach to bladder or rectum
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39
Q
  1. What is the amnion
  2. What is the chorion?
A
  1. the amnion that lines the inner surface of the amniotic sac interfacing with the fetus
  2. The chorion that is the outer layer in contact with maternal tissue.
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40
Q

What changes happen to amnion and chorion with monozygotic twins if division occurs in…
1. Day 1-3
2. Days 4-8
3. Days 9-12
4. Days 13+

A
  1. dichorionic and diamniotic
  2. chorion already developed so share one chorion but separate amnion
  3. Chorion and amnion already developed so share one chorion and amnion - “roommates” - but this is dangerous if they get tied up in eachothers umbilical cords
  4. This can result in conjoined twins
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41
Q
  1. What are the two prenatal screenings very often given to find out if there are any fetal abnormalities?
  2. What can each screening detect?
A
  1. Cell free fetal DNA - can detect aneuploidy (like trisomy 21, 18, 13)
  2. Nuchal Translucency US - Measuring nuchal fold thickness helps assess the risk for Down syndrome and other genetic problems in the baby.
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42
Q

Maternal Serum Analyte Testing: Quad Screen

Trisomy 21
1. MSAFP levels
2. Estriol levels
3. B-hCG levels
4. Inhibin levels?

A
  1. decreased
  2. decreased
  3. elevated
  4. elevated
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43
Q

Maternal Serum Analyte Testing: Quad Screen

Trisomy 18
1. MSAFP levels
2. Estriol levels
3. B-hCG levels
4. Inhibin levels?

A
  1. decreased
  2. decreased
  3. decreased
  4. decreased
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44
Q

Chorioamnionitis
1. What is this?
2. What causes this?

A
  1. inflammation of amnion and chorion
  2. Listeria can be acquired transplacentally
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45
Q

Ascending infections in pregnant women
1. what causes this?
2. What does this do to fetus?

A
  1. Group B strep
  2. associated with neonatal sepsis - give prophylaxis to mom before birth
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46
Q

Seminiferous tubules
1. Where are these found?
2. What are their purpose?

A
  1. these are found in the testes
  2. the site of spermatogenesis where germ cells develop into spermatozoa in close interaction with Sertoli cells.
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47
Q

The Male Gametogenesis

Spermatogenesis
1. What are the steps of spermiogenesis (include names of cells as the progress from Type A dark to spermatid

A
  1. Mitosis (2n->2n): germs cells go from Type A dark to type A pale to Type B cells [SPERMATOGONIAL PHASE]
  2. Meiosis I (2n -> n): From Type B cells to primary and then secondary spermatocyte [SPERMATOCYTE PHASE]
  3. Meiosis II (n->n): From secondary spermatocyte to early spermatid [SPERMATID PHASE]
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48
Q
  1. what process happens after spermatogenesis?
  2. What does this form in sperm?
A
  1. spermiogenesis - changes spermatids into spermatozoa (Mature sperm cells)
  2. acrosome, condensation of nucleus, formation of neck and tail, shedding of most of cytoplasm
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49
Q

Spermatogonia (Spermatogonial phase of spermatogenesis - Mitosis) - what are these described as?
1. Type A Dark cells:
2. Type A Pale cells
3. Type B cells

A
  1. stem cells, dark cells with dark nuclei
  2. differentiated cells, lighter in color - undergo mitosis and daughter cells remain linked
  3. differentiated, mitotically active, dark nuclei (still linked)
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50
Q
  1. Where are leydig cells found in seminiferous tubules?
  2. What are their function?
A
  1. found outside of the blood-testis barrier
  2. produce testosterone, oxytocin
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51
Q

Sertoli cells
1. What is their function?
2. What can they secrete?

A
  1. structural and nutritional support of the gametocytes undergoing spermatogenesis. they also form the blood testis barrier
  2. fructose solution to carry sperm, androgen binding protein (ABP), inhibin, activin, anti-mullerian hormone
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52
Q

Spermiogenesis - explain these phases
1. Golgi
2. Cap
3. Acrosome
4. Maturation

A
  1. Acrosomal vesicle forms, centrioles migrate to periphery to formaxoneme of flagellum
  2. acrosomal cap forms, nucleus condenses
  3. further nuclear condensation, manchette forms (part of tail)
  4. Discarding of cytoplasm, released into lumen of seminferous tubules, non-motile in testes though
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53
Q
  1. what the golgi apparatus become in mature sperm
  2. what the centrioles become in mature sperm
  3. what the mitochondria become in mature sperm
A
  1. becomes the acrosome
    1. sperm neck contains centrioles that form the cilium
    2. wrap around dense fibers and axoneme to produce energy (ATP) for the movement of sperm
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54
Q
  1. What part of male repro system is this?
  2. What does it connect/do?
A
  1. This is the ductuli efferentes - scalloped look
  2. conduct sperm from retes testes to epididymus
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55
Q
  1. What part of male repro system is this?
  2. What does it connect/do?
A
  1. this is within the epididymus [DUCTUS EPIDIDYMIS] - wrapped by smooth muscle and lumen has sterocilia
  2. store sperm until ejaculation - sperm fully mature in epididymis and become motile.
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56
Q
  1. What part of male repro system is this?
  2. What does it connect/do?
A
  1. this is the vas deferenes/ ductus deferens and found within the spermatic cord
  2. This conducts sperm during ejaculation. Has lots of blood vessels, nerves, and lymphatics
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57
Q
  1. What part of male repro system is this?
  2. What does it connect/do?
A
  1. this is the seminal vesicle
  2. secrete yellowish fluid with fructose, amino acids, prostaglandins - activate sperm
58
Q

ACCESSORY GLANDS OF MALE REPRO SYSTEM

  1. purpose of secretions of seminal vesicle?
  2. purpose of prostate glands?
  3. purpose of Cowpers/bulbourethral glands?
A
  1. secretions activate sperm
  2. secretions are alkaline and neutralize acidic environment of vagina - helps protect sperm
  3. lubricates the urethra
59
Q

Which gland in the male repro system make the most secretions?

A
  1. the seminal vesicles
60
Q

Corpora Amylacea
1. Where is this found?
2. when does this increase?

A
  1. this is found in the prostate stroma - they are concretions that may calcify (triangle)
  2. can increase with age
61
Q
  1. What artery supplies blood in the corpus cavernosum?
A
  1. Deep/central artery of the penis
62
Q
  1. What are the glands of littre?
A
  1. These are within the corpus spongiosum and lubricate the urethra (triangle)
63
Q

Phimosis
1. What is this
2. What can cause this?

A
  1. constricted fibrotic foreskin that cannot be retracted
  2. can be acquired from scarring or inflammation
64
Q

Paraphimosis
1. What is this?

A
  1. When foreskin is retracted and cannot be returned to normal position
65
Q

Condyloma Acuminatum
1. What is found in histology?

A
  1. (koilocytes) Nucleus looks like a rasin with clear cytoplasm around it
66
Q

Peyroinie Disease
1. What is this?
2. What causes this?
3. Sx?

A
  1. fibrosis in tunica albiguinea of the penis causes upward curvature of the penis
  2. Due to repeated minor trauma to penis during intercourse
  3. pain, nodule, ED
67
Q

SCC of penis
1. what part of penis does this occur on?
2. in what type of patient
3. risk factors?

A
  1. glans or shaft
  2. older men around 60
  3. uncircumcision, HPV infection 16 and 18, and smoking
68
Q

In vasectomy what is resected?

A
  1. the vas deferens
69
Q

Cryptochidism
1. What is this?
2. What is the tx or disease path?

A
  1. “hidden testes” - usually due to undescended testes. 3% of fetus have this and 80% descend by 3 months of age
  2. If it doesn’t fix on its own by age 6 then surgery can be done to correct (orchiopexy)
70
Q

Hydrocele
1. What is this?
2. How can you identify this on physical
3. What can cause this?
4. When can communicating hydrocele occur?

A
  1. accumulation of fluid in the tunica vaginalis (between visceral and parietal layers) which makes a small fluid filled sac attached to testicle
  2. with flashlight- if swelling transluminates then likely a hydrocele
  3. 2ndary to infection, torsion, truama
  4. incomplete closure of processus vaginalis in newborns -usually fixes itself by age 1
71
Q

Varicocele
1. Sx?
2. What is this?
3. What side of scrotum is this more common on and why?

A
  1. Scrotal pain and swelling + more pain with standing or valsalva maneuver
  2. Dilated veins in scrotum —- defective valves in the veins within the scrotum, just above the testicles. Normally, these valves regulate the flow of blood to and from the testicles. When normal flow doesn’t occur, the blood backs up, causing the veins to dilate (enlarge).
  3. Left side - because left spermatic vein has a longer course to get to left renal vein and left renal vein can have nutcracker effect which raises risk for varicocele
72
Q

Spermatocele
1. Sx?
2. What is this?
3. tx?

A
  1. asymptomatic but can be painful. Mass on top of testes
  2. an abnormal sac (cyst) that develops in the epididymis
  3. most dont require treatment
73
Q

Torsion of testes
1. patient age most common?
2. sx?
3. What is this?
4. What deformities can increase risk?

A
  1. adolescents, young adults
  2. painful swollen testicle, absence of cremaster reflex - this is an emergency
  3. When testicle rotates in scrotum and twists the spermatic cord.
  4. Bell clapper deformity (when testes are hanging more horizontally and more freely) - when scrotal ligament is abnormal and cannot secure testes correctly
74
Q

Torsion of testes
1. What are some complications with this if not treated?

A
  1. infertility, compression of veins and arteries can lead to hemorrhagic infarction
75
Q

Testes Germ Cell Tumors

Germ Cell Tumors: Classical Seminoma
1. morphology
2. histology
3. markers

A
  1. soft, well circumscribed, gray white tumor that bulges from the cut surface of the affected testes - usually no necrosis or hemorrhage
  2. large cells, clear cytoplasm, distinct cell borders, fried egg appearance - also can show lymphocytes
  3. HCG and lactate dehydrogenase
76
Q

Testes Germ Cell Tumors

Germ Cell Tumors: Classical Seminoma
1. What is the equivalent in female
2. benign or malignant?
3. sx

A
  1. dysgerminoma on ovaries
  2. malignant - but highly radiosensitive, metastasizes late, and excellent prognosis
  3. painless, testicular enlargement
77
Q

Testes Germ Cell Tumors

Germ Cell Tumors: Spermatocytic Seminoma
1. How is this different from classical seminoma?

A
  1. Spermatocytic seminoma tends to occur more commonly, in men aged over 50
  2. does not metastasize
  3. has polymorphous cell population (large, intermediate, and small cells)
78
Q
  1. What is the most common testicular tumor?
  2. What is the age range for these?
A
  1. seminoma
  2. 20-50 years old
79
Q

Testes Tumors (non-seminomas)

Embryonal Carcinoma
1. benign or malignant?
2. Sx?
3. Histology?
4. Pure or found in mixed tumors?

A
  1. malignant
  2. painful, hemorrhagic mass with necrosis
  3. Undifferentiated, alveolar, tubular, papillary patterns
  4. More often found in mixed tumors
80
Q

Testes Tumors (non-seminomas)

Embryonal Carcinoma
1. Markers (pure vs mixed)

A
  1. Pure: may have syncytiotrophoblast tissue that secretes beta hcg and normal AFP
  2. When mixed - AFP is elevated
81
Q

Testes Tumors (non-seminomas)

Yolk Sac Tumor
1. benign or malignant?
2. most common in what patient population
3. pure or mixed tumor?

A
  1. malignant - aggressive
  2. children less than 3 years old
  3. more often pure tumor
82
Q

Testes Tumors (non-seminomas)

Yolk Sac Tumor
1. Histology
2. Markers

A
  1. Schiller Duval bodies (resemble glomerulus)
  2. increased AFP
83
Q

Testes Tumors (non-seminomas)

Choriocarcinoma
1. benign or malignant?
2. what is wrong that causes this tumor?
3. sx?
4. Markers?
5. complications?

A
  1. malignant - frequent liver and lung mets
  2. disordered syncytiotrophoblasts and cytotrophoblasts
  3. Gynecomastia, sx of hyperthyroidism
  4. increased beta HCG
  5. Hyperthyroidism due to molecular similarity of HCG to TSH
84
Q

Testes Tumors (non-seminomas)

Teratoma
1. What can be found in tumor?
2. benign or malignant?

A
  1. many things like skin, cartilage, bone, hair, etc
  2. benign in children <3 years === malignant in adults (when part of mixed tumors)
85
Q
  1. What are the routes of spread of seminomas vs non-seminomas?
A
  1. seminomas spread to LN first then hematogenous spread - and its spreading is late onset
  2. non-seminomas - have early mets that are spread hematogenously
86
Q

Sex-Cord Stromal Tumors of Testes

Leydig Cell Tumor
1. Benign or malignant
2. morphology?
3. Histology?

A
  1. mostly benign
  2. golden browh color of tumor
  3. uniform round nuclei, Reinke crystals (eosinophilic cytoplasmic inclusions)
87
Q

Sex-Cord Stromal Tumors of Testes

Leydig Cell Tumor
1. Its effects on hormones?
2. Sx?
3. Most common ages to occur?

A
  1. Can become functional tumor and release androgens (at times both androgens and estrogens and even corticosteroids)
  2. testicular swelling, precocious puberty, gynecomastia
  3. 20-60 years old
88
Q

Sex-Cord Stromal Tumors of Testes

Sertoli Cell Tumor
1. benign or malignant?
2. affects on hormones?
3. morphology and histology?

A
  1. Benign
  2. hormonally silent - only present as testicular mass
  3. gray-white to yellow tumor —- on histology shows cold like structures and tubules, palisading cells, etc
89
Q

Non-testicular Tumors

Primary Testicular Lymphoma
1. benign or malignant?
2. type of lymphoma?
3. most common testicular cancer in what age group?

A
  1. malignant with poor prognosis, usually disseminated - found in groin LN
  2. Diffuse large B cell lymphoma
  3. older men >60 years old
90
Q

Acute Prostatitis
1. etiology?
2. sx
3. histology can show
4. Should bx be done?

A
  1. bacterial etiology such as e. coli, gram neg rods, staph
  2. fever, chills, dysuria, prostate may be tender and boggy
  3. Neutrophils in gland lumens
  4. no bx, it may result in sepsis
91
Q

Granulomatous/Autoimmune Prostatitis
1. etiology?
2. sx
3. histology can show

A
  1. Infectious (following BCG tx) or non infectious
  2. may show prostate induration
  3. caseating or noncaseating granulomatous inflammation and later stages of fibrosis
92
Q

Chronic prostatitis
1. etiology?
2. Clinical presentation?
3. Histology?

A
  1. bacterial or non bacterial
  2. asymptomatic or low back pain, dysuria, perinea discomfort
  3. Bacteria etiology shows infiltrates of lymphocytes, plasma cells, and macrophages
93
Q

Acute Orchitis/epididymitis
1. Etiology
2. Clinical Presentation
3. Histology presentation

A
  1. infectious of urinary tract that reach epididymis/testes through vas deferens or lymphatics. Usually Gram neg rods but also chlamydia, neisseria, syphilis
  2. testicular swelling and tenderness, pain
  3. acute inflammation, may lead to suppurative necrosis. May result in fibrous scarring and in some cases sterility
94
Q

Mumps Orchitis
1. Etiology
2. Clinical Presentation

A
  1. paramyxovirus (“mumps”)
  2. usualy 1 week after onset of parotid gland swelling, pain - 20-30% in postpubertal males
95
Q

Granulomatous (autoimmune) Orchitis
1. Etiology
2. Clinical Presentation
3. Histology

A
  1. idiopathic, autoimmune bases suspected
  2. painless testicular mass or moderatley tender testicular mass
  3. diffuse granulomatous inflammation involving spermatic tubules
96
Q

BPH
1. pathogenesis
2. How can this be differentiated from prostate cancer (histology)
3. Tx?

A
  1. elevated DHT stimulates stromal cell and this increases growth factors -> leads to proliferation of glands in prostate and stroma (hyperplasia)
  2. The prostate epithelium has two cell layers: the luminal layer, which is composed of columnar epithelial cells, and the basal layer, which is composed of cuboidal epithelial cells. If any of these layers is abnormal or missing then think cancer
  3. meds (alpha blockers or 5 alpha reductase inhibitors) or sx
97
Q

Prostatic Carcinoma
1. What changes in epithelial layer of prostate is found?
2. Histology changes?
3. What drives the disease?
4. Genetic mutations?

A
  1. small layer of cuboidal or low columnar epithelium + lacking basal cell layer.
  2. Nuclei are enlarged and contain one or more prominent nucleoli, small crowded glands, and changes in epithelial linings
  3. Androgens promote the growth of both normal and cancerous prostate cells by binding to and activating the androgen receptor in prostate cells. Those who have shorter CAG repeats have more receptor sensitivity and more risk for cancer.
  4. BRCA2, PTEN, increased level/sensitivity of androgen receptor (lower CAG repeats)
98
Q

Prostatic Carcinoma
1. Where in prostate does this occur (think zones)
2. Where does it often spread to?
3. prognosis

A
  1. peripheral zones (BPH is in transitional zone by urethra)
  2. often spreads to spine (low back pain)
  3. good prognosis
99
Q
  1. What are precursor in situ lesions of penile Squamous cell carcinoma? (3)
  2. Which never becomes squamous cell carcinoma?
A
  1. Bowen disease (in penile shaft, presents as leukoplakia “white plaque”),
  2. Erythroplasia of Queyrat (carcinoma in situ of the glans, presents as erythroplakia “red plaque”)
  3. Bowenoid papulosis (carcinoma in situ of unclear malignant potential, presenting as reddish papules).
  1. Bowenoid never becomes squamous cell carcinoma and often regresses
100
Q

Bowen Disease vs Bowenoid Papulosis
1. Age range

A
  1. Bowen - usually >35 years old
  2. Bowenoid - sexually active adults, younger age demographic
101
Q

Bipotential (INDIFFERENT) phase
1. What happens in this phase to create indifferent gonads?

A
  1. Gonadal ridges derived from mesenchyme develop at about 7 weeks
  2. Germ cells (future gametes) from wall of yolk sac migrate towards hindgut - invade gonadal ridges - and allow gonads to develop there
102
Q
  1. What happens if bipotentatial phase doesn’t happen or is abnormal?
  2. What disorders show this?
  3. What sx/physical presentations occur?
A
  1. There is gonadal dysgenesis
  2. turner syndrome
  3. strea ovary with no functional gametes, webbed neck, short stature, high arched palate, cardiac anomalies
103
Q
  1. At what point are mesonephric and paramesonephric ducts still present?
  2. What does each do/form eventually?
A
  1. at the bipotential phase - indifferent gonad that can become either male or female
  2. Mesonephric duct (wolffian) - develops into male structures
  3. Paramesonephric duct (mullerian) - develops into female structures
104
Q

Male vs Female body
1. what causes elimination of mullerian/paramesonephric duct?
2. What stimulates development of wolffian/mesonephric duct?

A
  1. If embryo is XY - then they have SRY gene (codes for testes determining factor) which leads to formation of testes. Sertoli cells release (MIF) mullerian inhibiting factor to supress development of paramesonephric duct (mullerian). Leydig cells release androgens to stimulate development of mesonephric/wolffian duct
  2. If embryo is XY then no SRY gene - ovaries develop bc mullerian/paramesonephric ducts are NOT inhibited.

This is just formation of internal gonads (other things effect external genitalia)

105
Q
  1. What is important about the cloaca in embryo?
A
  1. It is part of gut tube and divides to form urogenital sinus and anal canal
106
Q
  1. What is the Gartner’s duct?
A
  1. this is wolffian remnant in female body
  2. found on vaginal wall and can form cysts at times.
107
Q

Urogenital sinus
1. What does this form in males
2. What does this form in females?

A
  1. Male: upper: forms bladder;;; middle: forms prostate, prostatic urethra, bulbourethral glands;;; phallic portion: penile urethra
  2. Female: upper: bladder;;; pelvic portion: inferior vagina, paraurethral glands (skene) and bartholin glands
108
Q

Genital Tubercle
1. In males what does this become?
2. What about females?

A
  1. males: penis
  2. females: clitoris
109
Q

Urogenital folds
1. what does this form in males
2. What about in females?

A
  1. males: these close and form penile urethra/spongy urethra
  2. females: stays open and forms labia minora
110
Q

Genital Swellings
1. what does this form in males
2. What about in females?

A
  1. males: this becomes scrotum
  2. Females: this becomes labia majora- but need estrogen to be higher than androgen for this to occur
111
Q

Epispadius
1. What is this?
2. Associated with what other disorder?

A
  1. urethral opening on the dorsal side of the penis. Due to abnormal position of genital tubercle.
  2. Associated with exstrophy of the bladder and abnormal closure of the anterior body wall
112
Q

Hypospadius
1. What is this?

A
  1. when urethral folds fail to close in males and it causes ventral opening of the urethra somewhere along penis
  2. More common than epispadius
113
Q

Uterine Abnormalities
1. Septation of uterus is due to what?

A
  1. failed fusion of two sides of the uterus. remember the paramesonephric ducts had to fuse in the middle to make one uterus- if this is abnormal then it leads to septated uterus or two complete separate uterus
114
Q

Ovotesticular Disorder of Sexual Development
1. What is this?
2. What is common karyotype

A
  1. both ovarian and testicular tissue present - genitalia is always ambiguous with tendency towards masculinization
  2. 46 XX
115
Q

Congenital Adrenal Hyperplasia (CAH)
1. what does this present as?
2. Common karyotype?
3. Why does this occur?

A
  1. ambiguous genitalia
  2. 46 XX
  3. masculinization of the external genitalia due to excessive androstenedione secreted by adrenal glands
116
Q

Androgen Insensitivity Syndrome
1. What does this appear as?
2. What is common karyotype?
3. What causes this?
4. What happens during puberty?

A
  1. external genitalia that are female in appearance but there are no uterine tubes or uterus - vagina ends inblind sac. Testes are in inguinal canals or labia majora.
  2. 46 XY
  3. Defect in androgen receptor resulting in female-appearing genetic male.
  4. Normal development of female sex characteristics but no menstruation. Androgens made by testes are ineffective in creating male external genitalia because of lack of androgen receptors.
117
Q

5-𝛂-Reductase deficiency
1. what is this?
2. What happens in puberty

A
  1. Without this enzyme cannot change testosterone to DHT (the more potent androgen) - so you get ambiguous genitalia
  2. At puberty - increased levels of testosterone allows for full development of external genitalia in males
118
Q
  1. what is disorders of sex development mean?
A
  1. when person has certain chromosomal sex (xx or xy) but this does not match their gonads (internal) or genitalia (external)
119
Q

Precocious Puberty
Dx criteria for
1. female
2. male

A
  1. breast development before 8 years of age
  2. testicular enlargement before 9 years of age
120
Q

Precocious puberty - Etiology
1. GnRH dependent causes
2. GnRH independent

A
  1. CNS tumors, hydrocephalus that puts pressure on pituitary, head traama with early secretion of GnRH, idipathic
  2. increased androgen secretion by adrenals (CAH, Cushing’s), increased androgen secretion by testes (tumors), increased estrogen secretions by ovaries (cysts or neoplasm)
121
Q

Precocious Puberty - imaging locations
1. what imaging is done if GnRH dependent is suspected?
2. What about GnRH independent?

A
  1. MRI - look at head
  2. imaging of pelvis
122
Q

Delayed Puberty - Dx criteria
1. males
2. females

A
  1. No testicuar enlargement by 14 or more than 5 years between start of puberty and completion of genital development
  2. No breast enlargement by 13, No menses by 16, or more than 5 years between breast development and onset of menses
123
Q

In men
1. What does LH stimulate?
2. What does FSH stimulate?

A
  1. LH stimualtes leydig cells
  2. FSH stimulates sertoli cells
124
Q

What is the role of testosterone in
1. fetus stage
2. puberty
3. adult

A
  1. fetus - internal and external genitalia requires hormones like testosterone to develop
  2. Puberty - leads to enlargement of scrotum and testes, increase penis size, growth of pubic hair, hair on face and underarms, deepening of voice, acne
  3. Adult - steady levels, can lead to prostate growth or certain levels of DHT can lead to male pattern balding
125
Q
  1. What is the function of inhibin in men?
A
  1. Made by sertoli cells and this inhibits pituitary from releasing FSH (negative feedbac)
126
Q

Testosterone
1. What is the synthesis pathway in Leydig cells to create testosterone?

A
  1. Start with cholesterol which eventualy becomes androstenedione.
  2. Then Type III 17 beta HSD (specific to leydig cell) creates final testosterone in leydig cells that get excreted
127
Q
  1. Are adrenal glands able to make tesosterone?
  2. Where is testosterone metabolized?
A
  1. No but they can make precursors to testosterone which can then be changed elsewhere
  2. Liver- undergoes conjugation and is excreted in urine
128
Q
  1. what hormone is for development of internal male genitalia?
  2. What about external male genitalia?
A
  1. testosterone
  2. DHT
129
Q

Tanner stages of male pubertal development
1. Stage I
2. Stage II
3. Stage III
4. Stage IV
5. Stage V

A
  1. pre-pubescent, low testicular volume, no pubic hair
  2. Testicular growth, minimal coarse pigmented hair at penis
  3. Continued testicular growth - initial penile lengthening - coarse, dark, curly hair spread over pubis
  4. Increased testicular growth, scrotum darkens, cont. penile lengthening, pubic hair of adult quality
  5. Full maturity, adult pubic hair distribution
130
Q

Helicine arteries
1. what are their function when penis is flaccid vs erect?

A
  1. When flacid blood does not go into these arteries (constricted) but when erect blood does go here (dilation) and make penis fully erect/full
131
Q

Emission vs Ejaculation
1. What is the difference
2. What induces each one

A
  1. emission is when sperm are moved from the testes and the epididymis (where the sperm are stored) to the beginning of the urethra. Ejaculation is when the semen is moved through the urethra and expelled from the body.
  2. Emission is caused by sympathetic induction (sympathethic reflex)
  3. Ejaculation is caused by spinal reflex (filling of internal urethra with semen elicits a reflex in the sacral spinal cord and somatic nerves -pudendal nerve-leads to rhythmic contractions of muscles to propel semen through urethra)
132
Q

Testosterone (topical, parenteral, oral)
1. Clinical use?
2. Adverse effect
3. Contraindications?

A
  1. Hypogonadism or delayed puberty
  2. HTN, MI, reduced fertility, fluid retention, hepatotoxicity (oral form), etc
  3. Avoid in prostate/Breast cancer in male, severe BPH, pregnancy
133
Q

Leuprolide, Goserelin
1. MOA
2. Clinical use
3. Adverse effect

A
  1. GnRH agonist - chronic administration eventually leads to suppression of LH and thus suppression of testosterone
  2. Precocious puberty, advanced prostate cancer, Hormone therapy for transgender female
  3. impotence, hot flashes, testicular atrophy
134
Q

Relugolix, Degarelix
1. MOA
2. Clinical use
3. Adverse effect

A
  1. GnRH Antagonist - to inhibit axis and stop testosterone stimulation
  2. Advanced prostate cancer
  3. Hot flashes, hepatotoxicity, hyperglycemia
135
Q

Abiraterone
1. MOA
2. Clinical use
3. Adverse effect

A
  1. Androgen synthesis inhibitor - inhibits 17α-hydroxylase (image)
  2. Metastatic prostate cancer
  3. Hot flashes, hyperglycemia, edema
136
Q

Finasteride
1. MOA
2. Clinical use
3. Adverse effect

A
  1. 5 alpha reductase inhibitor - The enzyme 5-alpha reductase is present in small amounts in muscle and converts testosterone to dihydrotestosterone (DHT).
  2. BPH, alopecia
  3. Impotence
137
Q

Enzalutamide
1. MOA
2. Clinical use
3. Adverse effect

A
  1. androgen receptor antagonist
  2. Prostate cancer
  3. Hot flashes, edema, hyperglycemia
138
Q

Sildenafil, tadalafil, vardenafil, avanafil (avanafil is most recently approved)
1. MOA
2. Clinical use
3. Adverse effect

A
  1. PDE-5 inhibits which leads to arterial smooth muscle relaxation -> good for erection
  2. Erectile dysfunction
  3. Headaches, vasodilation, diarrhea, rhinitis, epistaxis, blue tinge to vision (for sidenafil mostly) some side effects vary depending on which drug is used
139
Q
  1. What is gonadoblastoma?
A
  1. gonad tumor with mix of germ cells and gonadal stromal elements - this is rare
140
Q

Squamous cell carcinoma of penis
1. What can cause this?
2. Risk factors
3. age range
4. sx?
5. Histology?

A
  1. HPV 16 and 18
  2. poor hygiene, uncircumscribed, cigarette smoking, phimosis, chronic inflammatory conditions
  3. middle aged to older patients (40-70)
  4. no pain unless ulceration or infection present
  5. keratinizing squamous cell carcinoma

Block 7 (4 decks)

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