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Pathophysiology III Reproductive Systems 1

Total questions: 89

Worksheet time: 45mins

Name
Class
Date
1.

X Chromosomes typically develop?

a)

Male Phenotype

b)

Female Phenotype

2.

XY Chromosomes typically develop?

a)

Male Phenotype

b)

Female Phenotype

c)

Hermaphroditism

3.

What determines gonadal (primary) sex determination?

a)

Genetic Sex

b)

Phenotypic Sex

c)

Sexual Hair

4.

Nonfunctional Ovary Chromosomal Arrangement?

a)

XX

b)

X0

c)

XY

5.

DAX1 and WNT4 function?

a)

Promote female sex development

b)

Represses male sex development

c)

Destroys the Mullerian Duct

6.

Follicular cells v.s. Theca Cells?

a)

Granulosa Cells are Present since Primordial stage

b)

Theca cells develop in secondary follicle + Membrana Granulosum as well = Antral Fluid Production

c)

Tertiary Follicle gives rise to Theca interna (Glandular) and Theca Externa (connective tissue)

7.

Follicular Cells and Theca Cells together form?

a)

Follicles that produce estrogen

b)

Follicles that produce testosterone

c)

Testes that produce Spermatozoa

8.

Mullerian duct develops into?

a)

Female internal Genitalia (Uterus, Cervix, Fallopian Tubes and Upper Vagina)

b)

Male External Genitalia (Testes and Penis)

9.

What genes are responsible for conversion of genital ridge to bipotential gonads?

a)

Steroidogenic Factor (SF1)

b)

Wilms Tumor Gene 1 (WM1)

c)

LHX9

d)

SOX9

10.

Bipotential Gonads become Testis through activation of what gene?

a)

SOX9

b)

SRY

c)

WNT4

d)

DAX1

11.

What is the role of SOX9 in testes development?

a)

regulation of Anti-Mullerian Hormone Transcription

b)

development of internal female genitalia

12.

Bipotential gonads can become ovaries by activation of which genes?

a)

WNT4

b)

DAX1

c)

SOX9

d)

SRY

13.

Function of sertoli cells?

a)

AMH Production

b)

Inhibin to regulate FSH Production

c)

Androgen Binding Protein to Increase testosterone in seminiferous tubules to stim Spermatogenesis

d)

Aromatase prod to convert TST to 17b-estradiol to direct spermatogenesis

14.

Leydig cells are stimulated by LH to produce?

a)

TST and DHEA

b)

Estrogen

15.

What hormone increases the response of leydig cells to LH?

a)

Prolactin

b)

ADH

16.

What enzyme stimulates the production of DHT?

a)

5-alpha reductase

b)

alpha 1 antitrypsin

17.

DHT acts on genital tubercle and urogenital sinus to form?

a)

Penis and Prostate

b)

Ovaries

c)

Uterus

18.

Male internal genitalia (epididymis, vas deferens, seminal vesicle) are formed from TST stimulating?

a)

Wolffian Duct

b)

Urogenital Sinus and Genital Tubercle

c)

Mullerian Duct

19.

Sertoli cells secete Mullerian Inhibiting Substance which causes?

a)

Wolffian Duct Degeneration

b)

Mullerian Duct Degeneration

20.

Activin and Inhibin function?

a)

TST Biosynthesis and Secretion

b)

LH Biosynthesis and Secretion

c)

FSH Biosynthesis and Secretion

d)

ADH Biosynthesis and Secretion

21.

Due to Leydig cells not being present and no testosterone available, what happens in the female Wolffian Duct?

a)

Wolffian Duct Degeneration

b)

Wolffian Duct Proliferation

c)

Mullerian Duct Degeneration

22.

FSH stimulates what in males?

a)

Sex hair destruction

b)

Testicular Degeneration and Enhanced production of Estrogen Binding Protein

c)

Testicular Growth and Enhanced production of Androgen Binding Protein

23.

Estrogen and the mullerian duct/wolffian duct?

a)

Destroys both of them

b)

Inhibits their development and is not needed for fertility in both sexes

c)

Promotes their development and needed for fertility in both sexes

24.

TST (leydig) can be converted by aromatase (sertoli) and to DHT by?

a)

5-Beta reductase

b)

5-alpha reductase

c)

10-alpha reductase

25.

LH Acts on Theca cells and causes production of?

a)

Testosterone

b)

ADH

c)

Estrogens and progestins

26.

Failure to form uterus and fallopian tubes is known as?

a)

Mullerian Genesis

b)

Mullerian Biopsy

c)

Mullerian Agenesis

27.

What factor produced by Leydig cells is needed for testes descent?

a)

Insulin Like Growth Factor - 3

b)

GH

c)

GnRh

28.

What is hydrometrocolpos?

a)

Constriction/Tightening of vagina/uterus caused by accumulation of cervical secretions from maternal estrogen stimulation

b)

Dilation of testes/penis caused by accumulation of cervical secretions from maternal estrogen stimulation

c)

Dilation of vagina/uterus caused by accumulation of cervical secretions from maternal estrogen stimulation

29.

Autosomal recessive mutation of MKKS gene can lead to?

a)

Kallman Syndrome

b)

Mckusick-Kaufman Syndrome

30.

Hydrometrocolpos causes?

a)

Imperforated Hymen

b)

Septate Uterus

c)

Atresia

31.

Mckusik-Kaufman syndrome presentation in females? (Remember this TRIAD)!

a)

HMC (Hydrometrocolpos)

b)

Polydactyly

c)

Congenital Heart Disease

32.

Mckusik-Kaufman syndrome presentation in males? (remember this TRIAD)!

a)

Genital Malformation

b)

Polydactyly

c)

Congenital Heart Disease

33.

Failure of testis to descend into scrotum?

a)

Cryptorchidism (Highly occurs in Inguinal region vs intraabdominal)

b)

Mullerian Agenesis

c)

Testicular Agenesis

34.

Kallman Syndrome is a type of hypogonadotropic hypogonadism. What is the pathophysiology?

a)

Olfactory Placode defect

b)

Lumbar Degeneration

c)

Testicular Maturation

35.

Symptoms of Kallman syndrome/presentation?

a)

Hyposmia/Anosmia

b)

Decreased GnRH

c)

Decreased LH/FSH

36.

Kallman syndrome decreases which hormone levels?

a)

Decreased TST and Estrogen/Progesterone

b)

ADH

c)

AMH

37.

Due to Decreased TST and Estrogen/Progesterone in Kallman Syndrome, what happens during development?

a)

Precocious Puberty

b)

Failure to start puberty

38.

Testicles must descend within 3-9 months or?

a)

must be surgically removed by age 3

b)

must be surgically removed by immediately at 9 months

c)

must be surgically removed by age 2

39.

Complications of cryptorchidism?

a)

infertility

b)

testicular torsion

c)

seminoma/germ cell carcinoma

40.

Where does the urethra open in epispadias and hypospadias, respectively?

a)

Urethra opens in dorsal surface in epispadias and ventrally in hypospadias

b)

Urethra opens in ventral surface in epispadias and dorsally in hypospadias

c)

Urethra opens in left lateral surface in epispadias and right lateral in hypospadias

41.

Risk factors for embryological malformations of the urethra?

a)

monozygotic twins

b)

stillbirths

c)

preterms

42.

Phimosis?

a)

Prepuce is too loose and floppy

b)

prepuce is too tight to be retracted

43.

Main complication of phimosis?

a)

Paraphimosis

b)

Infection

44.

Why is phimosis an increased risk factor for infection?

a)

Interferes with hygiene

b)

Prepuce needs air

c)

Unable to ejaculate

45.

Why is paraphimosis a medical emergency?

a)

Urethral constriction = unable to retract foreskin back in place = gangrene and amputation

b)

Unable to urinate afterwards

46.

Androgen insensitivity syndrome is also known as?

a)

Roid Rage

b)

Anabolic Rage

c)

Metabolic Acidosis

d)

Testicular femenization syndrome

47.

46XY individuals with x-linked recessive disorder and defect in androgen receptor?

a)

Kallman Syndrome

b)

Mckusik-Kaufman syndrome

c)

Androgen Insensitivity Syndrome (AIS)

48.

Androgen Insensitivity Syndrome presents as?

a)

Normal appearing male with female genotype

b)

Normal appearing female with male genotype

c)

Normal appearing male with hermaphroditism

49.

In androgen Insensitivity Syndrome, why is there degeneration of internal female sex organs even though there is a female phenotype?

a)

Mullerian Inhibiting Factor still works because of male genotype

b)

Prolactin Excess

c)

ADH Excess

50.

In androgen insensitivity syndrome, there is a loss of (-) feedback and this results in?

a)

Decreased TST and LH, and Increased Estrogen due to conversion of TST by aromatase

b)

Increased TST and LH, and Increased Estrogen due to conversion of TST by aromatase

c)

Decreased TST and LH, and decreased Estrogen due to conversion of TST by aromatase

51.

Testosterone unable to be converted to DHT results in?

a)

no external male sex organs

b)

Development of external male sex organs

52.

Physical exam of AIS?

a)

Rudimentary thyroid, Cryptorchidism and excessive sexual hair

b)

Rudimentary penis, Cryptorchidism and massive sexual hair

c)

Rudimentary vagina, Cryptorchidism and NO sexual hair

53.

Partial AIS is also known as?

a)

Reifenstein Syndrome

b)

Kallman Syndrome

c)

Mckusik-Kaufman Syndrome

54.

People with mild androgen insensitivity present with?

a)

Female sex characteristics but are infertile/may not develop breasts in puberty

b)

Female and male sex characteristics but are infertile/may or may not develop breasts in puberty

c)

Male sex characteristics but are infertile/may develop breasts in puberty

55.

Absence of breast development by age 12 or testicular enlargement by age 14?

a)

Precocious Puberty

b)

Delayed Puberty

c)

Early Puberty

56.

Most common cause of constitutional delay or growth and puberty?

a)

Genetic defect causing an extra chromosome

b)

Autoimmune defect that causes antibodies against GnRH

c)

Functional Defect in prod of GnRH

57.

Primary hypogonadism causes?

a)

Low gonadal steroids

b)

High gonadal steroids

58.

FSH/LH Labs for primary hypogonadism?

a)

Decreased LH/FSH

b)

Increased LH/FSH

c)

Always normal LH/FSH

59.

Conditions associated with primary hypogonadism?

a)

Turner Syndrome

b)

Klinefelter Syndrome

c)

Chemotherapy Injury/Cryptorchidism

d)

Mumps and TST synthesis

60.

Secondary Hypogonadotropic hypogonadism labs?

a)

Elevated LH/FSH and Excess GnRh or Gondatoropin Secretion

b)

Low or Normal LH/FSH and Deficient GnRh and/or gonadotropin secretion

61.

ANOS1 mutation?

a)

Kallman Syndrome

b)

Mckusick-Kaufman Syndrome

c)

Androgen Insensitivity Syndrome

62.

Renal Issue in Kallman Syndrome?

a)

Unilateral Renal Agenesis

b)

Bilateral Renal Agenesis

c)

Unilateral Renal Artery Stenosis

63.

What is Bimanual Synkinesis? What syndrome is this seen in?

a)

Contraction of one muscle causes contraction of another

b)

Kallman

c)

Failure to contract 2 groups muscles at once

d)

Mckusick-Kaufman

64.

Turner Syndrome gene defect? Clinical Presentation?

a)

45 X0 ; Short Stature, Hypogondism, delayed puberty, Infertility,

b)

45 X0 ; Webbed Neck, Low Hairline, Lymphedema hands/feet, renal and skeletal problems, Coractation of Aorta and Arotic Valve Problems

65.

Klinefelter syndrome has an extra chromosome. What is the sequence?

a)

XX

b)

XY

c)

XXY

66.

Klinefelter syndrome clinical presentation?

a)

Taller than average, Small Testis, Cryptorchidism, Hypospadias

b)

Low muscle tone, intellectual disability

67.

What is precocious puberty? What is Central Precocious Puberty?

a)

Precocious: Onset of secondary sex characteristics before age 8 (female) and 9 (Male) due to variants, normal Dev, or malignancy

b)

Central Precocious: Gonadotropin-Dependent or TRUE Precocious Puberty

68.

Pathophysiology of central precocious puberty?

a)

Early maturation of hypothalamic-pituitary-gonadal axis

b)

Late maturation of hypothalamic-pituitary-gonadal axis

69.

Central precocious puberty presentation?

a)

Early sequential maturation of breasts and pubic hair in females

b)

Early Testicular. penile and pubic hair growth in males

70.

Causes of central precocious puberty?

a)

Idiopathic

b)

CNS Lesions, Genetic Dysfunction

c)

Pituitary Gonadotropin Releasing Tumor

71.

Peripheral precocious puberty refers to?

a)

Gonadotropin independent precocious puberty

b)

Gonadotropin dependent precocious puberty

72.

Causes of peripheral precocious puberty?

a)

excess sex hormones from gonads, adrenals, exogenous or ectopic (germ cell tumor)

b)

XX

c)

xx

73.

Why precocity and not puberty?

a)

Puberty requires activation HPG axis

b)

Precocity requires activation of HPG axis

74.

Female causes of peripheral precocity?

a)

Ovarian Cysts and tumors

b)

Ovarian tumors can lead to granulosa cell tumors = isosexual

c)

Sertoli or Leydig Cell can cause contrasexual development

75.

Male causes of peripheral precocity?

a)

Leydig cell tumors (TST)

b)

HCG secreting cell tumors - increased TST

76.

Why does primary hypothyroidism cause peripheral precocity?

a)

excess TSH stimulating FSH receptors

b)

Low tsh causes high fsh= precocity

77.

McCune Albright Syndrome Triad?

a)

Peripheral Precocious Puberty

b)

Cafe Au Lait Spots

c)

Fibrous Dysplasia of Bone

78.

Mnemonic for McCune Albright? MCCUNE ABIG

a)

Menarche Comes early

b)

Cafe aU lait

c)

iNcreased Estrogen

d)

Aromatase inhibitors

e)

Bone gone wrong - Independent of Gnrh

79.

Pathophysiology of McCune Albright Syndrome?

a)

mutation of protein that activates adenylyl cyclase and leads to continued stimulation of endocrine function

b)

Liver/Heart Issues

c)

Cholestasis/Hepatic Issues

d)

Intestinal Polyps and Arrhythmias

80.

Benign Non-Progressive Variants refers to?

a)

isolated breast development in females (premature thelarche)

b)

isolated androgen mediated sex characteristic development in males (Pubic hair axillary acne apocrine)

81.

Benign Non Progressive Variants Diagnosis?

a)

mildly elevated levels of Dehydroepiandrosterone (premature adrenarche)

b)

Severely elevated levels of Dehydroepiandrosterone (premature adrenarche)

82.

Pseudohermaphroditism?

a)

mismatch between phenotypic sex and gonadal testes (ovary/testicle)

b)

xx

83.

Female Pseudohermaphroditism genotype and presentation?

a)

XX genotype

b)

excessive/inappropriate exposure to androgenic steroids during early gestation

84.

Female pseudohermaphroditism is most commonly seen?

a)

Congenital Adrenal Hyperplasia

b)

Exogenous Administration

c)

Aromatase Deficiency

85.

Male pseudohermaphroditism genotype and most common cause?

a)

XY

b)

XX

c)

Androgen Insensitivity Syndrome (testicular feminization)

d)

Lupus

86.

True hermaphroditism refers to?

a)

Presence of ovarian and testicular tissue in XX, XX/XY, or XY with varying degrees of ambiguous genitalia

b)

xx

87.

Causes of true hermaphroditism?

a)

Ovum splits and then fuses together again

b)

SRY gene mutation = some testicular development but not enough female suppression

88.

5 alpha reductase deficiency refers to?

a)

Autosomal recessive defect in XY chromosomes

b)

xx

89.

Pathophysiology of 5-alpha reductase deficiency?

a)

Impaired conversion of TST to DHT = impaired virilization, Normal TST/Estrogen prod, normal or elevated LH, normal internal genitalia

b)

Ambiguous genitalia

c)

No Gynecomastia