This quiz consists of 10 multiple-choice questions. To be successful with the weekly quizzes, it’s important to thoroughly read chapter 5 in the textbook. It will also be extremely useful to study the key terms at the end of the chapter and review the Test Your Knowledge activity at the end of the chapter.
Instruction
This quiz consists of 10 multiple-choice questions. To be successful with the weekly quizzes, it’s important to thoroughly read chapter 5 in the textbook. It will also be extremely useful to study the key terms at the end of the chapter and review the Test Your Knowledge activity at the end of the chapter. Keep the following in mind:
Multiple Attempts – You will have three attempts for this quiz with your highest score being recorded in the grade book.
Timing – You will need to complete each of your attempts in one sitting, as you are allotted 30 minutes to complete each attempt.
Answers – You may review your answer-choices and compare them to the correct answers after your final attempt.
To start, click the “Take the Quiz” button. When finished, click the “Submit Quiz” button.
Time Left: 30:00
Q. 1
Characteristic features of Rokitansky — Kuster Hauser syndrome are all of the following except :
A
Absent uterus
B
Absent vagina
C
Anovulation
D
46 — XX
Q. 1
Characteristic features of Rokitansky — Kuster Hauser syndrome are all of the following except :
A
Absent uterus
B
Absent vagina
C
Anovulation
D
46 — XX
Ans.
C
Explanation:
Anovulation
Mayer Rokitansky Kuser Syndrome (MRKH) is the complete failure in the development of the mullerian ducts resulting in absence of the fallopian tubes, uterus and most of vagina° (as of vagina is formed by Mullerian duct).
Mayer Rokitansky-Kuster Hauser syndrome
Karyotype = 46 XX°
Phenotype = Female
Associated abnormalities are :
Renal ectopy and agenesis (Horse shoe shaped kidney)°
Skeletal abnormalities° (most common – scoliosis)
Cardiac anomalies.°
Clinical features :
Patient present between 15-18 years of age with primary amenorrhoea.° (eugonadotropic amenorrhea).
Secondary sexual characteristics are normal° as ovaries are normal (because of their separate embryonic origin, so ovulation is also normal.)
P/V = Vagina is felt like a blind pouch and uterus is absent.°
Findings are confirmed by USG.°
Ideal method for demonstrating Uterine malformations is MRI.°
Management :
Repair of vaginal agenesis done either by frank dilatation or vaginoplasty.
Vaginoplast should onl be performed when the girls is just married or about to be marripri
Frank Dilatation :
This non-surgical procedure consists of a woman applying gradual pressure with progressively increasing dilators over the mullerian pit for 15 minutes twice a day. An indentation is created by the end of 3 to 6 month. Some have satisfactory intercourse, but in many, vaginal size is inadequate and they need a surgical procedure eventually.
Surgical management : Vaginoplasty either by Mc Indoe operation
Differential Diagnosis :
Testicular feminization syndrome.
Mayer Rokitansky-Kuster Hauser syndrome can be differentiated from testicular feminizing syndrome on the basis of :
Q. 2
Hysteroscopy is used in all EXCEPT :
A
Uterine synechiae
B
Abnormal vaginal bleeding
C
Infertility
D
None
Q. 2
Hysteroscopy is used in all EXCEPT :
A
Uterine synechiae
B
Abnormal vaginal bleeding
C
Infertility
D
None
Ans.
D
Explanation:
None
Q. 3
The Colposcopic features suggestive of malignancy are all except :
A
Condyloma
B
Vascular atypia
C
Punctation
D
White epithelium
Q. 3
The Colposcopic features suggestive of malignancy are all except :
A
Condyloma
B
Vascular atypia
C
Punctation
D
White epithelium
Ans.
D
Explanation:
White epithelium
Q. 4
Metropathica hemorrhagica is best treated by :
A
Curettage of uterus
B
Progestogen
C
Estrogen
D
Clomiphene
Q. 4
Metropathica hemorrhagica is best treated by :
A
Curettage of uterus
B
Progestogen
C
Estrogen
D
Clomiphene
Ans.
B
Explanation:
Ans. is b i.e. Progestogen
Metropathia hemorrhagica is a specialised form of DUB. Mostly seen in premenopausal women.
Maximum age incidence : between ages 40 – 45 years.
Pathology :
Changes in the Uterus : Symmetrical enlargement of the uterus to a size of 8 – 10 weeks due to hypertrophy of muscles.
Changes in Endometrium : Naked eye appearance : Endometrium looks thick, congested and often polypoidal.
Microscopic appearance :
Hyperplasia of all endometrial components.
Intense cystic glandular hypertrophy.
Some glands are small and some large giving appearance of “swiss cheese°.
Glands are empty and lined by columnar epithelium.
Secretory changes are absent.°
Follicular cysts containing estrogen present on ovaries.
Sign and Symptom : Patient complains of excessive painless bleeding (Anovular bleeding).
Treatment :
In DUB due to anovular causes : Progesterones are the mainstay of therapy.
They diminish the effects of estrogen on target cells by inhibiting oestrogen receptors.
To stop Acute severe bleeding :
Norethisterone (5 mg tab.) is given thrice daily till bleeding stops. Then norethisterone is stopped resulting in withdrawl bleeding (after 2-4 day). This is called as Medical curettage.
Thereafter cyclical progesterone – MPA (Medroxy Progesterone Acetate) 10 mg or Norethisterone 5 mg is given from day 5 – day 25 of the cycle for 3 cycles.
Q. 5
First site to be affected in genital tuberculosis :
A
Ovary
B
Cervix
C
Fallopian tube
D
Vagina
Q. 5
First site to be affected in genital tuberculosis :
A
Ovary
B
Cervix
C
Fallopian tube
D
Vagina
Ans.
C
Explanation:
Fallopian tube
Q. 6
Transverse vaginal septum corresponds to :
A
External Os
B
Vesical neck
C
Bladder base
D
Hymen
Q. 6
Transverse vaginal septum corresponds to :
A
External Os
B
Vesical neck
C
Bladder base
D
Hymen
Ans.
A
Explanation:
External Os
If there is a disorder in fusion of downgrowing Mullerian duct and upgrowing derivative of urogenital sinus. It results in Transverse vaginal septum which causes imperforate vagina (or vaginal agenesis).
In a series reported :
– 46% septa were located in upper part.° Ott ti2v-a
– 40% septa were located in middle part.°
– 14% septa were located in lower part.°
The upper part corresponds to external os therefore it is the option of choice.
Transverse vaginal septum can present either in :
A. Neonatal age group ?
The placental transfer of estrogen results in stimulatin the •lands of the endocervix which results in formation of Mucocolpos it can present as :
abdominal tumour.°
can compress the ureter resulting in hydroureter followed by hydronephrosis.°
can compress the rectum resultina in obstioation / intestinal obstruction.°
B. At puberty ?
Patient can present with Primary amenorrhea (actually called as Cryptomenorrheaa as uterus menstruates normally but blood does not come out due to outflow Tract obstruction).°
Secondary sexual characteristics are normal.°
Due to Cryptomenorrhoea, blood gradually collects and distends first the vagina (hematocolpos)° then cervix uterus (hematocervix and hematometra) and finally the tube (hematosaipinx)°. All these present as pelvic/ abdominal tumour.
The abdominal tumour can irritate the bladder followed by compression of internal urinary meatus leading to
complete retention of urine (This occurs 3 – 4 years after the onset of hidden menstruation and therefore patient is generally aged 15 – 18 years°).
Patient may complain of monthly cyclic pain (backache I lower abdomen pain).°
Management ?
Once the diagnosis of cryptomenorrhea is made, surgical treatment is urgently required° since every menstrual episode further dilates the genital tract and threatens permanent impairment of reproductive function.
Obstruction at the level of the cervix is managed by uterovaginoplasty. If uterovaginoplasty is unsuccessful hysterectomy is performed.
When the outflow menstrual blood is prevented by a thick vaginal membrane at any level, incision followed
by covering the deficiency with either vaginal epithelium or skin grafting is done.
When the obstructing membrane is thin and low down, the membrane is merely excised.°
Q. 7
All of the following are features of mullerian agenesis except :
A
46 XX karyotype
B
Normal breast development
C
Absent vagina
D
Ovarian agenesis
Q. 7
All of the following are features of mullerian agenesis except :
A
46 XX karyotype
B
Normal breast development
C
Absent vagina
D
Ovarian agenesis
Ans.
D
Explanation:
Ans:D.)Ovarian agenesis
Mullerian agenesis
It is Mayer Rokitansky-Kuster Hauser syndrome. .
Müllerian agenesis is a congenital malformation characterized by a failure of the Müllerian duct to develop, resulting in a missing uterus and variable degrees of vaginal hypoplasia of its upper portion. Müllerian agenesis (including absence of the uterus, cervix and/or vagina) is the cause in 15% of cases of primary amenorrhoea.
Because ovaries do not develop from the Müllerian ducts, affected women might have normal secondary sexual characteristics but are infertile due to the lack of a functional uterus.
Signs and Symptoms:
An individual with this condition is hormonally normal; that is, the person will enter puberty with development of secondary sexual characteristics including thelarche and adrenarche (pubic hair). The person’s chromosome constellation will be 46,XX. At least one ovary is intact, if not both, and ovulation usually occurs. Typically, the vagina is shortened and intercourse may, in some cases, be difficult and painful. Medical examination supported by gynecologic ultrasonography demonstrates a complete or partial absence of the cervix, uterus, and vagina.
Atypical MRKH – Uterovaginal aplasia/hypoplasia with renal malformation or uterovaginal aplasia/hypoplasia with ovarian dysfunction
Prevalence – 24 percent
MURCS syndrome – Uterovaginal aplasia/hypoplasia with renal malformation, skeletal malformation, and cardiac malformation
Prevalence – 12 percent
Q. 8
Find the wrong match :
A
Brenner’s tumor – puffed wheat nuclei
B
Krukenberg tumor – Signet ring appearance
C
Granulosa cell tumor – Cell exner bodies
D
Gonadoblastoma – Reinke’s crystals
Q. 8
Find the wrong match :
A
Brenner’s tumor – puffed wheat nuclei
B
Krukenberg tumor – Signet ring appearance
C
Granulosa cell tumor – Cell exner bodies
D
Gonadoblastoma – Reinke’s crystals
Ans.
D
Explanation:
Gonadoblastoma – Reinke’s crystals
Q. 9
In menopause, not seen is :
A
↓ FSH
B
↑Cholestsrol
C
↑ Androgen
D
↓ Cholesterol
Q. 9
In menopause, not seen is :
A
↓ FSH
B
↑Cholestsrol
C
↑ Androgen
D
↓ Cholesterol
Ans.
A
Explanation:
↓ FSH
Q. 10
Ovulation occurs due to :
A
Midcycle FSH surge
B
High prolactin level
C
Midcycle LH surge
D
a and c both
Q. 10
Ovulation occurs due to :
A
Midcycle FSH surge
B
High prolactin level
C
Midcycle LH surge
D
a and c both
Ans.
D
Explanation:
a and c both
Q. 11
The ovarian cycle is initiated by :
A
FSH
B
Oestrogen
C
LH
D
Progesterone
Q. 11
The ovarian cycle is initiated by :
A
FSH
B
Oestrogen
C
LH
D
Progesterone
Ans.
A
Explanation:
FSH
Initiated by the release of FSH (From Anterior pituitary) FSH stimulates the Growth of Multiple Follicles (Folliculogenesis)
Selection of a dominant Follicle (Graffian Follicle), by day 5-7. Graffian Follicle acquires FSH receptors on Granulosa cells and LH receptors on Theca cell. Under the influence of FSH, Graffian follicle secretes 178 estradiol (Day 7) 178 estradiol causes
4, i 4,
Proliferative changes Negative feedback on FSH Positive feedback on LH therefore
in the endometrium LH increases in amount.
Decreased Amount of FSH Increased LH leads to :
Production of androgen from Theca cells
which is converted peripherally to estrogen therefore Estrogen peak occurs (48 hours before ovulation)
LH surge (32-36 hours before ovulation) & LH peak (10-16 hours before ovulation) 1
Ovulation Occurs (14 days prior to next cycle)
Formation of corpus luteum & 2nd phase of ovulatory cycle i.e. Luteal Phase begins.
Secretes Progesterone
Stimulates Endometrium to undergo secretory changes 1.
In absence of Fertilisation corpus luteum degenerates
Oestradiol Progesterone Inhibin
(inhibin FSH production)
(Leads to menstruation in menstrual
cycle) & will release the negative Increased FSH as
feedback on GnRH, therefore compared to LH increases GnRH pulses
A patient is presenting with a non-painful swelling on the eye-lid as shown in the image.This condition occurs due to obstruction of which glands?
A. Zeis gland
B. Moll glands
C. Manz glands
D. Meibomian glands
Show Answer
Correct Answer » D
Explanation
Ans:D. Meibomian glands
Condition shown is Chalazion
Chalazion
Chalazion
It is a chronic noninfective granulomatous inflammation of the sebaceous glands of the eyelid.They commonly affect the meibomian glands in the tarsal plate, resulting clinically as a painless, firm nodule of the eyelid.It occurs due to due to blockage and swelling of meibomian glands.
Histologically, deep dermal or subcutaneous suppurative lipogranulomatous inflammation exists, containing neutrophils, plasma cells, lymphocytes, histiocytes, and giant cells in a zonal configuration around central lipid material. A pseudocapsule surrounds the cellular infiltrate.
Treatment:
Conservative treatment with lid massage, moist heat, and topical mild steroid drops .Intralesional steroid injection may also be used. These aid in reducing inflammation and increasing the local blood supply.
Antibiotics are usually unnecessary.
Incision and curettage is a conventional and effective treatment of chalazion
A chalazion clamp is applied to evert the lid and to control bleeding. A transconjunctival vertical incision is made (to avoid injury to other meibomian ducts)
If a chalazion threatens to break through the skin or has drained through, an external approach may be recommended. A horizontal incision is made in the skin (to have an invisible scar) at least 3 mm from the lid margin in an existing crease.
Alzheimer’s disease (AD) is a slowly progressive disease of the brain that is characterized by impairment of memory and eventually by disturbances in reasoning, planning, language, and perception.
Alzheimer’s disease is Common in 5th and 6th decade
Alzheimer’s disease is Atrophied gyri widened sulci
Cortical atrophy of temporoparietal cortex
ETIOLOGY:
It is likely that the causes include genetic, environmental, and lifestyle factors.
Some drug therapies propose that AD is caused by reduced synthesis of the neurotransmitter acetylcholine.
Other cholinergic effects have also been proposed, for example, initiation of large-scale aggregation of amyloid leading to generalized neuroinflammation.
Alzheimer’s disease is characterized by a build-up of proteins (Apo E gene) in the brain.
Trisomy 21 is associated with alzheimer’s dementia
Though this cannot be measured in a living person, extensive autopsy studies have revealed this phenomenon.
The build-up manifests in two ways:
Plaques– deposits of the protein beta-amyloid that accumulate in the spaces between nerve cells
Tangles – deposits of the protein tau that accumulate inside of nerve cells
Both amyloid plaques and neurofibrillary tangles are clearly visible by microscopy in brains of those afflicted by AD.
Plaques are dense, mostly insoluble deposits of amyloid – beta peptides and cellular material outside and around neurons.
Senile neural plaques correlates (increases) with age
Tangles (neurofibrillary tangles) are aggregates of the microtubule-associated protein tau which has become hyperphosphorylated and accumulate inside the cells themselves & are associated with severe dementia
Lateral geniculate body is resistant to neurofibrillary tangles.
SYMPTOMS:
Early Stage
This is considered as a mild/early stage and the duration period is 2-4 years.
Frequent recent memory loss, particularly of recent conversations and events.
Repeated questions, some problems expressing and understanding language.
Writing and using objects become difficult and depression and apathy can occur.
Drastic personality changes may accompany functional decline.
Need reminders for daily activities and difficulties with sequencing impact driving early in this stage.
Second stage
This is considered as a middle/moderate stage and the duration is 2-10 years.
Can no longer cover up problems.
Pervasive and persistent memory loss impacts life across settings.
Dementia of Alzheimer’s type is associated with Depressive symptoms, Delusions ,Apraxia and aphasia
Rambling speech, unusual reasoning, confusion about current events, time, and place.
Potential to become lost in familiar settings, sleep disturbances, and mood or behavioral symptoms accelerate.
Nearly 80% of patients exhibit emotional and behavioral problems which are aggravated by stress and change.
Slowness, rigidity, tremors, and gait problems impact mobility and coordination.
Need structure, reminders, and assistance with activities of daily living.
Moderate stage
Increased memory loss and confusion.
Problems recognizing family and friends.
Inability to learn new things.
Difficulty carrying out tasks that involve multiple steps (such as getting dressed).
Problems coping with new situations.
Delusions and paranoia.
Impulsive behavior.
In moderate AD, damage occurs in areas of the brain that control language, reasoning, sensory processing, and conscious thought
Last stage
This is considered as the severe stage and the duration is 1-3 years.
Confused about past and present.
Loss of recognition of familiar people and places
Generally incapacitated with severe to total loss of verbal skills.
Unable to care for self.
Falls possible and immobility likely.
Problems with swallowing, incontinence, and illness.
Extreme problems with mood, behavioral problems, hallucinations, and delirium.
Patients need total support and care, and often die from infections or pneumonia
DIAGNOSIS
Patient history, collateral history from relatives, and clinical observations
Characteristic neurological and neuropsychological features and the absence of alternative conditions.
Computed tomography (CT) or magnetic resonance imaging (MRI), and with single photon emission computer tomography (SPECT) or positron emission tomography (PET) can be used to help exclude other cerebral pathology or subtypes of dementia.
The fixative used in histopathology 10% buffered neutral formalin
The diagnosis can be confirmed with very high accuracy post-mortem when brain material is available and can be examined histologically.
TREATMENT:
Cholinesterase inhibitors: donepezil, rivastigmine, and galantamine.
These agents are orally active, have adequate penetration into the central nervous system.
Exam Question
In Alzheimer’s disease Cortical atrophy of temporoparietal cortex is involved.
Recent memory loss is feature of Alzheimer’s disease
Degenerated neurofilaments seen in patients with Alzheimer’s disease are Neurofibrillary tangles
Neurofibrillary tangles, Senile (neurotic) plaques & Amyloid angiopathy are feature of Alzheimer’s disease
Trisomy 21 is associated with alzheimer’s dementia
The area of the brain resistant to Neurofibrillary tangles of Alzheimer’s disease is Lateral geniculate body
Galantamine, Rivastigmine & Donepezil are used for treatment of Alzheimer’s disease
Protein involved in Alzheimer’s disease is Apo E gene
Biochemical etiology of Alzheimer’s disease relates it to Acetylcholine
Dementia of Alzheimer’s type is associated with Depressive symptoms, Delusions, Apraxia and aphasia
Alzheimer’s disease is Common in 5th and 6th decade
Alzheimer’s disease is Atrophied gyri widened sulci
In Alzheimer’s disease number of senile neural plaques correlates (increases) with age
In Alzheimer’s disease there is presence of tau protein suggest neurodegeneration
In Alzheimer’s disease number of neurofibrillary tangles is associated with the severity of dementia
Area of brain resistant to NFTs in Alzheimer’s disease Lateral geniculate body
Biochemical etiology of Alzheimer’s disease relates to acetylcholine
The fixative used in histopathology 10% buffered neutral formalin
Donepezil is a cerebroactive drug. It is used in Alzheimer’s disease (AD).
Don’t Forget to Solve all the previous Year Question asked on Alzheimer’s Disease
