Pelvic Organ Prolapse, Menstrual Disorders, Anemia In Pregnanxy

Question 1

What is a prolapse?
What’s the difference between prolapse and a fistula
State the risk factors for an obs fistula and examples of fistulas

Answer 1

Prolapse is defi ned as protrusion of the uterus and/or vagina beyond normal anatomical confi nes. The bladder, urethra, rectum, and bowel are also often involved. Pelvic organ prolapse is the abnormal descent or herniation of the pelvic organs from their normal attachment sites or their normal position in the pelvis. The pelvic structures that may be involved include the uterus (uterine prolapse) or vaginal apex (apical vaginal prolapse), anterior vagina (cystocele), or posterior vagina (rectocele).
•Genital prolapse is a group of clinical conditions that affect women and increases with age. It is defined as the protrusion of a pelvic organ beyond its normal anatomical confines. It is not life threatening but can severely affect the quality of life of many women. The term genital prolapse is synonymous with pelvic relaxation and pelvic organ prolapse (POP).

A fistula is an abnormal connection between two epithelial tissues or two body cavities.
Risk factors- Teenager, poor ANC attendance, obstetrics labour, prolonged labour, nulli parity,macrosmia,small pelvis,CPD,tears,advanced maternal age. Multiparity isn’t a risk factor for fistula but it can be a risk factor for pelvic prolapse

Examples- recto Vaginal, uterovesical fistula,vesicovaginal fistula

Fistulas for general surgery:
Anal fistula, enterocutaneous fistula

Question 2

What does the pelvic floor consists of
Name the major supports of the uterus
Who introduced the three levels of pelvi organ support
What are the three levels of pelvic organ support?
Damage to each support causes specific prolapses. Name the support and each prolapse

Answer 2

The pelvic fl oor consists of muscular and fascial structures that provide support to the pelvic viscera and the external openings of the vagina, urethra, and rectum . The uterus and vagina are suspended from the pelvic side walls by endopelvic fascial attachments that support the vagina at three levels.

•PELVIC SUPPORTS
•The pelvic viscera are supported by the pelvic floor fascia, ligaments (part of endopelvic fascia) and muscles. The major supports of the uterus are the • Transverse cervical ligaments (also called Cardinal or Mackenrodt’s ligaments), • Uterosacral ligaments
•In 1993, Delancey introduced 3 levels of pelvic organ support.
•Level 1 support (Apical):
• Transverse cervical ligaments (also called Cardinal or Mackenrodt’s ligaments).
• Uterosacral ligaments. damage results in prolapse of vaginal apex
•Level 2 support (Transverse or Horizontal)
•• Levator ani and arcus tendinous fascia.
• Pubocervical fascia. • Rectovaginal fascia
•Damage results in retrocele or a cystocele

•Level 3 support
•• The third level shows the superficial transvers perineal muscle and the urethra.Damage results in urethrocele

Level 1: the cervix and upper third of the vagina are supported by the cardinal (transverse cervical) and uterosacral ligaments. These are
attached to the cervix and suspend the uterus from the pelvic sidewall and sacrum respectively.
• Level 2: the mid portion of the vagina is attached by endofascial
condensation (endopelvic fascia) laterally to the pelvic side walls. created by vaginal attachment to arcus tendineus and fascia of levator ani
• Level 3: the lower third of the vagina is supported by the levator ani muscles and the perineal body. The levator ani, together with its
associated fascia, is termed the pelvic diaphragm.
damage resultsin urethrocele

Uterus on top of vag, rectum behind, bladder and ureters in front

Question 3

Pelvic organ prolapse is usually caused by weakness of the pelvic diaphragm. Descent of the pelvic diaphragm places stress on the endopelvic connective tissue support system. Subsequent increases in intra-abdominal pressure result in prolapse. In the majority of cases, labor and childbirth are thought to be the primary factors responsible for pelvic neuropathies and tissue damage that predispose to the development of POP.
DeLancey demonstrated that normal pelvic support is provided by the interaction between the levator ani muscle group and connective tissue attachments that stabilize the vagina at varying levels. Any weakness or tears within the connective tissue leads to the varying pathology of pelvic floor defects.[3]

With normal pelvic support, the vagina lies horizontally on top of the levator ani muscles. Damage causes the levator ani muscles to become more vertical in orientation, opening the vagina, and thus shifting support to the connective tissue attachments.
True or false ?

Answer 3

True

Question 4

What are the classifications of pelvic organ prolapse ( with respect to the compartments)
Name the other ways of classifying POP

Answer 4

ANTERIOR COMPARTMENT DEFECTS
 Urethrocele: the urethra is displaced from the suprapubic angle and displaced downwards on straining
 Cystocele: weakness of pubocervical fascia and pubourethral ligament leading to displacement of the bladder. Cystocele is prolapse of the anterior vaginal wall, involving the bladder. Often there is an associated prolapse of the urethra, in which case the term cysto-urethrocele is used.

POSTERIOR COMPARTMENT DEFECTS
 Rectocele -Rectocele is prolapse of the lower posterior wall of the vagina,
involving the anterior wall of the rectum.A posterior vaginal prolapse, also known as a rectocele, occurs when the wall of tissue that separates the rectum from the vagina weakens A rectocele is a bulging of the front wall of the rectum into the back wall of the vagina. The rectum is the bottom section of your colon (large intestine).

MIDDLE/APICAL COMPARTMENT DEFECT
 Enterocele: herniation of the pouch of Douglas through the posterior vaginal fornix. It may
contain bowel or omentum. Enterocele is prolapse of the upper posterior wall of the vagina. The resulting pouch usually contains loops of small bowel.

 Vaginal vault prolapse: Inversion of the apex of the vagina following abdominal/vaginal hysterectomy. vaginal vault prolapse-Vaginal prolapse, also known as vaginal vault prolapse, occurs when the top of the vagina weakens and collapses into the vaginal canal. In more serious cases of vaginal prolapse, the top of the vagina may bulge outside the vaginal opening. vaginal vault prolapse characterizes descent of the uterus, cervix, or apex of the vagina
 Uterovaginal prolapse-Uterine (apical) prolapse is the term used to describe prolapse of
the uterus, cervix, and upper vagina. If the uterus has been removed,
the vault or top of the vagina, where the uterus used to be, can itself
prolapse.

Classifications of POP . Methods for noting pelvic floor relaxation include (1) the Baden Walker classification or halfway system, (2) the International Continence Society (ICS) classification using the Pelvic Organ Prolapse Quantification (POPQ) system, and (3) the revised New York Classification (NYC) system. [11, 12, 13]

Question 5

Explain the POP Qclassification and the Baden Walker classification

Answer 5

Most clinicians routinely use the ICS classification (POP-Q) system, which is classified as follows:
Stage 0 - No prolapse
Stage I - Descent of the most distal portion of prolapse is more than 1 cm above the level of the hymen.
Stage II - Maximal descent of prolapse is between 1 cm above and 1 cm below the hymen.
Stage III - Prolapse extends more than 1 cm beyond the hymen, but no more than within 2 cm of the total vaginal length.
Stage IV - Total or complete vaginal eversion

Grading of urogenital prolapse (Baden–Walker
classifi cation)
• First degree: the lowest part of the prolapse descends halfway down
the vaginal axis to the introituse.
• Second degree: the lowest part of the prolapse extends to the level
of the introituse and through the introituse on straining.
• Third degree: the lowest part of the prolapse extends through the
introituse and lies outside the vagina.
2 Procidentia describes a third-degree uterine prolapse.

Stage I where the prolapse does not reach the hymen.
• Stage II where the prolapse reaches the hymen.
• Stage III when the prolapse is mostly or wholly
outside the hymen.
STAGE IV -When the uterus prolapses
wholly outside this is termed procidentia.

DON’T JUST WRITE POP ADD THE STAGING

Previously used, the Baden-Walker Halfway system is an alternative grading system for pelvic organ prolapse.[15] Normal pelvic support is defined as grade 0. Descent half the distance to the hymen is grade 1, distant at the hymen is grade 2, and distant distal to the hymen is grade 3. Stage 4 describes complete procidentia.

Baden–Walker half way system [6]. It consists of four grades: grade 0 – no prolapse, grade 1–halfway to hymen, grade 2 – to hymen, grade 3 – halfway past hymen, grade 4 –maximum descent.

Question 6

State five causes of POP
Name the most common cause

Answer 6

Pregnancy and vaginal delivery: prolapse is uncommon in nulliparous women. Vaginal delivery may cause mechanical injuries and denervation of the pelvic fl oor. The risk is increased with large babies, prolonged second stage, and instrumental delivery (particularly forceps).
• Congenital factors: abnormal collagen metabolism, for example, in Ehlers–Danlos syndrome, can predispose to prolapse.
• Menopause: the incidence of prolapse increases with age. This may be due to the deterioration of collagenous connective tissue that occurs following oestrogen withdrawal.
• Chronic predisposing factors: prolapse is aggravated by any chronic increase in intra-abdominal pressure, resulting from factors such as obesity, chronic cough, constipation, heavy lifting, or pelvic mass.
• Iatrogenic factors: pelvic surgery may also infl uence the occurrence of
prolapse:
• hysterectomy is associated with subsequent vaginal vault prolapse (particularly when the indication was prolapse)
• continence procedures, although elevating the bladder neck, may lead to defects in other pelvic compartments (Burch colposuspension may predispose to rectocele and enterocele
formation).

Question 7

State ten risk factors of POP

Answer 7

Increasing age
 Increasing parity
 Previous pelvic surgery (including hysterectomy)
 Congenital weakness in pelvic floor
 Menopause
 Obesity

Immediate precipitating factors to genital prolapse
 Increased intra-abdominal pressure from chronic cough and constipation
 intra-abdominal masses or ascites
 occupational activity requiring repetitive lifting of heavy objects
 menopausal state (lack of estrogens)

Increasing age has been found to be associated with denervation injury to the pelvic floor ligaments and musculature. This is increased by childbearing. Each vaginal delivery, no matter how well-conducted, is associated with some denervation injury. The degree of denervation injury is affected by duration of the 2nd stage of labour and by operative interventions such as episiotomies. Previous pelvic surgery also causes nerve damage to the pelvic floor muscles.
Estrogen helps tissues o be strong and as they go to menopause, it doesn’t work anymore. Vaginal delivery stretches delivery. Women who get cervical and perineal tears during delivery. Fam hx of prolapse due to fam hx of weak collagen. Ascites, abdominal masses, number of kids and if she delivered all by SVD, weight of baby., HOW IS IT AFFECTING YOUR LIFE (SEX LIFE, PROBLEMS WITH URINATION OR SHITTING
Symptoms- Wasit pain, BPV or discharge from ulcer on POP

Question 8

How will a patient with a prolapse present and what questions should you ask?

Answer 8

Age
Other demographics

PC- Something coming down’ or a feeling of a mass/lump in the vagina which worsens with
progression of the day, and relieved by lying down
 Dragging discomfort in vagina

So you have to ask if the thing worsens as the stands for long as the day progresses or if it is relieved when she lies down

ODQ- BPV or discharge from ulcer on POP . Dyspareunia. Vaginal discharge
CYSTO-URETHROCELE:
 Urinary symptoms such as incomplete bladder emptying despite straining,urgency,frequency. The patient may
digitally reduce the bulge in order to pass urine. Urinary retention
 Frequency and recurrent UTI
 Hydroureters and hydronephrosis due to kinking of ureters are rare
 Rectocele may present with constipation, difficulty with defecation and she may resort to splinting before
moving bowels(may digitally reduce it to defecate).
Symptoms tend to become worse with prolonged standing and towards the end of the day. In case of grade 3 or 4 prolapse, there may be mucosal ulceration and lichenifi cation, resulting in vaginal bleeding and discharge.

Number of pregnancies, number of deliveries. If she delivered by SVD or CS.If SVD, If there were any complications during deliveries such as cervical and perineal tears during delivery. The weight of the baby.
If they’ve had any surgery done(pelvic surgery such as hysterectomy is a risk factor for prolapse such as Vaginal vault prolapse), Fam hx of prolapse due to fam hx of weak collagen. Ascites, abdominal masses, number of kids and if she delivered all by SVD, HOW IS IT AFFECTING YOUR LIFE (SEX LIFE, PROBLEMS WITH URINATION OR SHITTING

Question 9

How will you diagnose someone with POP
Why will you examine in sims position

Answer 9

SIMS POSITION WHY-This allows retraction of the anteriorand posterior vaginal wall in turn, to allow full assessment of the degree of prolapse and to assess how much
descent of the cervix and uterus is present.

1. History: symptoms (urinary, bowel, sexual); complications (ulcer, pain, infection, bleeding)
2. Examination includes Sims speculum in lateral position, examination in supine and erect positions
3. Grading (Baden Walker or POP-Q system)

Question 10

What do you expect to see on physical examination

Answer 10

ASK TO COUGH WHEN LYING AND IF NOTHING OR SQUAT OR STRAIN AND THE THING WILL COME OUT

Exclude pelvic masses with a bimanual examination.
• Vaginal examination is best carried out with the woman in the left
lateral position OR LITHOTOMY POSITION, using a Sims speculum.
• The walls should be checked in turn for descent and atrophy.
• If absolutely necessary, a volsellum may be applied to the cervix so that traction will demonstrate the severity of uterine prolapse (this can cause marked discomfort and should be performed very gently).
• Sometimes, prolapse may only be demonstrated with the woman standing or straining.
Check for stress incontinence
• An assessment of pelvic fl oor muscle strength should be carried out
 Check for presence of rugae (estrogen effect)
 Check prolapse with valsalva or upright position, check for stress incontinence
 Speculum examination for type of prolapse and grading
 Rectovaginal examination is important to help differentiate between rectocele and enterocele

Question 11

Explain the modified Oxford
Investigations for POP

Answer 11

Modifi ed Oxford system for grading pelvic fl oor
muscle strength
A system of grading using vaginal palpation of the pelvic fl oor muscles.
• 0: No contraction.
• 1: Flicker.
• 2: Weak.
• 3: Moderate.
• 4: Good (with lift).
• 5: Strong.

USS to exclude pelvic or abdominal masses (if suspected clinically).
• Urodynamics are required if urinary incontinence is present. URINE R/E -
Urine sample, clean midstream to rule out infection in patients with incontinence and prolapse
• ECG, CXR, FBC, and U&E (if appropriate), to assess fi tness for
surgery.

Urodynamic testing is any procedure that looks at how well parts of the lower urinary tract—the bladder, sphincters, and urethra—work to store and release urine. Most urodynamic tests focus on how well your bladder can hold and empty urine. Urodynamic tests can also show whether your bladder is contracting when it’s not supposed to, causing urine to leak.

What urodynamic tests do health care professionals use?

Health care professional may use the following tests

uroflowmetry
postvoid residual urine measurement
cystometric test
leak point pressure measurement
pressure flow study
electromyography
video urodynamic tests

Question 12

State three differentials and five complications of POP

Answer 12

DIFFERENTIAL DIAGNOSIS
 vaginal wall cyst
 urethra diverticulum,
 cervical polyp,
 uterine inversion often associated with uterine (submucous fibroid) polyp

COMPLICATIONS
 Keratinisation of vaginal epithelium (trauma and exposure to air)
 Decubital ulceration: ulcer on the most dependent part of prolapse (circulatory changes)
 Hypertrophy and elongation of the cervix
 Congestion and edema of the cervix
 Incarceration of the prolapse
 Obstruction of the urinary tract
 Incomplete emptying resulting in hypertrophy of the bladder and trabeculation
 Constriction of the ureters may lead to hydroureters and hydronephrosis
Depression

Question 13

How is POP managed

Answer 13

You’ll refer to urogynaecologist for assessment of type and severity of prolapse and if they’ll do a prolapse surgery plus or minus a continence surgery

CONSERVATIVE MANAGEMENT AND SURGICAL MANAGEMENT.
CONSERVATIVE MANAGEMENT:
 Use of topical estrogen creams to promote healthy vaginal epithelium in postmenopausal women
 Physiotherapy-pelvic floor exercises. OR KAEGEL EXERCISES. Have limited value in minor degree of prolapse especially
during the first 6 months following delivery. They do not cure prolapse.
 Vaginal cones –pelvic floor re-education. Set of 3 or 5 of same size or shape of increasing weight
 Pessaries. A pessary is a vaginal device put in place to support the pelvic organs. There are a
variety of pessaries available, made of rubber, plastic, or silicone-based material. Pessaries
must be changed every 3-6 months.
Treat cause of prolapse
Indications for use of pessary
 Prolapse found within 6 months of delivery
 Patients who are unfit for or cannot withstand surgery
 Patient does not want/refuses surgery
 To promote healing of decubital ulcers before surgery
 Patient on a long waiting list for surgery
 Therapeutic test, where it is difficult to establish if symptoms are due to prolaps

Question 14

State the factors that influence the management of POP
When will you use physio as a management for POP?
At which stage of prolapse do you leave them or not do anything?
What is the management of POP at the health center?

Answer 14

Factors infl uencing management of prolapse
• Severity of symptoms.
• Extension of the signs (asymptomatic grade 1 prolapse does not
require treatment).
• Age, parity, and wish for further pregnancies.
• Patient’s sexual activity.
• Presence of aggravating features such as smoking and obesity.
• Urinary symptoms.
• Other gynaecological problems such as menorrhagia.

Physiotherapy
Physiotherapy has a role in the management of mild prolapse in younger
women, who fi nd intravaginal devices unacceptable and are not yet willing
to consider defi nitive surgical treatment.
• Pelvic fl oor muscle exercises (PFME): are most effective when taught
under the direct supervision of a physiotherapist; these will improve
the tone in young parous women, but are unlikely to benefi t older
women with signifi cant uterovaginal prolapse.
• Biofeedback and vaginal cones

STAGE I- LEAVE THEM

At HEALTH CENTER- PRESCRIBE TOP CREAM AND KAEGEL EXERCISES THEN REFER
Ulcers- warm water w salt

Question 15

State six types of pessaries
How often should be changed?

Answer 15

Intravaginal devices (pessaries)
Vaginal pessaries (Fig. 22.9) offer a further conservative line of therapy
for women who decline surgery, who are unfi t for surgery, or for whom
surgery is contraindicated. They should be changed 6 monthly and topical
oestrogen may be given to reduce the risk of vaginal erosion.
• Ring pessary: is most commonly used and is available in a number of
different sizes (52–129mm); the ring is placed between the posterior
aspect of the symphysis pubis and the posterior fornix of the vagina.
• Shelf pessary: can be used when a correctly sized ring pessary will not
sit in the vagina and/or where the perineum is defi cient (it may be
diffi cult to insert and remove, so its use is becoming less common).
• Hodge pessary: can be used to correct uterine retroversion. It is of
classical interest, but in practice is virtually never used now.
• Cube and doughnut pessaries: are, very rarely, used for signifi cant
prolapse, when others are not retained.

Question 16

State the surgical management and complications of the types of pelvic prolapse

Answer 16

Cystocele
 Anterior colporrhaphy
 Problems: Damage to the bladder or urethra, hemorrhage, urine retention, postoperative
infection, recurrence, dyspareunia (vaginal shortening or narrowing)

Rectocele
 Posterior colporrhaphy. , trans vaginal hysterectomy
 Problems: damage to rectum, hemorrhage, dyspareunia

Utero-vaginal prolapse
 Vaginal hysterectomy and pelvic floor repair
 Indicated in women who have completed their family
 Problems: Bleeding, damage to bladder, sometimes ureter, vault hematoma, pelvic abscess, vault
prolapse, dyspareunia

Question 17

State other surgical managements and their problems

Answer 17

Manchester Repair
 Cervical amputation
 Anterior plication of cardinal ligaments
 Anterior colporrhaphy and/or posterior colporrhaphy
 Problems: Recurrence of the prolapse, enterocele

Le Fort’s Colpocleisis
 Rarely performed these days
 Done in very frail elderly women when sexual intercourse is not contemplated
 Partial closure of vagina with narrow lateral channels for drainage of vaginal secretions
 Problems: DD&C and other investigation become impossible in the event of uterine bleeding
later.

Sacrospinous ligament fixation
 Done vaginally using non-absorbable sutures placed through sacrospinous ligament and attached
to the vaginal vault; this elevates the vault against the sacrospinous ligament
Sacral colpopexy
 Done via abdominal route using inorganic mesh (Mersilene mesh)
 The posterior vaginal wall is fixed to the periosteum overlying the sacral promontor

Question 18

How is POP

Answer 18

Prevent precipitating factors
Prevent from delivering SVD if big baby
• Reduction of prolonged labour.
• Reduction of trauma caused by instrumental delivery.
• Encouraging persistence with postnatal pelvic fl oor exercises.
• Weight reduction.
• Treatment of chronic constipation.
• Treatment of chronic cough (including smoking cessation).

Question 19

What is anaemia?
What is anaemia in pregnancy

Answer 19

Anaemia is defined as reduced haemoglobin concentration in blood more than the amount appropriate for that age, sex, race, and physiological status(e.g. pregnancy).

The WHO definition for anaemia in pregnant women is haemoglobin less than 11g/dl. it is severe if Hb is less thsn 7. The normal haemoglobin (Hb) is 12-16gm%
Non pregnant women Hb < 12gm% (Hct=38)

Pregnant women (WHO) Hb < 11 gm% (Hct=35))
1st & 3rd Trimester Hb <11 gm% (Hct<33%)
2nd trimester Hb < 10.5 gm% (Hct<32%)

Question 20

What is the WHO grading system for anemia in pregnancy

Answer 20

Grade 1 (Mild) = 9.5 – 11 g/dl Hb
Grade 2 (Moderate) =8 – 9.5 g/dl Hb
Grade 3 (Severe) = 6.5 – 8 g/dl Hb
Grade 4 (Life Threatening) =< 6.5 g/dl Hb

Question 21

state the types of anemia in pregnancy and examples

Answer 21

Physiological : Increase uptake (physiological) in all pregnancies
Pathological :
a.Decreased RBC production
Iron-deficiency anaemia -vitamin C increases iron absorption and tea reduces it . This type of anemia is called microcytic hypochromic anemia
Folate-deficiency anaemia- Macrocytic normochromic anemia
it. B12 deficiency (due to pernicious anemia which is a decrease in red blood cells when the body can’t absorb enough vitamin B12due to a lack of intrinsic factor in stomach secretions. Intrinsic factor is needed for the body to absorb vitamin B12., due to terminal ileum disease which can inhibit ansorption of vb12 since it is absorbed at the terminal ileum
b.RBC destruction(Hemolytic diseases)-Normocytic Hypochromic anemia
Diamond-Blackfan anemia

Diamond-Blackfan anemia is a rare (7 per 1 million) autosomal dominant disorder of pure red cell aplasia necessitating life-long transfusion
c.Blood loss(Hemorrhage)

Question 22

How does Vit b12 deficiency cause anemia
How does pernicious anemia cause anemia
Where is iron and folate absorbed
What are risk factors for folate deficiency
Diagnosis for folate deficiency is?

Answer 22

so for vitamin B12, it causes anemia by producing cells which die sooner than the normal red blood cell thereby which will lead to a low hb. vit b12 deficiency leads to delayed cell civion and impaired nuclear maturation leading to megaloblastic or big cells
You can get vitamin B12 deficiency if you can’t absorb vitamin B12 due to problems with your gut or if you have pernicious anemia, which makes it difficult to absorb vitamin B12 from your intestines. Intrinsic factor is a glycoprotein that binds ingested vitamin B12 and protects it from destruction in the upper gastrointestinal tract, thus permitting its absorption from the ileum. vit b12- alcohol consjmption too much whi prevents absorption of vitamin B12, medications such ash such as metformin.

pernicous anemia:autoimmune destruction of gastric parietal cells and subsequent reduction in intrinsic factor (IF) production

where is iron ansorbed -

Hemolysis in vitamin B12 deficiency is thought to be related to elevated levels of homocysteine .Folate and cobalamin interact with each other in the methionine cycle via the remethylation of homocysteine to methionine

Hemolytic anemia
•Acquired- immune-mediated, infection, microangiopathic, blood transfusion-related, and secondary to hypersplenism

•Hereditary- enzymopathies, disorders of hemoglobin (sickle cell), defects in red blood cell metabolism (G6PD deficiency, pyruvate kinase deficiency), defects in red blood cell membrane production (hereditary spherocytosis and elliptocytosis)

risk factors for folate deficiency include poor nutritional status , haemolytic anemia,haemoglobinopathies, drug intrraction with folate metabolism example anti epileptics, trimethoprim in first trimester since its a folate antagonist

at risk group for patients to give birth to babies with neural tube defects jnclude women on anticonvulsants,woman with a previous child affected eith a neural tibe defect( The two most common NTDs are spina bifida (a spinal cord defect) and anencephaly (a A baby born with an underdeveloped brain and an incomplete skull.brain defect).), woman with diabetes, with a BMI more than 35(Individuals with higher Body Mass Indexes have less supplement use, unhealthier diets and donot consume sufficient vegetables and fruits, all of which can affect decrease in folate levels. Furthermore, adiposity may affect folate absorption by intestinal epithelium.) , with SCD

diagnosis for folate def is high MCV( MCV stands for mean corpuscular volume. An MCV blood test measures the average size of your red blood cells. ),low serum folate

Folic acid function-Folic acid is a water-soluble vitamin used in nucleic acid synthesis. Required for normal erythropoiesis, it is an important cofactor for enzymes used in production of RBCs.

and vitamin B 12 -Etiology
Vitamin B12 deficiency is a cause of macrocytosis. Because DNA synthesis requires cyanocobalamin (vitamin B12) as a cofactor, a deficiency of the vitamin leads to decreased DNA synthesis in the erythrocyte, thus resulting in macrocytosis. A dietary deficiency of vitamin B12 is rare and usually only occurs in elderly persons on a “tea-and-toast diet” or in strict vegan vegetarians. However, deficiency can result from the following:

• Lack of intrinsic factor in patients who have undergone gastrectomy or who have pernicious anemia

• Malabsorption of vitamin B12 secondary to small bowel bacterial overgrowth, tapeworm, familial factors, drugs, ileal bypass, ileal enteritis, or sprue
• and intrinsic factor deficiency ( people with this respond to IV vitamin b12 but no response to injection) -Intrinsic factor is a glycoprotein that binds ingested vitamin B12 and protects it from destruction in the upper gastrointestinal tract, thus permitting its absorption from the ileum.

iron functions in erythropoiesis -

The most common cause of macrocytic anemia is megaloblastic anemia, which is the result of impaired DNA synthesis. Although DNA synthesis is impaired, RNA synthesis is unaffected, leading to a buildup of cytoplasmic components in a slowly dividing cell. This results in a larger-than-normal cell. The nuclear chromatin of these cells also has an altered appearance. [7]

Vitamin B12 and folate coenzymes are required for thymidylate and purine synthesis; thus, their deficiency results in retarded DNA synthesis. In vitamin B12 deficiency and folic acid deficiency, the defect in DNA synthesis affects other rapidly dividing cells as well, which may manifest as glossitis, skin changes, and flattening of intestinal villi.

DNA synthesis may also be delayed when certain chemotherapeutic agents are used, including folate antagonists, purine antagonists, pyrimidine antagonists, and even folate antagonist antimicrobials.

Question 23

State four causes of anemia

Answer 23

Physiological anaemia of pregnancy due to volume expamsion in pregnancy (on FBc there shouldnt be any change in MCV and MCHc)
„Nutritional / Iron deficiency anemia
Pre-pregnancy poor nutrition very important
Besides Iron, folate and B12 deficiency also important
Bone marrow insufficiency(hypoplasia or Aplastic anemia rare)
Acute blood loss in APH, PPH
malaria, chronic infections such as HIV,TB
Recurrent infections (UTI) - anemia due to impaired erythropoiesis
Hemolytic anemia in PIH
Hemoglobinopathies like Thalassemia, sickle cell anemia,G6pD deficency
parasitic infections – Hookworm ,schistosomiasus

Urinary schistosomiasis is caused by S haematobium and deposition of eggs in the bladder and ureters. The subsequent granulomatous inflammation causes nodules, polypoid lesions, and ulcerations in the lumens of the ureter and bladder, which in turn causes urinary frequency, dysuria, and end stream haematuria.

Question 24

Why does a pregnant woman need more iron?
What tests are done for suspected iron deficiency anemia
State the symptoms, consequences of iron deficiency anemia
What hormones, trace elements,vitamins, proteins and minerals are needed for erythropoiesis

Answer 24

woman who is pregnant often has insufficient iron stores to meet the demands of pregnancy. Pregnant women are encouraged to supplement their diet with 60 mg of elemental iron daily. An MCV less than 80 mg/dL and hypochromia of the RBCs should prompt further studies, including total iron-binding capacity, ferritin levels, and Hb electrophoresis if iron deficiency is excluded.
Clinical symptoms of iron deficiency anemia include fatigue, headache, restless legs syndrome, and pica (in extreme situations).
The clinical consequences of iron deficiency anemia include preterm delivery, perinatal mortality, and postpartum depression. Fetal and neonatal consequences include low birth weight and poor mental and psychomotor performance. [

Hormones – Erythropoietin (produced from Kidney, stimulates stem cells in Bone Marrow)
Trace elements – Zinc (also important for protein synthesis & Nucleic acid metabolism), Cobalt, Copper
Vitamins – Vit C,Vit B12 ,Folic acid (Vitamin B9)
Proteins for synthesis of Globin
Mineral – Iron for synthesis of heme

Question 25

physiology of anemia in normal pregnancy

Answer 25

With normal pregnancy, blood volume increases, which results in a concomitant hemodilution. Although red blood cell (RBC) mass increases during pregnancy, plasma volume increases more, resulting in a relative anemia. This results in a physiologically lowered hemoglobin (Hb) level, hematocrit (Hct) value, and RBC count, but it has no effect on the mean corpuscular volume (MCV).

Blood volume increases 40-45% in pregnancy
Iron stores are depleted with each pregnancy

MCH stands for Mean Corpuscular Hemoglobin, and is a calculation of the average amount of hemoglobin contained in each of a person’s red blood cells.

HCT-Hematocrit is the percentage by volume of red cells in your blood.

Question 26

State ten risk factors for anemia in pregnancy

Answer 26

pregnant women with hemoglobinopathies
2. pregant women who are vegetarian
3.poverty -pregnant women who who do not eat enough food contaning iron,vit b12,folate
4.pregant women who dont attend ANC
5.women who atend ANc but do not take their routine medications
6.autoimmune diseases such as pernicious anemia
7.women who frequently fale alcohol during pregnancy
8.pregant women with long term kidney disease
9.pregnant women who frequently drink tea because it inhibits iron absorption
10.pregnant women in rual areas who bath in rivers because it can lead to schistosomiasis infection

Larval schistosomes (cercariae) can penetrate the skin of persons who come in contact with contaminated freshwater, typically when wading, swimming, bathing, or washing. Over several weeks, the parasites migrate through host tissue and develop into adult worms inside the blood vessels of the body.

Question 27

Anemia occurs as a result of the sickle hemoglobinopathies. Deoxygenation of the abnormal red blood cells (RBCs) results in sickling. These permanently damaged RBCs are then removed by the reticuloendothelial system, with the average RBC lifespan reduced to 17 days. The result is a chronic compensated anemia, with Hb typically measured between 6.5 and 9.5 g/dL.
true or false
How is anemia diagnosed ?

Answer 27

History
Physical Examination
Basic Investigations

Question 28

State four signs and symptoms of anemia

Answer 28

symptoms(asymptomatic or symptomatic)
Easy fatiguability and weakness
Palpitations due to ectopic heart beats
Dizziness
Headache
Anorexia
Indigestion
Dypsnea
Sweling of the legs etc

signs:
palmar pallor
conjuctival pallor
if there is a long standing kidney problem, there will be bilateral edema
spoon shaped nails in long standing iron deficiency anemia and vitamin B12 deficiency
There is pallor of mucous membranes or palms
Jaundice (conjunctival, skin)
Delayed capillary refill
Tachypnea
Tachycardia
Low blood pressure
Cold hands and feet
Koilonychia - long standing iron deficiency
Angular stomatitis
Glossitis -Vit B12 and iron deficiency
Edema of the legs may be due to hypoproteinemia or associated preeclampsia.
Crepitations may be heard at the base of the lungs due to congestion.

Question 29

What do you want to know in the history of someone with anemia

Answer 29

ODQ- your signs and symptoms, diet, chronic bleeding , loss of appetite, vomiting, worm infestation,etc
INDEX OR CURRENT PREGNANCY– ANC visit and iron supplementation, planned or planned, BPV,
GYNE Hx- frequency of her menses, volume etc
PAST OBST Hx- number of pregnancies, interval, lactational history,
PMHx- past history of anaemia, G6PD, sickle cell disease, leukemia
DRUG Hx- current medications, herbal medications
FMHx- sickle cell disease, multiple pregnancies,
SOCIAL Hx- whether patient sleeps under a treated mosquito net, occupation, condition of her house(environment)

Question 30

State ten investigations for anemia

Answer 30

FBC can be checked at first visit, then 28-30weeks and 36weeks
Sickling test
Stool R/E for parasites such as hookworm eggs
G6PD
BF for MPs malaria
HIV antibodies or retro screen
Peripheral blood film comment
serum iron,ferritin and total iron binding cspacity
Urinalysis for schistosoma ova and urobilinogen
blood film comment-

Complete blood count (CBC) including differential
•Calculate the corrected reticulocyte count = percent reticulocytes x (patient’s HCT/normal HCT)
•For normal HCT, use 45% in men and 40% in women
•If result > 2, this suggests hemolysis or acute blood loss, while results < 2 suggests hypoproliferation.

After calculating the reticulocyte count, check the MCV.
MCV (<80 fl)
•Iron deficiency- decreased serum iron, percent saturation of iron, with increased total iron-binding capacity (TIBC), transferrin levels, and soluble transferrin receptor
•Lead poisoning- basophilic stippling on the peripheral blood smear, ringed sideroblasts in bone marrow, elevated lead levels
•Thalassemia- RBC count may be normal/high, low MCV, target cells, and basophilic stippling are on peripheral smear. Alpha thalassemia is differentiated from beta-thalassemia by a normal Hgb electrophoresis in alpha thalassemia. Elevated Hgb A2/HgbF is seen in the beta-thalassemia trait

Question 31

How is anemia in pregnancy managed
Side effects of iron

Answer 31

Choice of therapy depends on: (1) Severity of anemia (2) Gestational age, and (3) compliance and tolerability of iron.
Oral therapy
60 mg elemental iron & 400 ug of folic acid daily during pregnancy and 3 months there after (ferrous sulphate 325 mg 8hrly and folic acid 5mg daily )
In anemia, therapeutic doses are 180-200 mg /d
Oral iron can have side effects like nausea, vomiting, gastritis, diarrhoea, constipation

Question 32

State three sources of iron and folate and B12 each from food

Answer 32

egg liver citrus fruits lentils folate
banana peanutsvegetables (especially dark green leafy vegetables), fruits and fruit juices, nuts, beans, peas, seafood, eggs, dairy products, meat, poultry, and grains (Table 2) [4,12].30 Nov 2022

egg milk salmonVitamin B12 Rich Foods Name List. Eggs. Milk. Soymilk. . Chicken. Tuna. …
Vitamin B12 Rich Fruits. Apple. Banana. . Orange. Mango.
Vitamin B12 Rich Vegetables. . Beetroot. Mushroom. Potato. vit b12

iron-fortified bread and breakfast cereal.
legumes (mixed beans, baked beans, lentils, chickpeas)
dark leafy green vegetables (spinach, silver beet, broccoli)
oats.iron-red meat , green leafy vegetables,ascorbic acid and meat, fish and poultry- iron

Question 33

What are the iron requirements and losses during pregnancy

Answer 33

During pregnancy Total 800-1000 mg extra iron is required
300 mg for Fetus & 50 mg for Placenta
400-500 mg for increased red cell mass
250 mg iron lost during delivery
Due to cessation of menses & reduction of blood volume after delivery conservation of iron is around 400 mg

Question 34

How does iron deficiency cause anemia

Answer 34

Iron deficiency anemia, the most common form, is effectively treated with supplemental dietary iron. This type of anemia, which develops over time, is characterized by pallor, fatigue, dizziness, exertional dyspnea, and other generalized symptoms of tissue ischemia. Iron forms the nucleus of the iron-porphyrin heme ring, which, together with globin chains, forms hemoglobin (Hb). Hemoglobin reversibly binds oxygen, which is critical for oxygen delivery from the lungs to other tissues. In the absence of adequate iron, small erythrocytes with insufficient hemoglobin are formed, giving rise to microcytic hypochromic anemia (Fig. 2).

Patients with iron deficiency anemia have low serum iron and low ferritin, as well as high soluble transferrin receptor and high total-iron binding capacity.

pregannt women need more iron because their babies need more iron to produce nomal red blood cells eith heme component. if heme componenrt isnt there then it means no haemoglobin which means the rbc wont csrry oxygen

Question 35

How is anemia managed in ANC
general, treating a pregnant woman who has sickle cell disease requires close observation. Obtain blood cell counts frequently because anemia can worsen quickly. Folic acid supplementation is recommended because of the quick turnover of erythrocytes. One should monitor the pregnancy with serial sonograms for assessment of fetal growth, and implementation of fetal surveillance in the third trimester is reasonable. Pneumococcal and meningococcal vaccines should be provided.
true or false

Answer 35

Depending on severity or grading, mostly deals with mild to moderate anaemia.
ROUTINE MANAGEMENT OF ANAEMIA- mild to normal anaemia
iron iii polymatose 1 twice daily for 30 days
folic acid 5mg daily for 30 days
albendazole 400mg start at 16weeks of gestation
sulfadoxine pyrimethamine(SP) after quickining or at 16 weeks of gestation and at least every other four weeks for 5 times
Vitamin C 100mg three times daily to aid iron absorption
the iron drugs are given every other visit till delivery.

HB below 9g/dl -moderate anaemia.
tothema 10mls twice daily for 14 days
folic acid 5mg daily for 30 days
iron iii polymatose twice daily for 30 days.
Vitamin C 100mg three times daily
check HB after two weeks if there is HB build up, routine management of anaemia continues if no, refer to physician.
NOTE- if HB is below 7g/dl at first visit, refer to physician for further management.

Question 36

State four indications for blood transfusion

Answer 36

Severe anemia first seen after 36 weeks of pregnancy
Anemia due to acute blood Loss – APH & PPH
Patient not responding to oral or parenteral therapy
Anemic & symptomatic pregnant women (dyspneic, with heart failure etc) irrespective of gestational age

Question 37

State ten complications of anemia
On mother and baby

Answer 37

Preeclampsia may be related to malnutrition and hypoproteinemia
Intercurrent infection impairs erythropoiesis
Heart failure at 30–32 weeks of pregnancy.
Preterm labour
During labour
PPH
Cardiac failure
Shock
Puerperium
Puerperal sepsis
Subinvolution
Poor lactation

Anemia (by causing hypoxia) and iron deficiency (by increasing serum norepinephrine concentrations) can induce maternal and fetal stress, which stimulates the synthesis of corticotropin-releasing hormone (CRH). - preterm labour

Effects on baby
Preterm birth, IUGR
Low APGAR at birth
Neonate more susceptible for anemia & infections
Anemic infant with cognitive dysfunction
LBW
Neural tube defects of brain & spine
Delayed growth in infants and children
. Intrauterine death due to severe maternal anoxemia

The clinical consequences of iron deficiency anemia include preterm delivery, perinatal mortality, and postpartum depression. Fetal and neonatal consequences include low birth weight and poor mental and psychomotor performance.

Question 38

State ten preventions of anemia in pregnancy

Answer 38

PRIMARY
Routine screening for anemia in high risk group(childbearing age and pregnancy)
Diet (iron rich diet,folate,protein)
Encourage iron supplementation during adolescence and pregnancy.
Malaria preventive measures
Encourage regular antenatal visits during pregnancy
The need to aviod teenage pregnancy
Importance of adeequate intervals between pregnancie and multipregnancies

Secondary-
This includes screening for:
Dianosis
Treating the deficiency-iron therapy(oral or intravenously)
Blood transfusion with packed red cells in severe anaemia
Treating the cause

Question 39

What are Menstrual disorders? (Dysmenorrhea isn’t part though)
What is the normal Menstrual cycle, how many mls of blood is usually lost during menstruation in a day

Answer 39

Menstrual disorders refer to conditions that affect a woman’s menstrual cycle including menorrhagia, amenorrhea,dysmenorrhea,oligomenorrhea, post menopausal bleeding,Inter menstrual bleeds. Loss of 80ml of blood that persists for more than 7 days is an indication of a menstral disorder. Normal is 20-80mls per day
Abnormal menstrual bleeding may be identified in either the length of the cycle or the amount of blood loss. Menstrual cycle abnormalities are mainly hormone–determined. In ovulatory cycles, the luteal phase is virtually constant, lasting 14 days. Changes in cycle length are therefore due mainly to changes in the follicular phase.
Normal Menstrual cycle-Menstruation is the periodic shedding of the functional layer (stratum functionalis) of the endometrium when fertilisation has not occurred or there is failure of implantation. The normal menstrual cycle lasts between 21 and 35 days with menstrual flow lasting 2–7 day (2-10days according to Dr Buernor)
Menarche is the first menses a woman experiences. The age range is 11-15 years. Cyclic changes occur in the ovaries, endometrium, the cervix and vagina during the menstrual cycle. This rythmic integrated process is intricately controlled by the gonadotropins produced along the HPO(hypothalamus pituitary ovarian) axis.

Question 40

Explain the menstrual cycle
State the three types of oestrogen produced in females

Answer 40

The gonadotropic hormones exert 3 primary effects on the gonads
a. Stimulation of oogenesis
b. Stimulation of gonadal hormone production (estrogen and progesterone)
c. Maintenance of the structure of the gonads
The levels of production of gonadotropic hormones are influenced by both positive and
negative feedback mechanisms from the sex steroids. Three main types of oestrogens are
produced in females: oestradiol (E2
, major type produced during menstrual cycle), oestriol
(E3
, produced by placenta during pregnancy) and oestrone (E1, main oestrogen during the
menopause).

The hypothalamus begins to secrete gonadotropin-releasing hormone (GnRH), and as this secretion continues, the pituitary gonadotropins (luteinizing hormone [LH] and follicle-stimulating hormone [FSH]) are released and ovarian follicles become more sensitive to stimulation.
These increases in GnRH pulsatility lead to gonadotropin secretion, eventually resulting in a dominant follicle. As the follicle grows, it produces estrogen. The estrogen provides positive feedback on the gonadotropins to cause a surge in LH and thus ovulation. This estrogen from the dominant follicle also causes the endometrium to proliferate and prepare for potential implantation.
After ovulation, a corpus luteum develops as the granulosa cells become luteinized. The corpus luteum secretes progesterone, which transitions the endometrium into a more stable environment for implantation. Without implantation of an embryo, the corpus luteum involutes, and progesterone and estradiol levels decrease. Thus, the endometrium sheds its lining as it loses its blood supply

The ovarian follicle represents the basic functional unit of the ovary. It consists of an
oocyte surrounded by granulosa and theca cells. Luteinizing hormone (LH) induces androgen biosynthesis by theca interna cells, whereas both follicle-stimulating hormone
(FSH) and LH stimulate aromatase activity by granulosa cells. The joint action of these two
types of cells and pituitary hormones forms the basis of the 2-cell, 2-gonadotropin theory
for biosynthesis of estrogen.
The 2 cells are the granulosa and theca cells. The 2 gonadotropins are LH and FSH.
According to this theory, the growth and maturation of the follicle depends on follicle
stimulating hormone (FSH) and luteinizing hormone (LH). In addition, FSH increases the
number of FSH receptors on granulosa cells, the number of LH receptors on theca cells and
granulosa cell aromatase activity. In theca cells, under the influence of LH, cholesterol is
converted to pregnenolone and metabolised through a series of substrates ending in
androgen production. The 2-cell, 2-gonadotrophin model comes into play with androgens
produced by the theca cells transported to the granulosa cells where they are aromatised
to oestrogens

Question 41

Another explanation of Menstrual cycle from osmosis

Answer 41

The menstrual cycle refers to the regular changes in the activity of the ovaries and the endometrium that make reproduction possible.
The endometrium is the layer of tissue lining the inside of the uterus.
This lining consists of a functional layer, which is subject to hormonal changes and is shed during menstruation, and a thin basal layer which feeds the overlying functional layer.
The menstrual cycle actually consists of two interconnected and synchronized processes: the ovarian cycle, which centers on the development of the ovarian follicles and ovulation, and the uterine or endometrial cycle, which centers on the way in which the functional endometrium thickens and sheds in response to ovarian activity.
Menarche, which refers to the onset of the first menstrual period, usually occurs during early adolescence as part of puberty.
Following menarche, the menstrual cycle recurs on a monthly basis, pausing only during pregnancy, until a person reaches menopause, when her ovarian function declines and she stops having menstrual periods.
The monthly menstrual cycle can vary in duration from 20 to 35 days, with an average of 28 days.
Each menstrual cycle begins on the first day of menstruation, and this is referred to as day one of the cycle.
The menstrual cycle refers to the regular changes in the activity of the ovaries and the endometrium that make reproduction possible.
The endometrium is the layer of tissue lining the inside of the uterus.
This lining consists of a functional layer, which is subject to hormonal changes and is shed during menstruation, and a thin basal layer which feeds the overlying functional layer.
The menstrual cycle actually consists of two interconnected and synchronized processes: the ovarian cycle, which centers on the development of the ovarian follicles and ovulation, and the uterine or endometrial cycle, which centers on the way in which the functional endometrium thickens and sheds in response to ovarian activity.
Menarche, which refers to the onset of the first menstrual period, usually occurs during early adolescence as part of puberty.
Following menarche, the menstrual cycle recurs on a monthly basis, pausing only during pregnancy, until a person reaches menopause, when her ovarian function declines and she stops having menstrual periods.
The monthly menstrual cycle can vary in duration from 20 to 35 days, with an average of 28 days.
Each menstrual cycle begins on the first day of menstruation, and this is referred to as day one of the cycle.
Ovulation, or the release of the oocyte from the ovary, usually occurs 14 days before the first day of menstruation (i.e., 14 days before the next cycle begins).
So, for an average 28-day menstrual cycle, this means that there are usually 14 days leading up to ovulation (i.e., the preovulatory phase) and 14 days following ovulation (i.e., the postovulatory phase).
During these two phases, the ovaries and the endometrium each undergo their own set of changes, which are separate but related.
As a result, each phase of the menstrual cycle has two different names to describe these two different parallel processes.
For the ovary, the two weeks leading up to ovulation is called the ovarian follicular phase, and this corresponds to the menstrual and proliferative phases of the endometrium.
Similarly, the two weeks following ovulation is referred to as the ovarian luteal phase, which also corresponds to the secretory phase of the endometrium.
So, let’s first focus on the preovulatory period, starting with the ovarian follicular phase.
This phase starts on the first day of menstruation and represents weeks one and two of a four-week cycle.
The whole menstrual cycle is controlled by the hypothalamus and the pituitary gland, which are like the masterminds of reproduction.
The hypothalamus is a part of the brain that secretes gonadotropin-releasing hormone, or GnRH, which causes the nearby anterior pituitary gland to release follicle stimulating hormone, or FSH, and luteinizing hormone, or LH.
Before puberty, the gonadotropin-releasing hormone is released at a steady rate, but once puberty hits, the gonadotropin-releasing hormone is released in pulses, sometimes more and sometimes less.
The frequency and magnitude of the gonadotropin-releasing hormone pulses determine how much follicle stimulating hormone and luteinizing hormone will be produced by the pituitary.
These pituitary hormones control the maturation of the ovarian follicles, each of which is initially made up of an immature sex cell, or primary oocyte, surrounded by layers of theca and granulosa cells, the hormone-secreting cells of the ovary.
Over the course of the follicular phase, these oocyte-containing groups of cells, or follicles, grow and compete for a chance at ovulation.
During the first ten days, theca cells develop receptors and bind luteinizing hormone, and in response secrete large amounts of the hormone androstenedione, an androgen hormone.
Similarly, granulosa cells develop receptors and bind follicle stimulating hormone, and in response produce the enzyme aromatase.
Aromatase converts androstenedione from the theca cells into 17β-estradiol, which is a member of the estrogen family.
During days 10 through 14 of this phase, granulosa cells also begin to develop luteinizing hormone receptors, in addition to the follicle stimulating hormone receptors they already have.
As the follicles grow and estrogen is released into the bloodstream, increased estrogen levels act as a negative feedback signal, telling the pituitary to secrete less follicle stimulating hormone.
As a result of decreased follicle stimulating hormone production, some of the developing follicles in the ovary will stop growing, regress and die off.
The follicle that has the most follicle stimulating hormone receptors, however, will continue to grow, becoming the dominant follicle that will eventually undergo ovulation.
This dominant follicle continues to secrete estrogen, and the rising estrogen levels make the pituitary more responsive to the pulsatile action of gonadotropin-releasing hormone from the hypothalamus.
As blood estrogen levels start to steadily climb higher and higher, the estrogen from the dominant follicle now becomes a positive feedback signal – that is, it makes the pituitary secrete a whole lot of follicle stimulating hormone and luteinizing hormone in response to gonadotropin-releasing hormone.
This surge of follicle stimulating hormone and luteinizing hormone usually happens a day or two before ovulation and is responsible for stimulating the rupture of the ovarian follicle and the release of the oocyte.
You can think of it this way: for most of the follicular phase, the pituitary saves its energy, then when it senses that the dominant follicle ready for release, the pituitary uses all its energy to secrete enough follicle stimulating hormone and luteinizing hormone to induce ovulation.
While the ovary is busy preparing an egg for ovulation, the uterus, meanwhile, is preparing the endometrium for implantation and maintenance of pregnancy.
This process begins with the menstrual phase, which is when the old endometrial lining, or functional layer, from the previous cycle is shed and eliminated through the vagina, producing the bleeding pattern known as the menstrual period.
The menstrual phase lasts an average of five days and is followed by the proliferative phase, during which high estrogen levels stimulate thickening of the endometrium, growth of endometrial glands, and emergence of spiral arteries, which grow a little under the influence of estrogen, from the basal layer to feed the growing functional endometrium.
Rising estrogen levels also help change the consistency of the cervical mucus, making it more hospitable to incoming sperm.
The combined effects of this spike in estrogen on the uterus and cervix help to optimize the chance of fertilization, which is highest between day 11 and day 15 of an average 28-day cycle.
Following ovulation, the remnant of the ovarian follicle becomes the corpus luteum, which is made up of luteinized theca and granulosa cells, meaning that these cells have been exposed to the high luteinizing hormone levels that occur just before ovulation.
Luteinized theca cells keep secreting androstenedione, and the luteinized granulosa cells keep converting it to 17β-estradiol, as before.
However, luteinized granulosa cells also respond to the low luteinizing hormone concentrations that are present after ovulation by increasing the activity of cholesterol side-chain cleavage enzyme, or P450scc for short.
This enzyme converts more cholesterol to pregnenolone, a progesterone precursor.
So luteinized granulosa cells secrete more progesterone than estrogen during the luteal phase.
Progesterone acts as a negative feedback signal on the pituitary, decreasing release of follicle stimulating hormone and luteinizing hormone.
At the same time, luteinized granulosa cells begin secreting inhibin, which similarly inhibits the pituitary gland from making follicle stimulating hormone.
Both of these processes result in a decline in estrogen levels, meaning that progesterone becomes the dominant hormone present during this phase of the cycle.
Together with the decreased level of estrogen, the rising progesterone level signals that ovulation has occurred and helps make the endometrium receptive to the implantation of a fertilized gamete.
Under the influence of progesterone, the uterus enters into the secretory phase of the endometrial cycle.
During this time spiral arteries grow the most and become coiled, and the uterine glands begin to secrete more mucus.
After day 15 of the cycle, the optimal window for fertilization begins to close.
The cervical mucus starts to thicken and becomes less hospitable to the sperm.
Over time, the corpus luteum gradually degenerates into the nonfunctional corpus albicans.
The corpus albicans doesn’t make hormones, so estrogen and progesterone levels slowly decrease.
When progesterone reaches its lowest level, the spiral arteries collapse, and the functional layer of the endometrium prepares to shed through menstruation.
This shedding marks the beginning of a new menstrual cycle and another opportunity for fertilization.

Summary
All right, so as a quick recap - the menstrual cycle begins on the first day of menstruation.
For an average 28-day menstrual cycle, the changes which occur in the ovary during the first 14 days are called the follicular phase.
Ovulation usually occurs at day 14, as a result of the estrogen-induced surge in luteinizing hormone.
The last 14 days of the cycle are the luteal phase, during which progesterone becomes the dominant hormone.
While the length of the follicular phase can vary, the luteal phase almost always precedes the onset of menses by 14 days.
The uterus also goes through its own set of changes.
During the first 14 days of the cycle, the endometrium goes through the menstrual phase and the proliferative phase, and during the last 14 days it goes through the secretory phase.

Question 42

PHASES OF MENSTRUAL CYCLE;
Ovarian cycle-Divided into 2 phases: Follicular and Luteal, with an intervening period called Ovulation
Endometrial cycle-This is made of the menstrual, proliferative and secretory phases. The cycle length is
21-35 days with an average of 28 days.

Problems in any of these will result in a menstrual disorder

Another explanation of Menstrual cycle

Answer 42

The follicular phase starts with development of about 20-50 Graafian follicles in
the ovary under stimulation of FSH released from the pituitary gland.
• These follicles grow steadily under FSH and produce oestrogen that is released into
the blood stream
• The oestrogen acts on the endometrium and stimulates it to proliferate to start the
proliferative phase of the endometrial cycle
• At around the 10th day of the follicular phase, one of the follicles becomes
distinctly larger than the others.
• It continues to grow, becoming larger and larger and is termed the ‘dominant
follicle’
• The growth of the other follicles in the cohort is arrested. and they become atretic.
• The granulosa cells of the dominant follicle secrete increasing amounts of
oestradiol (E2) which reach a peak by day 12
• Rising E2 levels has a positive feedback on the hypothalamus which then releases
increasing amounts of LH leading to the LH surge, and a smaller surge in FSH
• LH surge begins 36hr before ovulation
• The dominant follicle ruptures when it is about 18 – 20 mm in size and releases an ovum on Day 14 of the menstrual cycle: this process is called ‘ovulation’
• The released ovum is a secondary oocyte surrounded by the zona pellucida and corona radiata
• If it is fertilised, it completes the 2nd meoitic division
• If not fertilised, it degenerates within 36hrs
• The follicular phase ends at this stage and the Luteal phase begins
• Cells of the follicle undergo changes under influence of LH: fat globules get deposited in them, they grow larger and assume a yellowish colour
• The follicle is thus transformed into a corpus luteum
• Cells of the corpus luteum start to produce progesterone in addition to oestradiol
• Progesterone acts on the endometrium transforming it into the secretory phase
• Progesterone levels reach a peak between days 22 – 26 of the cycle
• If fertilization has occurred, the corpus luteum continues to increase in size under influence of human chorionic gonadotrophin (hCG) produced by the developing zygote
• It continues to produce progesterone which supports the early embryo
• If fertilization does not occur, the corpus luteum decreases in size, gets atrophic and becomes the corpus albicans
• Progesterone levels begin to fall in tandem with the decreasing action of the corpus luteum
• When levels of progesterone reach a minimum critical level, the endometrium is no
longer supported and is shed as the menses
• As soon as menstruation starts, it denotes the beginning of another menstrual
cycle.

The Endometrial Cycle
This is made of the menstrual, proliferative and secretory phases. The cycle length is
21-35 days with an average of 28 days.
Menstrual Phase
• Begins when spiral arteries rupture secondary to ischemia in the endometrium,
releasing blood into the uterus
• The stratum functionalis is completely shed
• Blood loss is 10-80 ml with an average of 35ml- 3-6 pads each day
• About 80% of total menstrual blood loss occurs in the first 2 days of menses
• Arterial and venous blood, remnants of endometrial stroma and glands and
leukocytes are present in menstrual blood
• Blood that is shed into the cavum uteri forms a clot immediately. The clot is then
acted upon by plasmin (a serine protease) which dissolves it

•The first day of menstrual flow is designated as Day 1
•Levels of all hormones involved with the cycle are low at this time
•Symptoms such as lower abdominal pain, irritability and breast tenderness may
accompany menses
• This phase normally lasts 2-7 days and is actually part of the proliferative phase
Proliferative Phase
The proliferative phase occurs while the ovary is in the follicular phase. It lasts for 14 days
in a 28-day cycle.
•From about Day 4 onwards proliferation of the endometrium begins from the
stratum basalis
• Secretion of estrogen from the growing ovarian follicle is responsible for this
proliferation
• At this stage epithelial cells equipped with cilia can be recognized
• The endometrial glands grow longer and the spiral arteries wind themselves lightly
into the stroma.
The Secretory Phase
This occurs while the ovary is in the luteal phase. It lasts for 14 days.
• Occurs from Day 14-28 of the cycle
• Endometrium differentiates itself under influence of progesterone (produced from
the corpus luteum) and attains its full maturity
• The glands and arteries become tortuous
• The connective tissue stroma becomes oedematous
• The endometrium is well prepared to accept and nourish a zygote should
fertilization occur
• Days 20-23 is the period of maximal reception ability for the blastocyst and is called
the ‘Implantation Window

Question 43

What is oligomenorrhea
State six causes of oligomenorrhea and explain how each causes

Answer 43

OLIGOMENORRHEA- It is a menstrual disorder characterized by infrequent menstrual periods.
This is when the menstrual cycle is longer than 35 days. This is so because the follicular phase is
prolonged.

Causes
1. Familial
2. Emotional, usually due to stress
3. Anovulation from any cause
 Hypothalamic
 Pituitary
 Ovarian
 Uterine
 Hyperthyroidism

4. Drugs e.g. long-acting progestogens such as Depo-Provera
5. Post-menarche - during the first few years after menarche about 20% of girls have Oligomenorrhea cuz HPO axis is still developing and may not be matured
   PCOS
   THYROID DISEASE
   RAPID WEIGHT LOSS LEADING TO LESS ESTROGEN

ANYTHING THAT PRODUCES LESS OESTROGEN DELAYS OVULATION AND WILL LENGTHN THE FOLLICULAR PHASE
FAMILIAL- TURNER SYNDROME, KALLMAN SYNDROME- GENETIC DEFECT THAT AFFECTS HYPOTHALAMUS AND PITUITARY, FA MHX OF PCOS
HYPERHTYROIDISM AFFECTS LEVELS OF ESTROGEN AND PROGESTERONE BY PRODUCING SEX HORMONE BINDING GLOBULIN WHICH BINDS TO THEM AND MAKES THEM LESS AVAILABLE IN THE BODY

turner ayndrome-In Turner syndrome, the ovaries may not function properly because of the absence of all or part of one of the X chromosomes. The ovaries are responsible for producing and releasing hormones, such as estrogen and progesterone, which regulate the menstrual cycle and control the development of female secondary sex characteristics. In Turner syndrome, the ovaries may not develop and function normally, which can lead to hormonal imbalances and menstrual irregularities, including oligomenorrhea or amenorrhea. Hormone replacement therapy can be used to replace the hormones that the ovaries are not producing, which can help regulate the menstrual cycle and prevent complications associated with Turner syndrome, such as osteoporosis.

kallman-Kallmann syndrome is a genetic condition in which the hypothalamus, which is the part of the brain that regulates the production of hormones, does not function properly. This can lead to a deficiency in gonadotropin-releasing hormone (GnRH), which is a hormone that stimulates the production of follicle-stimulating hormone (FSH) and luteinizing hormone (LH), which are responsible for regulating the menstrual cycle. Oligomenorrhea can occur in Kallmann syndrome because of the hormonal imbalances caused by the deficiency in GnRH, FSH, and LH. Treatment for Kallmann syndrome may involve hormone replacement therapy to replace the hormones that the body is not producing, which can help regulate the menstrual cycle and promote the development of secondary sex characteristics.

pCOS- high level of testosterone causes few eggs to be produced leasing to anovulation and oligomeonorhea
Testosterone can interfere with the production of estrogen by the ovaries by inhibiting the activity of an enzyme called aromatase. Aromatase is responsible for converting androgens, such as testosterone, into estrogens, such as estradiol. In women, aromatase is primarily found in the ovaries, although it is also present in other tissues, such as adipose (fat) tissue.
When testosterone levels are high, the activity of aromatase can be inhibited, which can reduce the production of estrogen by the ovaries. This can lead to a variety of symptoms, including menstrual irregularities, hot flashes, and vaginal dryness. High levels of testosterone can also interfere with the production of other hormones that are involved in the menstrual cycle, such as follicle-stimulating hormone (FSH) and luteinizing hormone (LH), which can further disrupt the balance of hormones that regulate the menstrual cycle. If you are experiencing symptoms of high testosterone or low estrogen, it is important to speak with your healthcare provider to determine the underlying cause and appropriate treatment.

PCOS-Women with PCOS usually have low to normal levels of FSH, but high levels of LH. Because LH is already high, there is no LH surge that occurs. Without an LH surge, the ovaries cannot release an egg and you may have irregular menstrual cycles.

proposed mechanism for anovulation and elevated androgen levels suggests that, under the increased stimulatory effect of luteinizing hormone (LH) secreted by the anterior pituitary, stimulation of the ovarian theca cells is increased. These cells, in turn, increase the production of androgens (eg, testosterone, androstenedione). Because of a decreased level of follicle-stimulating hormone (FSH) relative to LH, the ovarian granulosa cells cannot aromatize the androgens to estrogens, which leads to decreased estrogen levels and consequent anovulation.

bnormality of the hypothalamic-pituitary-ovarian or adrenal axis has been imposed in the pathophysiology of polycystic ovarian disease. A disturbance in the secretion pattern of the gonadotrophin-releasing hormone (GnRH) results in the relative increase in LH to FSH release (6). Ovarian estrogen is responsible for causing an abnormal feedback mechanism that caused an increase in LH release (7). Usually, in healthy women, the ratio between LH and FSH usually lies between 1 and 2. In polycystic ovary disease women, this ratio becomes reversed, and it might reach as high as 2 or 3 (8).

As a result of raised LH/FSH ratio, ovulation does not occur in polycystic ovary disease patients

The pituitary gland can cause anovulation by producing an excess amount of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), which are the hormones that regulate the menstrual cycle. In a typical menstrual cycle, the levels of LH and FSH rise and fall in a specific pattern, which triggers the ovaries to produce and release an egg. In women with anovulation, this process is disrupted, and the ovaries do not produce and release an egg. This can be caused by a variety of factors, including hormonal imbalances, stress, weight changes, or underlying medical conditions. When the pituitary gland produces too much LH and FSH, it can disrupt the balance of hormones that regulate the menstrual cycle, which can lead to anovulation. Women with anovulation may experience irregular menstrual cycles or may not have a period at all. If you are experiencing symptoms of anovulation or have concerns about your menstrual cycle, it is important to speak with your healthcare provider to determine the underlying cause and appropriate treatment.

Depo-Provera works by suppressing ovulation, which is the process by which the ovaries release an egg each month. The active ingredient in Depo-Provera is a synthetic form of the hormone progesterone called medroxyprogesterone acetate (MPA). MPA works by inhibiting the production of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in the pituitary gland. These hormones are responsible for stimulating the ovaries to produce and release an egg each month. By suppressing the production of LH and FSH, Depo-Provera prevents ovulation from occurring. Additionally, Depo-Provera thickens the cervical mucus, which makes it more difficult for sperm to reach the egg. This dual mechanism of action makes Depo-Provera a highly effective form of contraception. If you have concerns about your contraceptive options or are experiencing side effects from Depo-Provera, it is important to speak with your healthcare provider.

Question 44

State six risk factors do oligomenorrhea
How is it managed

Answer 44

RISK FACTORS-
PCOS
OBESITY
UNDERWEIGHT WOMEN
THYROID DISORDERS
HORMONAL CONTRACEPTIVE USE
PATIENTS ON CHEMOTHERAPY OR RADIATION THERAPY
PATIENTS ON ANTIDEPRESSANTS SUCH AS SELECTIVE SEROTONIN UPTAKE INHIBITORS EXAMPLE SERTRALINE
Pituitary gland disorders-

MGT-
TREAT UNDERLYING CAUSE
IF DUE TO WEIGHT LOSS, GAIN SUFFICIENT WEIGHT
IF DUE TO STRESS, STRESS REDUCTION
HORMONAL REPLACEMENT THERAPIES

Serotonin is a neurotransmitter that plays a role in regulating mood, appetite, and sleep, among other functions. It has also been shown to affect the production of hormones such as follicle-stimulating hormone (FSH) and luteinizing hormone (LH), which are important for regulating the menstrual cycle. Specifically, serotonin can inhibit the release of FSH and LH from the pituitary gland, which can lead to menstrual irregularities. This is because FSH and LH are responsible for stimulating the growth and development of ovarian follicles, which in turn produce estrogen and progesterone. Changes in the levels of these hormones can affect the timing and regularity of the menstrual cycle.

Chemotherapy can cause oligomenorrhea, which is a condition characterized by infrequent or irregular menstrual periods, by affecting the production of hormones in the body. Specifically, chemotherapy drugs can damage the ovaries, which can lead to a decrease in the production of estrogen and progesterone. These hormones are important for regulating the menstrual cycle, and changes in their levels can lead to menstrual irregularities.
However, it is important to note that not all women who undergo chemotherapy will experience menstrual irregularities, and the severity of these symptoms can vary depending on the individual and the specific treatment regimen.

Pituitary adenoma affects production of thyroid hornones, LH,FSH thus leading to menstrual irrgularities

Treatment of PCOS depends on the patient’s goals, as follows:
For patients who wish to conceive,
clomiphene citrate has been historically the first-line treatment, followed by gonadotropins [18] ; there has been debate regarding whether aromatase inhibitors (specifically, letrozole) replace clomiphene as first-line treatment, especially in obese patients [44]

For those who are not attempting to conceive,
a combined oral contraceptive pill (COCP) is usually the first line of treatment, provided that there are no contraindications; COCPs are therapeutic for multiple reasons, including regulating menstrual cycles, suppressing ovarian and adrenal androgen production, and increasing circulating levels of sex hormone–binding globulin, thus lowering levels of free testosterone in serum [15]

In addition to these treatment options, lifestyle modifications are recommended for overweight and obese PCOS patients so as to decrease their risk for cardiovascular disease, diabetes, and metabolic syndrome.

Question 45

What is dysmenorrhea
State the two types
State the treatment for primary dys

Answer 45

is menstruation associated with pain such as to prevent normal activity and warrant medication.
There are 2 main types: Primary (no organic cause) and Secondary (pathologic cause present).

PRIMARY-Primary dysmenorrhoea describes painful periods since onset of menarche and is unlikely to be associated with pathology
Primary dysmenorrhea has been associated with ovulatory cycles. The mechanism has been attributed to prostaglandin activity as well as leukotrienes and vasopressin. Psychologic factors such as attitudes passed from mother to child and emotional anxiety are believed to be co-factors.
Clinical findings
 The pain typically occurs a day to onset of menses or at the onset of flow.
 Nausea and vomiting may occur.
 There is generalized lower abdominal tenderness.
Treatment
1. NSAIDS or other pain-killers
2. Ovulation may be stopped by giving drugs such as the Combined Pill in intractable cases
3. Psychological counsellin

Question 46

What is secondary dysmenorrhea
State the causes and how each causes it

Answer 46

SECONDARY; Secondary dysmenorrhoea describes painful periods that have developed over time and usually have a secondary cause.

CAUSES-• Endometriosis. • Adenomyosis. • PID. • Pelvic adhesions. • Fibroids (though not always causal). • Cervical stenosis (iatrogenic post-LLETZ or instrumentation). • Asherman’s syndrome. • Congenital abnormalities causing genital tract obstruction, e.g. non-communicating cornua. , Pelvic congestion syndrome

Endometriosis is a condition in which the tissue that normally lines the inside of the uterus (the endometrium) grows outside of the uterus, such as on the ovaries, fallopian tubes, or other pelvic organs. This can cause a variety of symptoms, including dysmenorrhea, which is painful menstrual cramps. Dysmenorrhea occurs because the endometrial tissue outside of the uterus responds to hormonal changes during the menstrual cycle in the same way as the endometrial tissue inside the uterus. This means that the tissue swells and sheds, just like the endometrium inside the uterus, which can cause inflammation and pain. Additionally, endometrial tissue can form adhesions or scar tissue, which can cause pain and discomfort during menstruation. While dysmenorrhea is a common symptom of endometriosis, it is important to speak with your healthcare provider if you experience any changes in your menstrual cycle or have concerns about your reproductive health.

Adenomyosis is a condition in which the tissue that normally lines the inside of the uterus (the endometrium) grows into the muscular wall of the uterus (the myometrium). This can cause the uterus to become enlarged and tender, and can lead to heavy, painful menstrual bleeding.

Dysmenorrhea occurs because PID can cause inflammation and scarring of the reproductive organs, which can make the uterus and surrounding tissues more sensitive to hormonal changes during the menstrual cycle. Additionally, scarring and adhesions can cause the uterus to become misshapen, which can lead to pain and discomfort during menstruation.

Dysmenorrhea occurs because fibroids can cause the uterus to become enlarged and distorted, which can make it more sensitive to hormonal changes during the menstrual cycle. Additionally, fibroids can cause heavy menstrual bleeding, which can also contribute to pain and discomfort during menstruation.
Fibroids, also known as leiomyomas, are noncancerous growths that develop in or on the uterus.

Cervical stenosis is a condition in which the opening of the cervix is narrow or completely closed. This can cause dysmenorrhea, which is painful menstrual cramps, because it can lead to a buildup of menstrual blood and pressure inside the uterus. This pressure can cause the uterus to contract more strongly than usual, leading to more severe menstrual cramps.

Asherman’s syndrome is a condition in which adhesions, or scar tissue, form inside the uterus. This can cause dysmenorrhea, painful menstrual cramps, because it can lead to a buildup of menstrual blood and pressure inside the uterus. The adhesions can also make it more difficult for menstrual blood to flow out of the uterus, which can cause pain and discomfort during menstruation. it causes build up because the adhesions or scar tissue creates blockages or narrows the cervical canal

non communicating horn or cornua means the lumen of the fallopian tube is not connected to the uterine cavity. this causes dysmenorhea because it leads to build up of blood and increased pressure in the uterus and build up of fluid in the non communicsting horn leads to paid and discomfort during menstruation

Question 47

Clinical presentation of secondary dysmenorrhea

Answer 47

SYMPTOMS-
LAP,DYSPAREUNIA, menstrual pain that precedes the period (a vital clue in endometriosis) and pain that only occurs with
Bleeding, SUDDEN, CRAMPING OR COLICKY PAIN,RADIATES TO LEGS,LOWER BACK,DULL OR CONSTANT PAIN, Nausea, vomiting, headaches and dizziness may sometimes be associated with the pain, RELIEVED BY PAIN KILLERS,
vaginal discharge
Increased weight gain,acne, - hirsutism(unwanted male pattern hair growth on a womans face chest and back),OLIGOENORRHEA
SIGNS-
PALLOR, pelvic mass (if an endometrioma is present), a fixed uterus (if adhesions are present) and endometriotic nodules
(palpable in the pouch of Douglas or on the uterosacral ligaments). An enlarged uterus may be found with fibroids. Abnormal discharge and tenderness may be seen with PID.

Question 48

State six risk factors for dysmenorrhea

Answer 48

There are several risk factors that can increase the likelihood of experiencing dysmenorrhea. These risk factors include being younger than 20 years old, having heavy or irregular menstrual periods, never having given birth, having a family history of dysmenorrhea or other menstrual disorders, and having an underlying condition such as endometriosis or uterine fibroids. Additionally, lifestyle factors such as smoking, stress, and a diet high in fat or sugar may increase the risk of dysmenorrhea.

Being younger than 20 years old can increase the risk of experiencing dysmenorrhea because the hormonal changes associated with puberty can cause the uterus to contract more strongly during menstruation. Additionally, younger women may have less experience managing menstrual pain and may be more likely to delay seeking treatment for their symptoms. However, while dysmenorrhea is more common in younger women, it can affect women of all ages.

Heavy menstrual periods can cause dysmenorrhea because the uterus has to work harder to expel the excess blood and tissue. This increased activity of the uterus can lead to more painful contractions during menstruation. Additionally, women with heavy menstrual periods may be more likely to experience other menstrual disorders, such as endometriosis or uterine fibroids, which can also cause dysmenorrhea.

Nulliparity, or never having given birth, can increase the risk of dysmenorrhea because the uterus may contract more strongly during menstruation in women who have not given birth. This increased activity of the uterus can lead to more painful contractions during menstruation. Additionally, women who have not given birth may be more likely to experience other menstrual disorders, such as endometriosis or uterine fibroids, which can also cause dysmenorrhea. However, while nulliparity is a risk factor for dysmenorrhea, it is important to note that many women who have never given birth do not experience dysmenorrhea.

A high sugar diet can cause inflammation in the body by promoting the production of pro-inflammatory cytokines, which are proteins that contribute to the inflammatory response. Additionally, consuming high amounts of sugar can cause fluctuations in blood sugar levels, which can lead to insulin resistance and hormonal imbalances in the body. These hormonal imbalances can contribute to menstrual pain and discomfort by affecting the levels of estrogen and progesterone in the body

Question 49

What do you want to know in the history of someone with dysmenorrhea and on examination too

Answer 49

History
• Timing and severity of pain (including degree of functional loss):
commonly premenstrual pain or in the fi rst 1–2 days of bleeding, then
eases.
• Pelvic pain and deep dyspareunia (may signify pelvic pathology).
• Previous history of PID or STIs.
• Previous abdominal or genital tract surgery (may cause adhesions).
Examination
• Abdominal exam to exclude pelvic masses.
• Pelvic exam; cervical excitation, adnexal tenderness, mobility, and
masses. abnormal cervix on examination, pelvic mass that is not obviously the uterus

Question 50

State five investigations and complications done for someone with dysmenorrhea

Answer 50

Investigations
FBC,SICKLING TEST
• STI screen (including Chlamydia swab). High vaginal and endocervical swabs
• Pelvic USS to check for endometriomata, PID sequelae, fi broids, congenital abnormalities
• Laparoscopy is usually reserved for women with when the history is suggestive of endometriosis; when swabs and ultrasound scan are normal yet symptoms persist; USS abnormalities,(IDK)
medical treatment failures, or those with concomitant subfertility.

Dysmenorrhea can lead to a number of complications, including decreased quality of life, missed school or work, and difficulty performing daily activities. In some cases, dysmenorrhea can also be a symptom of an underlying condition, such as endometriosis or uterine fibroids, which may require medical treatment. Additionally, severe menstrual pain can be a sign of a more serious condition, such as ovarian cysts or pelvic inflammatory disease, which may require emergency medical attention.

Question 51

How is dysmenorrhea managed

Answer 51

Appropriate reassurance and analgesia may be all that is required.
y Bed rest
y Warm pads applied to the lower abdomen

• Symptom control:
Mild pain,paracetamol
• in severe pain mefenamic acid 500mg tds with each period is effective
• COCP to abolish ovulation in those who dont plan to give birth again
• TENS, vitamin B1, and magnesium may be of benefi t to some
women.

Treat any underlying causes:
• Endometriosis—COCP, progestagens, GnRH analogues, LNG-IUS:
• antibiotics for PID
• relief of obstruction (usually surgical). congenital abnormalities causing genital tract obstruction
FIBROIDS- HYSTERECTOMY
• Therapeutic laparoscopy—for above indications: gold standard for
diagnosis + management of endometriosis/adhesions/complicated PID.
Refer to a gynaecologist if pain interferes with normal activity
especially if treatment is ineffective or an underlying cause is identified.

Transcutaneous electrical nerve stimulation (TENS) is a non-invasive therapy that involves the use of a small device to deliver electrical impulses to the skin. TENS has been used as a complementary therapy in the management of dysmenorrhea, or painful menstrual cramps. The electrical impulses are thought to stimulate the release of endorphins, which are natural pain-relieving chemicals produced by the body. TENS may also help to reduce muscle tension and improve blood flow to the affected area. While TENS is generally considered safe, it is important to speak with your healthcare provider before using this therapy, particularly if you have a pacemaker or other implanted medical device.

it is used in patient with chronic pain

Vitamin B1, also known as thiamine, is an essential nutrient that is important for the proper functioning of the nervous system, muscles, and heart. While there is limited scientific evidence to support the use of vitamin B1 in the management of dysmenorrhea, some studies have suggested that it may be helpful in reducing menstrual pain and discomfort. Vitamin B1 may help to reduce inflammation and improve circulation, which can help to alleviate menstrual cramps. er to determine if it is an appropriate treatment option for your specific condition.

Magnesium is an essential mineral that is important for many bodily functions, including muscle and nerve function, blood sugar regulation, and bone health. Some studies have suggested that magnesium may be helpful in the management of dysmenorrhea, or painful menstrual cramps. Magnesium may help to reduce muscle tension and improve blood flow to the affected area, which can help to alleviate menstrual cramps. In addition, magnesium may have a calming effect on the nervous system, which can help to reduce stress and anxiety, both of which can contribute to menstrual pain and discomfort.

Question 52

Still on dysmenorrhea

Answer 52

Endometriosis

NSAIDs are a common first-line treatment for endometriosis, though there is no current evidence that these agents reduce endometriosis-related pain. [57] Oral contraceptives, progestins, androgens, and gonadotropin-releasing hormone (GnRH) analogues are the mainstays of medical therapy.

LNG-IUS: there is evidence that this is beneficial
for dysmenorrhoea and indeed can be an effective
treatment for underlying causes, such as endometriosis and adenomyosis. It is often used as a firstline treatment before laparoscopy.The Levonorgestrel intrauterine system (LNG IUS) is a type of birth control that is also used in the management of endometriosis. The LNG IUS releases a small amount of the hormone levonorgestrel into the uterus, which can help to reduce the growth of endometrial tissue outside the uterus. The LNG IUS may also help to reduce the severity of endometriosis symptoms, such as pain and heavy bleeding.

• GnRH analogues: this is not a first-line treatment
nor an option for prolonged management due to
the resulting hypo-oestrogenic state. These are
best used to manage symptoms if awaiting hysterectomy or as a form of assessment as to the
benefits of hysterectomy. If the pain does not settle with the GnRH analogue, it is unlikely to be
resolved by hysterectomy.
• Surgery: signs or symptoms of pathology such as
endometriosis may warrant surgical laparoscopy
to perform adhesiolysis or treatment of endometriosis/drainage of endometriomas.

Question 53

What is polymenorrhea
Causes and management

Answer 53

POLYMENORRHEA
This refers to cycle lengths that are shorter than 21 days. In effect, the woman has more menstrual in years than expected from the norm. The causes include:
 Imperfect follicular development
 Defective corpus luteum, ANOVULATION,SHORT LUTEAL PHASE, SHORT FOLLICULAR PHASE.
COMMON IN PUBERTY AND ADOLESCENCE DUE TO IMMATURE HP GONADAL AXIS
COMPLICATIONS:
Anemia and complications of the undelrying cause

management:
The management of polymenorrhea depends on the underlying cause of the condition. Treatment options may include hormonal therapies, pain relief medications, or surgery in some cases. Hormonal therapies, such as hormonal contraceptives or medications that regulate hormone levels, may be recommended to regulate the menstrual cycle and reduce symptoms of polymenorrhea. Pain relief medications, such as nonsteroidal anti-inflammatory drugs (NSAIDs), may be recommended to manage cramping and other symptoms associated with frequent menstrual periods. In some cases, surgery may be needed to remove uterine fibroids or other abnormalities that are causing polymenorrhea. Additionally, lifestyle changes such as stress reduction techniques, exercise, and a healthy diet may help to regulate the menstrual cycle and reduce symptoms of polymenorrhea. If you are experiencing polymenorrhea, it is important to speak with your healthcare provider to determine the underlying cause of your symptoms and to develop an appropriate treatment plan.

Question 54

What is hypomenorrhea
Causes and how each cause problem

Answer 54

HYPOMENORRHEA
This is diminished flow or shortening of the days of menstrual flow. It is unusually light menstrual flow,
sometimes presenting as spotting only. It is blood loss than 30ml per day

The causes include:
 anovulation
 hymenal obstruction
 cervical stenosis
 Asherman’s syndrome- scarring of the uterus usually after dilation and curettage

Asherman syndrome is a condition in which the walls of the uterus become scarred, usually as a result of a medical procedure, such as a dilation and curettage (D&C) or a cesarean section. This scarring can prevent the uterus from shedding its lining during menstruation, which can cause amenorrhea, or the absence of menstrual periods. The scarring can also cause menstrual periods to become lighter or shorter than usual. If you are experiencing amenorrhea or other menstrual irregularities, it is important to speak with your healthcare provider to determine the cause and appropriate treatment. Treatment for Asherman syndrome may involve surgery to remove the scar tissue and restore the normal function of the uterus.

Anovulation, which is a condition characterized by the lack of ovulation, can cause hypomenorrhea, which is a condition characterized by light or infrequent menstrual periods. This is because ovulation is necessary for the production of progesterone, which is a hormone that helps to regulate the menstrual cycle. Without ovulation, the levels of progesterone in the body can be low, which can cause the lining of the uterus to become thin and result in a lighter menstrual flow. Additionally, anovulation can be associated with other symptoms such as irregular menstrual periods, acne, and excess hair growth.

Hymenal obstruction, which is a condition characterized by a blockage of the hymen, can cause hypomenorrhea, which is a condition characterized by light or infrequent menstrual periods. This is because the hymen is a thin membrane that partially covers the vaginal opening, and if it is obstructed, it can prevent menstrual blood from flowing out of the body. This can lead to a buildup of menstrual blood in the uterus, which can cause the periods to become lighter or less frequent. Additionally, hymenal obstruction can be associated with other symptoms such as pelvic pain, discomfort during intercourse, and difficulty inserting tampons.

Question 55

What is early puberty ageC

Answer 55

Also called prerecourse puberty. Less than 8yrsrs

Question 56

What is menorrhagia
State ten causes of this

Answer 56

MENORRHAGIA
This is heavy or prolonged menses occurring at regular intervals. With menses occurs >7 days, blood loss
is usually >80ml. It is synonymous with hypermenorrhea. The causes may be organic or dysfunctional
(endocrine).

CAUSES; ORGANIC CAUSES DYSFUNCTIONAL CAUSES
Systemic Reproductive Tract Ovulatory
 Disorders of coagulation  Fibroids ,PID Anovulatory (this is commoner)
LEUKEMIA  Adenomyosis
IDIOPATHIC , CIRRHOSIS  Endometrial polyps
THROMBOCYTOPENIA  Endometrial hyperplasia
HYPERSPLENISM, Hypothyroidism  Cervical polyp
Drug therapy (e.g. warfarin). Endometrial/cervical carcinoma.
Coagulation disorders (e.g. von Willebrand disease) • Intrauterine devices (IUDs).

Leukemia is a type of cancer that affects the blood and bone marrow, and it can cause heavy menstrual bleeding due to a number of factors. According to the American Cancer Society, leukemia can affect the production and function of platelets, which are cells that help the blood to clot. When the body does not have enough platelets, it can lead to abnormal bleeding, including heavy menstrual bleeding. Additionally, leukemia can cause anemia (a condition in which the body does not have enough red blood cells to carry oxygen to the tissues), which can also contribute to heavy menstrual bleeding. Other symptoms of leukemia can include fatigue, weakness, and bruising or bleeding easily. If you are experiencing heavy menstrual bleeding or other symptoms of leukemia, it is important to speak with your healthcare provider to determine the underlying cause of your symptoms and to develop an appropriate treatment plan.

Question 57

State six risk factors for menorrhagia

Answer 57

Age: Menorrhagia is more common in women who are in their 40s or approaching menopause.

2. Hormonal imbalances: Hormonal imbalances, such as those that occur during puberty, perimenopause, or as a result of certain medications, can affect the menstrual cycle and lead to heavy bleeding.
3. Uterine fibroids: These are noncancerous growths in the uterus that can cause heavy menstrual bleeding and pain.
4. Endometrial polyps: These are growths in the lining of the uterus that can cause heavy menstrual bleeding.
5. Adenomyosis: This is a condition in which the tissue that lines the uterus grows into the muscular wall of the uterus, causing heavy bleeding and pain.
6. Inherited bleeding disorders: Some women may have a genetic condition that affects their blood’s ability to clot, leading to heavy menstrual bleeding.
7. Certain medications: Some medications, such as blood thinners, can increase the risk of heavy menstrual bleeding.
8. Medical conditions: Certain medical conditions, such as liver or kidney disease, can increase the risk of heavy menstrual bleeding.

According to Medscape, von Willebrand factor is a protein that is involved in blood clotting. Von Willebrand disease, a genetic disorder that affects the ability of the blood to clot, can cause heavy menstrual bleeding because it can affect the platelets (the blood cells that help with clotting) and the lining of the blood vessels in the uterus. This can lead to heavier and longer-lasting menstrual bleeding. Other symptoms of von Willebrand disease can include frequent nosebleeds, easy bruising, and prolonged bleeding after injury or surgery. If you are experiencing heavy menstrual bleeding or other symptoms of von Willebrand disease, it is important to speak with your healthcare provider to determine the underlying cause of your symptoms and to develop an appropriate treatment plan.

Hemophilia A and B, von Willebrand disease, and rare factor deficiencies (such as factors I, II, V, VII, X, XI, and XIII) are examples of inherited bleeding disorders. These disorders affect the body’s ability to form blood clots, which can result in prolonged bleeding after injury or surgery, as well as spontaneous bleeding into muscles and joints. If you suspect that you or a family member may have an inherited bleeding disorder, it is important to speak with a healthcare provider who can perform diagnostic tests and help develop an appropriate treatment plan.

The kidneys play a role in the production and metabolism of hormones, including estrogen. According to the National Kidney Foundation, when the kidneys are not functioning properly, they may not be able to metabolize estrogen effectively, leading to an accumulation of estrogen in the body. This can cause a range of symptoms, including heavy menstrual bleeding. Additionally, the liver is responsible for metabolizing hormones, and when the kidneys are not functioning properly, the liver may also be affected, further contributing to hormonal imbalances.

As per the information provided by Medscape, Menorrhagia is more common in women who are in their 40s or approaching menopause. This is because as women age, their hormone levels change, and the balance between estrogen and progesterone can become disrupted. This can cause changes in the menstrual cycle and lead to heavy bleeding. Additionally, as women approach menopause, the lining of the uterus may become thicker, which can also lead to heavy menstrual bleeding.

hormonal im alance/According to Medscape, hormonal imbalances during puberty, such as an excess of estrogen or a deficiency in progesterone, can cause changes in the menstrual cycle and lead to heavy menstrual bleeding. This is because estrogen stimulates the growth of the lining of the uterus, while progesterone helps to stabilize and prepare the lining for possible pregnancy. If there is an imbalance between these hormones, the lining of the uterus may grow too thick or become unstable, which can cause heavy bleeding. Additionally, it can take time for the menstrual cycle to become regular and for the body to adjust to the changes in hormone levels during puberty. This can cause menstrual irregularities, including heavy bleeding.

medications such as anti coagulants:Anticoagulants (blood thinners) can cause heavy menstrual bleeding because they affect the body’s ability to form blood clots. This can make it more difficult for the body to control bleeding during menstruation, leading to heavier bleeding. Additionally, some anticoagulants can cause irritation of the lining of the uterus, which can also contribute to heavy bleeding.
herbal medication such as ginseng can also affect blood clotting

According to Medscape, uterine fibroids can cause heavy menstrual bleeding because they can increase the surface area of the endometrium (the lining of the uterus) and disrupt the normal menstrual flow. This can cause the menstrual bleeding to become heavier and last longer than usual. Additionally, fibroids can cause the uterus to contract more strongly during menstruation, which can also contribute to heavy bleeding. Other symptoms of uterine fibroids can include pelvic pain, pressure, and discomfort.

According to Medscape, adenomyosis can cause heavy menstrual bleeding because it can cause the uterus to become enlarged and the lining of the uterus to become thicker than usual. This can lead to heavier and longer-lasting menstrual bleeding. Additionally, adenomyosis can cause the uterus to contract more strongly during menstruation, which can also contribute to heavy bleeding. Other symptoms of adenomyosis can include pelvic pain, pressure, and discomfort.

Question 58

What do you want to know in the history and exam of someone with menorrhagia

Answer 58

Irregular bleeding abnormality IMB, PCB SUGGESTIVE OF Endometrial or cervical polyp or other cervical
Coagulation disorder (coagulation disorders will be present in 20% OF those presenting with ‘unexplained’ HMB:
Excessive bruising/bleeding from other site, History of PPH, Excessive postoperative bleeding, Excessive bleeding with dental extractions, Family history of bleeding problems.
Unusual vaginal discharge SUGGESTIVE OF PID
Urinary symptoms, abdominal mass or abdominal fullness Pressure from fibroids
Weight change, skin changes, fatigue Thyroid disease
The relevant questions to determine heaviness of the period and the extent to which is disrupts the woman’s life and SYMPTOMS OF ANEMIA. In younger women it is important to question whether HMB started at menarche, as this is much less likely to be associated with pathology. The regularity of the menstrual cycle is also important as heavy anovulatory bleeds may be associated with early puberty, polycystic ovary syndrome or the perimenopause.

PHYSICAL EXAM-
PALLOR, V/E,PELVIC EXAM
After examining the patient for signs of anaemia,
it is important to perform an abdominal and pelvic
examination in all women complaining of HMB.
This enables any pelvic masses to be palpated, the
cervix to be visualized for polyps/carcinoma, swabs
to be taken if pelvic infection is suspected or a cervical smear to be taken if one is due.

Question 59

What are the investigations for menorrhagia

Answer 59

Full blood count (FBC) should be performed
in all women (but serum ferritin should not be
performed).
• Coagulation screen only if coagulation HMB
since menarche or family history of coagulation Defects
Hb Electrophoresis
PELVIC ULTRASOUND, High vaginal and endocervical swabs.
Thyroid function tests should only be carried out
when the history is suggestive of a thyroid disorder.

Question 60

How is menorrhagia managed

Answer 60

Admit.
WIDE BORE CANNULAS,HYDRATEIntravenous access and resuscitation or
transfusion as required, TRANSFUSE DEPENDING ON HB
• Pelvic examination.
• FBC, coagulopathy screen, biochemistry.
• Tranexamic acid oral or IV.
• TVUSS.
• High-dose progestogens to arrest bleeding.
• Consider suppression with GnRH or ulipristol acetate in the medium term.
• Longer-term plan when a diagnosis has
been made.

Question 61

State five complications of menorrhagia

Answer 61

According to the American College of Obstetricians and Gynecologists, some of the potential complications of heavy menstrual bleeding include anemia (a condition in which the body does not have enough red blood cells to carry oxygen to the tissues), fatigue, and decreased quality of life. Sickle cell crisis
. Additionally, heavy menstrual bleeding can interfere with daily activities and may require time off from work or school. In some cases, heavy menstrual bleeding may be a symptom of an underlying medical condition, such as fibroids, polyps, or endometriosis, which may require further evaluation and treatment.
Heavy menstrual bleeding can be particularly concerning for individuals with sickle cell anemia. According to the American Society of Hematology, heavy menstrual bleeding can lead to anemia and can trigger a sickle cell crisis, which is a painful episode that occurs when sickle-shaped red blood cells clump together and block blood flow to the tissues. Additionally, heavy menstrual bleeding can interfere with daily activities and may require time off from school or work. If you have sickle cell anemia and are experiencing heavy menstrual bleeding, it is important to speak with your healthcare provider to determine the underlying cause of your symptoms and to develop an appropriate treatment plan.

Question 62

What is METRORRHAGIA

Answer 62

METRORRHAGIA

This is bleeding occurring between menstrual periods. The causes include:
 bleeding at ovulation (i cant explain)
 endometrial polyps
 cervical polyps
 cervical cancer

Endometrial and cervical ervical polyps are growths that occur on the lining of the cervix, and they can cause metrorrhagia (irregular bleeding between menstrual periods) due to a number of factors. According to the American College of Obstetricians and Gynecologists, endocervical polyps can cause bleeding by irritating the surrounding tissue and causing inflammation. Additionally, polyps can be fragile and can bleed easily, leading to spotting or heavy bleeding. Other symptoms of endocervical polyps can include vaginal discharge, pain during intercourse, and pain or pressure in the pelvic region. If you are experiencing metrorrhagia or other symptoms of endocervical polyps, it is important to speak with your healthcare provider to determine the underlying cause of your symptoms and to develop an appropriate treatment plan.

According to Medscape, cervical cancer can cause intermenstrual bleeding (bleeding between menstrual periods) due to the fact that cancer cells can cause inflammation and irritation of the cervix. Additionally, cervical cancer can cause the cervix to become friable (easily damaged), which can lead to bleeding. Cervical cancer can also cause bleeding by invading the blood vessels in the cervix. Other symptoms of cervical cancer can include pelvic pain, pain during intercourse, and vaginal discharge. If you are experiencing intermenstrual bleeding or other symptoms of cervical cancer, it is important to speak with your healthcare provider to determine the underlying cause of your symptoms and to develop an appropriate treatment plan. Regular cervical cancer screening, such as a Pap test, can help detect cervical cancer in its early stages when it is most treatable.

According to Medscape, bleeding at ovulation can cause intermenstrual bleeding (bleeding between menstrual periods) due to the release of an egg from the ovary. This can cause a small amount of bleeding or spotting, which may be mistaken for intermenstrual bleeding.
However, some individuals may experience heavier bleeding or bleeding outside of ovulation, which may be indicative of an underlying medical condition.

Treatment of endometrial polyps may depend on the individual’s symptoms and the size and location of the polyps. According to the American College of Obstetricians and Gynecologists, small polyps may not require treatment, while larger polyps may need to be removed surgically. Surgical removal of endometrial polyps can be done through hysteroscopy, a minimally invasive procedure in which a thin, lighted tube is inserted through the cervix to view the inside of the uterus and remove the polyp. Hormonal medications, such as birth control pills or progestin therapy, may also be used to help regulate the menstrual cycle and reduce the risk of polyp formation. If you have been diagnosed with endometrial polyps, it is important to speak with your healthcare provider to determine the best treatment plan for your individual needs.

Question 63

State the complications and differentials and management

Answer 63

COMPLICATIONS:
Anemia

DDX:
Ectopic
Implantation bleeding
Mollar pregnancy
Uterine Fibroids

Treat underlining cause

Question 64

What is MENOMETRORRHAGIA
What is amenorrhea
State the types of amenorrhea
What is primary and secondary amenorrhea

Normal menstruation requires functional female reproductive system consisting of
 Hypothalamus that produces GnRH that stimulate pitutary
 Pituitary gland produces FSH and LH that stimulate the ovary
 Ovary: functional ovarian follicles produce estrogen (E2) and inhibin in response to FSH; and Corpus
Luteum that produces progesterone in response to LH
 Uterus with endometrium that responds to changes in levels estrogen and progesterone
 Normal outflow tract that allows menstrual blood to flow ou

Answer 64

MENOMETRORRHAGIA
This is heavy or prolonged menses occurring at irregular intervals. The causes are those found in
menorrhagia and metrorrhagia

Amenorrhea:
This is the absence of menses during the reproductive years.
It can be physiologic (pregnancy,
postpartum) or pathologic. If it is pathologic, it is further classified as primary or secondary. Common physiological states associated with amenorrhea include pre-menarche, pregnancy, lactation,
and menopause. Pathological causes of amenorrhea occur at levels of the Hypothalamus, Pituitary
gland, Ovaries, Uterus and the outflow tract. Evaluation of amenorrhea should therefore target these
levels.
• 1° amenorrhoea is lack of menstruation by age 16 in the presence of sexual characteristics or 14 in their absence.
• 2° amenorrhoea is an absence of menstruation for 6mths. (oxford)

PRIMARY AMENORRHEA
This is the absence of menses in a girl by age 14 years in the absence of secondary sexual characteristics,
or in a girl aged 16 years who has developed some secondary sexual characteristics. The incidence of
primary amenorrhea is 2-3%. Amenorrhea, or absent menstruation, can be either primary or secondary. Primary amenorrhea is defined as either (a) the lack of menstruation by the age of 15 years (or within 3 years after thelarche) with otherwise normal pubertal development or (b) the lack of secondary sexual characteristics by the age of 13 years. [1] Secondary amenorrhea is defined as the lack of menses for 6 months, though it is uncommon even in adolescents to lack menses for more than 3 months.(medscape)

Question 65

What do you want to know in the history of someone with amenorrhea

Answer 65

Diagnosis
History
Emphasis on:
• Sexual activity, risk of pregnancy, and type of contraceptive used.
• Galactorrhoea or androgenic symptoms (weight gain, acne, hirsutism).
• Menopausal symptoms (night sweats, hot fl ushes).
• Previous genital tract surgery (intrauterine instrumentation or LLETZ).
• Issues with eating or excessive exercise.
• Drug use (especially dopamine antagonists for psychiatric conditions).

Examination
• BMI <17/>30, hirsutism, 2 ° sexual characteristics (Tanner staging).
• Stigmata of endocrinopathies (including thyroid) or Turner’s syndrome.
• Evidence of virilization (deep voice, male pattern balding,
cliteromegaly).
• Abdominal: may show masses due to tumours or genital tract
obstruction.
• Pelvic: imperforate hymen, blind ending vaginal septum, absence of
cervix and uterus.
Physical examination for primary amenorrhea begins with measurement of height, weight, body mass index (BMI), and vital signs. One should also evaluate for staging of thelarche and adrenarche, as well as for signs of hyperandrogenism, including hirsutism, acne, and clitoromegaly.
Thelarche marks the beginning of breast development and includes five Tanner stages, as follows [4] :
Stage 1 - No palpable breast tissue
Stage 2 - Development of breast buds with elevation of the papilla
Stage 3 - Enlargement of the breast without separation of the areola
Stage 4 - Formation of a secondary mound, as the areola and papilla project above the breast
Stage 5 - Recession of the areola to the contour of the breast
Adrenarche indicates the activation of the adrenal cortex to produce androgens; it is associated with pubarche, or the development of pubic hair.
The examination should also include evaluation of physical features consistent with Turner syndrome, such as short stature, webbed neck, shield chest, and widely spaced nipples. If feasible, a genital examination should be performed to evaluate for presence of an imperforate hymen, absent or blind-ending vagina, or transverse vaginal septum, as well as the presence of a cervix, a uterus, and ovaries. If this is not possible, imaging can be performed to evaluate for the presence of müllerian structures.

Question 66

Name the risk factors for amenorrhea

Answer 66

Medscape notes that the risk factors for amenorrhea include pregnancy, breastfeeding, menopause, certain medications, such as hormonal contraceptives or chemotherapy drugs, and medical conditions that affect the ovaries, hypothalamus, or pituitary gland, such as polycystic ovary syndrome (PCOS), thyroid disorders, or hypothalamic amenorrhea
Mosaicsm and other chromosomal disorders
. Additionally, certain lifestyle factors, such as excessive exercise or low body weight, can also lead to amenorrhea. Other risk factors for amenorrhea may include stress, eating disorders, or a family history of amenorrhea.

Question 67

Cause of primary amenorrhea
What’s the Clinical approach to evaluating primary amenorrhea

Answer 67

Causes OF PRIMARY AMENORRHEA range from congenital enzymatic deficiencies through hypothalamic-pituitary problems to structural abnormalities in the genital tract. Clinical approach to evaluating primary amenorrhea
includes History, Physical Examination and Laboratory Investigations. Pelvic ultrasound and or
laparoscopy may be done in evaluating the pelvis for presence of uterus. It is clinically useful to group
the causes and relate them to the presence or absence of secondary sexual characteristics (breasts) and
female internal genitalia (the uterus).

Thus, there are four clinical categories of causes kf primary amenorrhea.
 Breast absent, uterus present
 Breast present, uterus absent
 Breast absent, uterus absent
 Breast present, uterus presen

Question 68

Explain breast absent uterus present

Answer 68

Breast Absent, Uterus Present
Breast absent implies low sex steroid (estrogen) production (hypogonadism). The cause can be at the level of the ovaries or higher centres as outlined below.

It’s in three levels

I. Gonadal failure or gonadal dysgenesis
 Turner’s Syndrome (45 X0)
 Pure gonadal dysgenesis (46XX, 46XY) i.e. congenital absence of the gonad (ovary) 46X,
abnormal X
 17α-hydroxylase deficiency (46XX)-17α-hydroxylase deficiency is a genetic condition that affects the production of certain hormones in the body. People with 17α-hydroxylase deficiency are unable to produce enough cortisol and sex hormones, which can lead to a range of symptoms, including high blood pressure, low potassium levels, and a lack of menstrual periods in people with XX chromosomes. The absence of menstrual periods in people with 17α-hydroxylase deficiency is due to a lack of estrogen, which is required for the development of female sex organs and the onset of menstruation. Treatment for 17α-hydroxylase deficiency may involve hormone replacement therapy to address the hormonal imbalances caused by the condition. It is important to speak with a healthcare provider to determine the most appropriate treatment plan for 17α-hydroxylase deficiency.
 Mosaicsm (X/XX, X/XX/XXX)-Mosaicism is a genetic condition that occurs when an individual has two or more genetically distinct populations of cells in their body.
-Mosaicism can affect menstruation in a variety of ways, depending on the specific genetic factors involved. In some cases, mosaicism can lead to a range of physical differences that affect the development of the reproductive system, which can result in amenorrhea, or the absence of menstrual periods. In other cases, mosaicism may have little or no effect on menstruation. The specific effects of mosaicism on menstruation can vary widely depending on the underlying genetic factors and other individual factors. It is important to speak with a healthcare provider to determine the most appropriate treatment plan for any menstrual irregularities that may be related to mosaicism.

II. Pituitary Failure: (failure of FSH secretion)
III. Hypothalamic failure: Failure of GnRH secretion

Question 69

Explain the second and third levels of breast absent uterus present

Answer 69

II. Pituitary Failure: (failure of FSH secretion)
 Pituitary tumours (chromophobe adenoma)
 Mumps encephalitis-
 Kernicterus
 Pre-pubertal hypothyroidism

III. Hypothalamic failure: Failure of GnRH secretion
 Neurotransmitter deficiencies
 Kallman syndrome
 Congenital anatomic defects in CNS
 CNS neoplasia (eg craniopharyngiomas)

Mumps encephalitis is a rare complication of mumps, a viral infection that primarily affects the salivary glands. In some cases, mumps encephalitis can lead to inflammation of the brain and other neurological symptoms. This can affect the hypothalamus, a part of the brain that plays a key role in regulating the menstrual cycle. Damage to the hypothalamus can disrupt the normal hormonal signals that control the menstrual cycle, leading to amenorrhea, or the absence of menstrual periods. The specific effects of mumps encephalitis on menstruation can vary widely depending on the severity and duration of the infection, as well as other individual factors.

Kernicterus is a rare neurological condition that occurs when high levels of bilirubin build up in the blood and enter the brain, leading to brain damage. In some cases, kernicterus can affect the hypothalamus, a part of the brain that plays a key role in regulating the menstrual cycle. Damage to the hypothalamus can disrupt the normal hormonal signals that control the menstrual cycle, leading to amenorrhea, or the absence of menstrual periods. The specific effects of kernicterus on menstruation can vary widely depending on the severity and duration of the condition, as well as other individual factors.

Hypothyroidism can cause a disruption of hormones that are necessary for the menstrual cycle. When the thyroid gland does not produce enough thyroid hormone, it can lead to an increase in the hormone prolactin, which can suppress the production of estrogen and progesterone. These hormones are essential for regulating the menstrual cycle, and a deficiency of these hormones can disrupt the normal hormonal signals that control the menstrual cycle, leading to amenorrhea, or the absence of menstrual periods. Thyroid hormone insufficiency can lead to increased prolactin levels in the blood. Prolactin is a hormone that is normally produced by the pituitary gland in response to signals from the hypothalamus. However, when thyroid hormone levels are low, it can disrupt the normal hormonal signals that control prolactin production, leading to an increase in prolactin levels. High levels of prolactin can suppress the production of estrogen and progesterone, which are essential for regulating the menstrual cycle.

Congenital anatomic defects in the central nervous system (CNS) can cause amenorrhea by disrupting the normal hormonal signals that control the menstrual cycle. For example, a congenital defect in the hypothalamus or pituitary gland can lead to insufficient production of gonadotropin-releasing hormone (GnRH) or luteinizing hormone (LH), which are essential for the production of estrogen and progesterone. Without these hormones, the menstrual cycle cannot proceed normally, leading to amenorrhea. Some examples of congenital anatomic defects that can cause amenorrhea include septo-optic dysplasia, Kallmann syndrome, and hypothalamic hamartoma

Question 70

Explain breast present uterus present

Answer 70

B. Breast Present, Uterus Present
Adequate sex steroid (estrogen) present; genotype 46XX; commonly implies outflow obstruction
 Imperforate hymen
 Vaginal agenesis/atresia
 Transverse vaginal septum
 Cervical agenesis
 Congenital endometrial hypoplasia or aplasia

An imperforate hymen is a congenital condition in which the hymen, a thin membrane that partially covers the vaginal opening, completely blocks the passage of menstrual blood. This can cause amenorrhea, or the absence of menstrual periods, because the blood cannot exit the body. The menstrual blood may accumulate in the uterus and cause abdominal pain or discomfort. Imperforate hymen is usually diagnosed during adolescence when girls fail to start their menstrual periods. Treatment for imperforate hymen typically involves a minor surgical procedure to create an opening in the hymen to allow menstrual blood to pass through. It is important to speak with a healthcare provider to determine the most appropriate treatment plan for any menstrual irregularities that may be related to an imperforate hymen.

Cervical agenesis is a rare congenital condition in which the cervix, which is the lower part of the uterus that connects to the vagina, does not develop properly or is absent. This can cause amenorrhea, or the absence of menstrual periods, because the menstrual blood cannot exit the body. Women with cervical agenesis often have a normal uterus and ovaries, and they may experience cyclic pelvic pain or discomfort due to the buildup of menstrual blood in the uterus. Treatment for cervical agenesis typically involves surgical creation of an opening in the cervix to allow menstrual blood to pass through. It is important to speak with a healthcare provider to determine the most appropriate treatment plan for any menstrual irregularities that may be related to cervical agenesis.

Congenital endometrial hypoplasia is a rare congenital condition in which the endometrium, which is the inner lining of the uterus, does not develop properly or is absent. This can cause amenorrhea, or the absence of menstrual periods, because the endometrium is necessary for the growth and shedding of the uterine lining during the menstrual cycle. Women with congenital endometrial hypoplasia may have a normal uterus and ovaries, but they may not ovulate or have regular menstrual cycles due to the absence of endometrial tissue. Treatment for congenital endometrial hypoplasia typically involves hormonal therapy to promote the development of endometrial tissue, or in some cases, assisted reproductive technologies may be necessary to achieve pregnancy.

Question 71

Explain breast present uterus absent

Answer 71

C. Breast Present, Uterus Absent
Adequate estrogen production
 Androgen insensitivity syndrome (peripheral estrogen production from androgens)
 Congenital absence of uterus (Rokitansky-Mayer-Kuster-Hauser syndrome)

D. Breast Absent, Uterus Absent
 17,20-desmolase deficiency
 Agonadism
 17α-hydroxylase deficiency (46XY

According to Medscape, primary amenorrhea, or the absence of menstrual periods in girls who have not yet reached the age of 16, can be caused by a variety of factors. Some of the causes of primary amenorrhea include genetic disorders, such as Turner syndrome or androgen insensitivity syndrome, structural abnormalities of the reproductive system, such as an imperforate hymen or vaginal septum, hormonal imbalances, such as hypothyroidism or hyperprolactinemia, and chronic illnesses or medications that affect the reproductive system. Additionally, certain lifestyle factors, such as excessive exercise or low body weight, can also lead to primary amenorrhea. If you or someone you know is experiencing primary amenorrhea, it is important to speak with a healthcare provider to determine the underlying cause of the condition and to develop an appropriate treatment plan.

Androgen insensitivity syndrome (AIS) can affect the menstrual cycle by causing amenorrhea, or the absence of menstrual periods, due to the underdevelopment or absence of female reproductive organs such as the uterus, fallopian tubes, and ovaries. In some cases, women with AIS may have peripheral estrogen production from androgens, which can lead to the development of secondary sexual characteristics, but may not result in regular menstrual cycles. Hormone therapy may be used to promote the development of secondary sexual characteristics and may also help regulate the menstrual cycle in some cases. It is important to speak with a healthcare provider to determine the most appropriate treatment plan for any menstrual irregularities that may be related to AIS.

Congenital absence of the uterus, also known as Mayer-Rokitansky-Küster-Hauser (MRKH) syndrome, is a rare congenital condition in which the uterus and upper portion of the vagina do not develop properly or are absent. This can cause amenorrhea, or the absence of menstrual periods, because the uterus is necessary for the growth and shedding of the uterine lining during the menstrual cycle. Women with MRKH syndrome may have normal ovaries and external genitalia, but they may not ovulate or have regular menstrual cycles due to the absence of the uterus. Treatment for MRKH syndrome typically involves surgical reconstruction of the vagina and may involve assisted reproductive technologies such as in vitro fertilization (IVF) to achieve pregnancy. It is important to speak with a healthcare provider to determine the most appropriate treatment plan for any menstrual irregularities that may be related to MRKH syndrome.

Question 72

State ten investigations for amenorrhea

Answer 72

Laboratory investigations
 Pregnancy test
 Check FSH/LH to differentiate ovarian failure from failure of higher centres (pituitary or
hypothalamus)
 Check Karyotype for chromosomal studies to resolve gonadal problems
 X-ray, CT scan, MRI for suspected pituitary and hypothalamic lesionPregnancy test.
• FSH/LH: i in premature ovarian failure (POF), d hypothalamic causes
(not useful in PCOS).
• Testosterone and sex hormone-binding globulin (SHBG) are most
useful for PCOS.
• Prolactin should always be tested.
• TFTs.
• Pelvic ultrasound:
• can defi ne anatomical structures, congenital abnormalities,
Asherman’s syndrome, haematometra, and PCOS morphology
• can indicate physiological activity or endometrial atrophy in POF.
• Karyotype if uterus absent or suspicion of Turner’s syndrome.
• Specifi c tests for endocrinopathies where there is clinical suspicion. s

levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), estradiol, thyroid-stimulating hormone (TSH), and prolactin. For interpretation of FSH and LH test results, the estradiol and progesterone levels must be low. In young women with no menses, it is sometimes necessary to draw weekly estradiol and progesterone levels until they indicate that the patient is in the early follicular phase, and then draw FSH and LH levels.
If the FSH is elevated, primary hypogonadism is likely, and karyotyping should be performed to determine whether there is evidence of Turner syndrome (45,X or 45,X/46,XX mosaic) or Swyer syndrome (46,XY). If the FSH is low or normal, the cause is likely hypothalamic, and further workup may include imaging of the head if no apparent, obvious cause (eg, stress- or exercise-induced hypothalamic dysfunction) is identified.
If the prolactin level is elevated, it is important to make sure that it was obtained in the fasting state without any recent nipple stimulation; if the level was not obtained in this state, the test may have to be repeated. If the prolactin level remains elevated and there is no recent medication use, including psychotropic medications to explain the elevation, magnetic resonance imaging (MRI) of the pituitary should be performed to evaluate for a pituitary microadenoma or adenoma.

Question 73

What is secondary amenorrhea

Answer 73

Secondary amenorrhea is the absence of menses for 3 consecutive months in a woman with previously
regular (normal) menstrual cycles or for 6months in a woman with previously irregular menstrual cycles
(oligomenorrhea). It is commoner than primary amenorrhea. The commonest cause of secondary
amenorrhea is pregnancy. Other causal factors includePsychological
Hypothalamic
Pituitary
Thyroid
Adrenal
Ovarian
Uterine and outflow tracT

Like primary amenorrhea the causal factors commonly occur at the level of the outflow tract and the
uterus, ovaries, pituitary and hypothalamus and other endocrine organs such as thyroid and adrenal
glands. Secondary amenorrhea may also be classified as hypergonadotropic (high FSH/LH),
hypogonadotropic (lowFSH/LH), normo-gonadotropic (normal FSH/LH) and hyperprolactinaemic.

Common causes of amenorrhoea

Physiological causes:
1 Pregnancy must always be excluded.
• Lactation.
• Menopause.
Iatrogenic causes
• Progestagenic contraceptives: Depo-Provera ® , Mirena IUS ® ,
Nexplanon ® , POP.
• Therapeutic progestagens, continuous COCP use, GnRH analogues,
rarely danazol.

Question 74

State the types of secondary amenorrhea

Answer 74

Hyperprolactinaemic amenorrhea

Hypergonadotropic hypogonadism

Hypogonadotropic hypogonadism

Normogonadotropic hypogonadism

Question 75

What is Hyperprolactinaemic amenorrhea

Answer 75

Hyperprolactinaemic amenorrhea
 Breastfeeding
 Breast stimulation
 Pituitary adenoma
 Empty sella syndrome
 Hypothyroidism
 Medications, eg oral contraceptives, antipsychotics, antidepressants
 Altered metabolism as in liver and renal failure
 Ectopic production, e.g. gonadoblastoma, teratoma

Empty sella syndrome (ESS) is a rare condition in which the sella turcica, a small depression in the skull where the pituitary gland is located, is partially or completely filled with cerebrospinal fluid. ESS can cause a range of symptoms, including amenorrhea, or the absence of menstrual periods, due to hormonal imbalances. The pituitary gland produces hormones that regulate the menstrual cycle, and ESS can interfere with the normal functioning of the gland, leading to menstrual irregularities. Treatment for ESS typically involves hormone therapy to correct any hormonal imbalances and may involve surgery to relieve pressure on the pituitary gland. It

Question 76

What is Hypergonadotropic hypogonadism and Hypogonadotropic hypogonadism

Answer 76

Hypergonadotropic hypogonadism
 Premature ovarian failure
 Gonadal dysgenesis

Hypogonadotropic hypogonadism
 anorexia nervosa
 chronic illnesses
 excessive exercises
anorexia nervosa
 chronic illnesses
 excessive exercises
 excessive weight loss
 Sheehan’s syndrome
Hypothalamic/pituitary destruction

Hypergonadotropic hypogonadism is a condition in which the body is unable to produce normal levels of sex hormones, such as estrogen and progesterone problem with the ovaries, which can lead to a hormonal imbalance. The pituitary gland produces hormones that stimulate the ovaries to produce estrogen and progesterone. If the pituitary gland is not functioning properly, it may not produce enough of these hormones, leading to hypergonadotropic hypogonadism. This condition can cause menstrual irregularities, such as amenorrhea (absence of menstrual periods), as well as other symptoms such as hot flashes, vaginal dryness, and reduced sex drive. Treatment for hypergonadotropic hypogonadism typically involves hormone replacement therapy to replace the deficient hormones and may involve other treatments to address any underlying causes of the condition. .

Premature ovarian failure (POF) is a condition in which the ovaries stop functioning normally before the age of 40, leading to a decrease in the production of estrogen and progesterone. This hormonal imbalance can cause menstrual irregularities, including amenorrhea (absence of menstrual periods). Amenorrhea occurs because the ovaries are not producing enough estrogen to stimulate the lining of the uterus to build up and be shed during a menstrual period. In some cases, POF may also cause other symptoms such as hot flashes, vaginal dryness, and reduced sex drive. Treatment for POF typically involves hormone replacement therapy to replace the deficient hormones and may involve other treatments to address any underlying causes of the condition. It is important to speak with a healthcare provider to determine the most appropriate treatment plan for any menstrual irregularities or other symptoms that may be related to POF.

Hypogonadotropic hypogonadism (HH) is a medical condition in which the body is unable to produce normal levels of sex hormones due to a problem with the hypothalamus or pituitary gland, which are part of the endocrine system that regulates hormone production. This can lead to a decrease in the production of estrogen and progesterone in females, which can cause menstrual irregularities, including amenorrhea (absence of menstrual periods). Amenorrhea occurs because the ovaries are not receiving enough stimulation from the pituitary gland to produce the hormones necessary to stimulate the lining of the uterus to build up and be shed during a menstrual period.

Gonadal dysgenesis is a condition in which the gonads (ovaries or testes) do not develop properly. This can lead to a variety of symptoms, including primary amenorrhea (the absence of menstrual periods) in women.

In women with gonadal dysgenesis, the ovaries do not develop properly, which can lead to a lack of estrogen production and the absence of menstrual periods. Gonadal dysgenesis can be caused by a variety of factors, including genetic abnormalities such as Turner syndrome or Swyer syndrome.

Amenorrhea is a common symptom of gonadal dysgenesis, as the ovaries are responsible for producing estrogen, which is necessary for the development and maintenance of the menstrual cycle.

Hypogonadotropic hypogonadism (HH) and hypergonadotropic hypogonadism (HH) are two types of medical conditions that can cause a decrease in the production of sex hormones in the body.

HH is a condition in which the body is unable to produce normal levels of sex hormones due to a problem with the hypothalamus or pituitary gland, which are part of the endocrine system that regulates hormone production. This can lead to a decrease in the production of estrogen and progesterone in females, and testosterone in males.

On the other hand, HH is a condition in which the body is unable to respond to normal levels of sex hormones due to a problem with the testes or ovaries. This can lead to a decrease in the production of estrogen and progesterone in females, and testosterone in males.

The main difference between these two conditions is the underlying cause of the hormone deficiency. In HH, the problem is with the hypothalamus or pituitary gland, while in HH, the problem is with the testes or ovaries. Treatment for both conditions typically involves hormone replacement therapy to replace the deficient hormones and may involve other treatments to address any underlying causes of the condition. It is important to speak with a healthcare provider to determine the most appropriate treatment plan for any symptoms that may be related to either condition.

Question 77

What is Normogonadotropic hypogonadism

Answer 77

Normogonadotropic hypogonadism
 Outflow tract obstruction, eg Asherman’s syndrome, cervical stenosis, Genital tract outfl ow obstruction:,• imperforate hymen ,• transverse vaginal septum ,• cervical stenosis ,• Asherman’s syndrome (iatrogenic intrauterine adhesions).
 Polycystic ovaries
 Thyroid disease
 Cushing’s syndrome
 Acromegaly

Normogonadotropic hypogonadism (NGH) is a medical condition in which the body is unable to produce normal levels of sex hormones despite having normal levels of gonadotropins, which are hormones produced by the pituitary gland that stimulate the production of sex hormones in the testes or ovaries. This can lead to a decrease in the production of estrogen and progesterone in females, and testosterone in males.

NGH is a rare condition that can be caused by a variety of factors, including genetic mutations, autoimmune disorders, and certain medications.

Asherman’s syndrome is a condition in which there is scarring or damage to the lining of the uterus, which can interfere with the normal hormonal signals that regulate the menstrual cycle and the production of sex hormones.

During a normal menstrual cycle, the lining of the uterus (the endometrium) thickens in response to rising levels of estrogen. This thickened lining is then shed during menstruation if fertilization and implantation of an embryo do not occur.

In Asherman’s syndrome, scarring or damage to the endometrium can interfere with the normal thickening and shedding of the lining of the uterus. This can cause menstrual abnormalities, such as decreased or absent menstrual flow, or irregular cycles.

The scarring can also interfere with the normal hormonal signals that regulate the menstrual cycle and the production of sex hormones. This can lead to decreased levels of estrogen and progesterone, which can cause symptoms such as infertility, decreased libido, and other symptoms related to low levels of sex hormones.

Question 78

State six causes of amenorrhea
Check the sldies for picture approach to primary and secondary amenorrhea

Answer 78

Pathological causes of amenorrhoea
• Hypothalamic:
• functional—stress, anorexia, excessive exercise, pseudocyesis
• non-functional— space-occupying lesion (SOL), surgery,
radiotherapy, Kallman’s syndrome (1° GnRH defi ciency).
• Anterior pituitary:
• micro- or macroadenoma (prolactinoma) or other SOL
• surgery
• Sheehan’s syndrome (post-partum pituitary failure).
• Ovarian:
• PCOS
• POF
• resistant ovary syndrome
• ovarian dysgenesis, especially due to Turner’s syndrome (45XO).
• Genital tract outfl ow obstruction:
• imperforate hymen
• transverse vaginal septum
• cervical stenosis
• Asherman’s syndrome (iatrogenic intrauterine adhesions).
• Agenesis of uterus and müllerian duct structures: sporadic or
associated with AIS.
• Endocrinopathies:
• hyperprolactinaemia
• Cushing’s syndrome
• severe hypo/hyperthyroidism
• CAH.
Oestrogen—or androgen—secreting tumours: usually ovarian or adrenal,
e.g. granulosa-thecal cell tumours and gynandroblastoma.

Question 79

How is amenorrhea

Answer 79

Management
Must be guided by the diagnosis and fertility wishes. Options include:
• Treat any underlying causes including attaining normal BMI.
• Cabergoline or surgery for hyperprolactinaemia.
• Cyclical withdrawal bleeds (COCP for PCOS).
• HRT for POF.
• Relief of genital tract obstruction: cervical dilation, hysteroscopic
resection, incision of hymen.
• Specifi c treatment for endocrinopathies and tumours.
2 Major congenital abnormalities, AIS, etc. should be managed by multidisciplinary teams in specialist centres.

Question 80

State four complications

Answer 80

According to Medscape, amenorrhea can be associated with a number of complications, including:

1. Infertility: Amenorrhea can make it difficult or impossible to conceive a child, as it can be caused by factors that interfere with ovulation and fertility.
2. Osteoporosis: Amenorrhea can lead to decreased levels of estrogen, which can increase the risk of osteoporosis, or thinning of the bones.
3. Cardiovascular disease: Amenorrhea can be associated with other hormonal imbalances, such as changes in thyroid function or insulin resistance, which can increase the risk of cardiovascular disease.
4. Endometrial cancer: Amenorrhea can be caused by factors that interfere with the normal shedding of the lining of the uterus, which can increase the risk of endometrial cancer.
5. Psychological effects: Amenorrhea can be associated with psychological stress and anxiety, particularly in women who are trying to conceive.

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Amenorrhea can lead to an increased risk of endometrial cancer because it is associated with a lack of menstrual periods. Menstrual periods are important for shedding the lining of the uterus, which helps to prevent the buildup of abnormal cells and tissues that can lead to cancer.

When a woman experiences amenorrhea, the lining of the uterus may continue to grow and thicken, which can increase the risk of abnormal cell growth and the development of endometrial cancer. This risk is particularly high in women who have other risk factors for endometrial cancer, such as obesity, diabetes, or a family history of the disease.

Osteoporosis is a condition in which the bones become thin, brittle, and weak, which can increase the risk of fractures and other injuries. Estrogen is a hormone that plays an important role in maintaining bone density and strength, particularly in women.

Estrogen helps to regulate the activity of cells called osteoclasts and osteoblasts, which are responsible for breaking down and building up bone tissue, respectively. When estrogen levels are low, as they may be in women who are experiencing menopause or other hormonal imbalances, the activity of osteoclasts can increase, leading to a loss of bone density.

Estrogen replacement therapy (ERT) may be used to help manage osteoporosis in women who are experiencing low levels of estrogen. ERT can help to slow or prevent the loss of bone density, reducing the risk of fractures and other injuries.

Amenorrhea can cause thyroid dysfunction through a number of different mechanisms. For example, amenorrhea can be caused by conditions such as polycystic ovary syndrome (PCOS) or hypothalamic amenorrhea, which can also affect thyroid function.

PCOS is a condition in which the ovaries produce high levels of androgens, or male hormones, which can interfere with ovulation and menstrual cycles. PCOS is also associated with insulin resistance, which can affect the body’s ability to regulate thyroid hormones.

Hypothalamic amenorrhea is a condition in which the hypothalamus, a part of the brain that helps to regulate the menstrual cycle, does not function properly. This can be caused by factors such as stress, excessive exercise, or low body weight. Hypothalamic amenorrhea can also affect thyroid function, as the hypothalamus is involved in regulating the production of thyroid hormones.

In addition, thyroid dysfunction can also be caused by autoimmune conditions such as Hashimoto’s thyroiditis or Graves’ disease, which can also affect the menstrual cycle and lead to amenorrhea.

It is important to speak with a healthcare provider if you are experiencing symptoms related to amenorrhea or thyroid dysfunction, as there may be treatment options available to help manage these conditions and prevent complications.

s. One of the most significant complications of amenorrhea is infertility, or the inability to conceive a child. Amenorrhea can be caused by a variety of factors that can also interfere with ovulation and fertility, such as polycystic ovary syndrome (PCOS) or hypothalamic amenorrhea.

Other complications of amenorrhea may include an increased risk of osteoporosis, or thinning of the bones, due to decreased levels of estrogen. Amenorrhea can also be associated with other hormonal imbalances, such as changes in thyroid function, which can lead to symptoms such as fatigue, weight gain, and other issues.