Human Development 2 Flashcards

1
Q

when you put your hands on your hips what bony land mark are u putting hands on?

A

when you put your hands on your hips your putting your hands on each iliac crest

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2
Q

what kind of joint is the pubic symphysis

A

cartilaginous joint

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3
Q

what bone do you sit on when you sit on ur bum

A

when you sit on your bum, you are sitting on the ischial tuberosities. These are the rounded bony prominences of the ischium, which is part of the pelvic bone.

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4
Q

which 2 bony landmarks does the inguinal ligament run between

A

inguinal ligament runs between ASIS and pubic tubercle

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5
Q

The umbilical artery is a paired vessel that arises from the internal iliac artery. During the prenatal development of the fetus, it is a major part of the fetal circulation. What happens to it after birth?

A

After birth, the distal part of the artery obliterates and becomes the medial umbilical ligament.

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5
Q

what neurovasculature runs through each of the following:

-greater sciatic foramen
-lesser sciatic foramen
-obturator foramen
-inguinal ligament

A

greater sciatic foramen
-gluteal arteries,veins + nerves
-sciatic nerve
-pudendal nerve

lesser sciatic foramen
-pudendal nerve

obturator foramen
-obturator artery, vein + nerve

inguinal ligament
-femoral artery, vein + nerve

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6
Q

what is the site of convergence between perineal and pelvic floor muscles which often tears during childbirth

A

the perineal body, is a fibromuscular mass which is the site of convergence between perineal and pelvic floor muscles. The perineal body is the final support of the pelvic viscera, disruption of the perineal body can therefore result in prolapse of pelvic viscera

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7
Q

The pudendal nerve is a somatic nerve, which spinal roots does it emerge from and explain its branching + what it innervates

A

The pudendal nerve; is a somatic nerve; emerges from spinal root S2-S4.

It branches from the sacral plexus + leaves the pelvis through the greater sciatic foramen to enter perineum

The pudendal nerve is responsible for sensory + motor innervation to perineum + is sensory to the genitals and motor to external urethral and anal sphincters

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8
Q

what is the most common site of fertilisation in the uterus

A

Ampulla is the most common site of fertilisation

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9
Q

what is an ectopic pregnancy

A

ECTOPIC PREGNANCY IS WHEN THE EMBRYO IMPLANTS outside of the body of the uterus

when a fertilized egg implants and grows outside the main cavity of the uterus

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10
Q

what is the normal position of the uterus (not pregnant)

A

anteverted and anteflexed

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11
Q

What are the 3 different types of nerve blocks or analgesic used for childbirth

A

1) spinal block= blocks all sensation
used ofr cesarean; all sensation below spinal block is numbed; can be carried out below L3 (but can be as high as T4 tho to ensure all sensation gone)

2) epidural= administered into epidural space (fat filled space around dura mater) takes away pain but not other sensation
- delivered in lumbar regions (below L3)

3) pudendal nerve block (lowest level of anaesthesia)
- used in more than just childbirth
e.g. surgery on perineum
-block all sensory and motor activity of pudendal nerve

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12
Q

what part of the prostate is effected by BPH (benign prostate hyperplasia)

A

BPH effects the transition zone (TZ) of the prostate. TZ becomes enlarged. The TZ surrounds the urethra, in BPH this compresses the urethra making urination difficult

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13
Q

BPH (benign prostate hyperplasia) aka BPE (benign prostate enlargement). Symptoms, causes , diagnosis + treatment

A

causes:
-advance age
-androgen problems (high testosterone, low oestrogen or general imbalance so higher oestrogen than testosterone)

symptoms:
-weak/interrupted urine flow
-frequent urination (nocturia)
-trouble urinating
-pain or burning during urination
-blood in urine or semen

FUN acronym= frequency, urgency, nocturia

diagnosis:
-history (fam history of prostate cancer or high testosterone/low oestrogen)
-digital rectal exam (DRE)
-blood test; prostate specific antigen (PSA) or gamma-seminprotein or kallikrein-3
-ultrasound biopsy

treatment:
-wait + see (if asymptomatic)

if symptoms
-alpha1 adrenergic blockers (relax smooth muscle to help urine flow)
-5-alpha-reductase inhibitors (dutasteride + finasteride) block the conversion of testosterone to DHT so reduces drive for growth cuz less potent (slows any further growth)

-surgery if significant enlargemen
-UroLift; transurethral resection or prostatectomy
-REZUM procedure (steam cook the prostate)= NICE recommended procedure now

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14
Q

Differences between direct and inguinal hernias

A

direct hernia:

indirect hernia:

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15
Q

What is Peyronie’s disease (bent penis); causes, symptoms, treatment

A

-scar tissue forms in shaft of penis causing bending or deformity of penis

causes
-scar tissue as a result of injury e.g. sex
-connective tissue disorders
-autoimmune reaction of body attacking penile tissue

symptoms:
-painful erections difficulties with sexual intercourse

treatment:
non-surgical;
-stretching/traction
-injections of collagenase (breaks down scar tissue)
-topical verapamil (disrupts production of collagen)
-interferon alpha 2b injections reduces fibrosis
-para-aminobenzoate may reduce plaque size

or
surgical

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16
Q

what is varicocele?

A

quite common (10-15%) can cause infertility (15% of men with varicocele are infertile as it increases the temp of the sperm)

varicose veins of the scrotum (pampiniform venous plexus)

most cases on left scrotum (on lefty they go up and join at a right angle making ti easier for them to varicose)

treatment is lasering the pampiniform veins to close them

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17
Q

Explain what gestational diabetes (GDM) is; pathophysiology, risk factors, complications, management, consequences for fetus vs mother

A

gestational diabetes (GDM) = glucose intolerance during pregnancy

pathophysiology:
thought to be exaggerated maternal response as pregnancy is intrinsically a state of insulin resistance + glucose intolerance. Placenta secretes anti-insulin hormones (hPL,PCRH= increase cortisol + PGH) to achieve this state (attacks beta islets)

risk factors:
-50% will develop T2D 10-15yrs post-partum
-indian/ southeast asian background
-family history diabetes
-BMI 30+ (obesity)
-age 35+
-has PCOS
-previous macrosomic bby
-glycosuria (glucose in urine)
-large for gestational age in current pregnancy

complications:
-preeclampsia
-fetal hyperinsulinaemia
-developing T2D
-large bby weight (macrosomia)
-polyhydramnios (excess amniotic fluid)

management:
-IV insulin
-lose weight (of overweight)
- diet + exercise
- monitor blood glucose
- Metformin and glyburide (sulfonylureas) can be used instead of IV insulin but with immense care/ not recommended as these oral drugs become concentrated in the fetus!

consequences for fetus:
-Macrosomia: birth trauma risk (Erb’s palsy, fetal asphyxia,shoulder dystocia)
- Neonatal Hypoglycemia: Occurs post-delivery due to abrupt removal of maternal glucose supply but persistent fetal hyperinsulinemia.
- Respiratory Distress Syndrome: Delayed lung maturation in poorly controlled GDM.
- Congenital Abnormalities: Slightly higher risk if GDM was unrecognized early in pregnancy.
- Stillbirth: Rare but increased risk in poorly controlled cases.

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18
Q

if the mother uses one of these drugs whil pregnant, what affect can they have on birth weight;

-metformin
-glyburide (sulfonylureas)

A

METFORMIN= decreases birth weight of baby
GLYBURIDE= increases birth weight of baby

19
Q

what is oligohydramnios vs polyhydramnios and how is it defined clinically

A

oligohydramnios (11% pregnancies)= low amniotic fluid (less than 300ml in 3rd trimester= can be caused by amniotic fluid leak or fetal kidney abnormalities= can cause Potter facies (bby becomes squashed but it will reverse after a couple days born) if early stage
treat: (if its a tear it heals and the fluid will increase again), drink lots of water, rest, amnioinfusion, depends on cause.

polyhydramnios (1+ pregnancies)= excess amniotic fluid (greater than 2000ml at any period of gestation), caused by fetal GI, kidney abnormalities, GDM, T2D
treatment: drain fluid + give indomethacin (reduces fluid production)

20
Q

what is Potter facies/ Potter syndrome?

A

Potter facies is characterized by prominent epicanthic folds, low set ears, flattened nose due to uterine pressure, and recessed chin.

On physical examination, infants have characteristics facies, defects in lower extremities, and genital tracts.

other characteristics:
Limb anomalies (abnormal positioning, hip dislocation, short lower limb, clubbed feet), absent anal opening, hemivertebrae, and sacral agenesis are the common skeletal deformities.

Stage of fetal lung development, degree, and duration of oligohydramnios determine the extent of pulmonary hypoplasia.

21
Q

what kind of anaemia do pregnant women get?

A

dilutional anaemia (ak physiological anaemia of pregnancy)

most women get this as plasma volume increases at a faster rate than haemoglobin volume

iron-deficiency anaemia (90% cases in 3rd trimester) this can cause lots of bleeding from mother at time of delivery; so fetus is draining mother of iron in 3rd trimester

n.b. hepcidin goes up in the 1st trimester and blocks ferroportin meaning she ma

treatment:
oral iron tablets or syrup, iron infusion, blood transfusion

22
Q

explain simply the role of hepcidin, ferroporton in the production of haemoglobin (Hb)

A

Ferroportin: (iron gatekeeper)
- protein found on the surface of cells that store or absorb iron.
- Acts like a “gate” that lets iron out of these cells into the bloodstream.

Hepcidin (iron regulator)
-produced by liver
-controls how much iron released into blood
-when hepcidin levels high= blocks ferroportin= decreases blood iron levels
-when hepcidin levels low= allows ferroportin to work (open gate)= increases blood iron levels

23
Q

How does cytomegalovirus effect baby?

A

prevelance : 0.7% live births (13% of those symptomatic at birth)

  • primary infection more likely to cause congenital CMV

symptoms in bby:
-sensorineural hearing loss 1st 5-7yrs
-75% bbies with symptomatic CMV develop hearing loss

24
Q

how does toxoplamosis effect baby? What are the risk factors of catching toxoplasmosis and what causative agent causes it.

A

causative agent= toxoplasma gondii

natural hosts: cats

risk factors; cat ownership (0.7), gardening (2), eating raw meat (2.6), eating cured meat (2.9)

infection is commonly asymptomatic; but symptoms include fever and lymphadenopathy. 40% adults are IgG positive tho

if woman is newly infected she can pass to bby (if she had before preg she n bby protected)

clinical features in b by:
choriorentitis (inflammation of the choroid and retina), hydrocephalus, intracranial atherosclerosis

25
Q

how does HSV effect baby?

A
26
Q

how does influenza effect mother, but not baby?

A
27
Q

UTIs are more common in pregnancy. How does this affect mother and baby. What is the treatment?

A

causative organisms; e.coli, p.mirabilis, k.pneumonae

must treat asymptomatic women too

maternal complications:
-pyelonephritis (kidney infection)

fetal complications;
-preterm labour
-growth restriction

treatment;
-penicillin’s
-cephalosporins
-nitrofurantoin

28
Q

Explain the stages of syphilis and if left untreated what risk it poses to baby (if mother with syphilis pregnant)

A

bacterial infection caused by: treponema pallidum (spirochete)

-50% risk of congenital syphilis

earlier the disease stage the worse the prognosis= associated w miscarriage, still birth and premturity

primary; chancre (SHANG-kur) first lil spore that is painless and indicates syphilis

secondary; rash

tertiary; GPI, tabes dorsalis (effects spinal cord; sensory loss) , neurosyphilis (affects brain + therefore spinal; motor loss/mixed deficits)

29
Q
A
30
Q

what does rubella (german measles) cause to bby

A

n.b. no cases of rubella in uk since 2019 so we no longer screen

  • rubella effects eye development in babies; heart defects, low birth weight, glaucoma, cataracts

outside pregnancy; rubella causes rash, lymphadenopathy (swollen lymph nodes), arthralgia (joint pain without visible inflammation)

31
Q

what is hyperemesis gravidarum?

A

Hyperemesis gravidarum is extreme morning sickness and causes you to vomit several times per day during pregnancy. In severe cases, it leads to dehydration and may cause premature birth

32
Q

Define the following:
-antepartum, intrapartum, postpartum

-define the 1st, 2nd and 3rd trimester

A

antepartum= early (before 24wks) late (after 24wks)

intrapartum= in labour (1st + 2nd stages)

postpartum= from delivery of fetus till 6wks later

1st trimester= 0-12 wks

2nd trimester= 13-27

3rd trimester= 28- chilbirth (40wks)

33
Q

Explain the function/role of hormones produced by the placenta and where they’re made

A

hCG: Maintains corpus luteum for progesterone production; supports fetal gonads; modulates immunity. Produced by the syncytiotrophoblast of the placenta.

Progesterone: Maintains uterine lining; prevents contractions; modulates immune response; supports lactation. Initially by the corpus luteum, later by the syncytiotrophoblast (8–10 weeks onward).

Estrogens (e.g., Estriol): Promotes uterine growth, placental blood flow, mammary gland development, and fetal growth. Formed in the syncytiotrophoblast from androgens (DHEAS) supplied by fetal adrenal glands.

hPL (Human placental lactogeb) / (aka Human Chorionic Somatomammotropin hCS) : Alters maternal metabolism for fetal energy needs; stimulates mammary glands for lactation. Secreted by the syncytiotrophoblast.

CRH (Corticotropin-Releasing Hormone) : Regulates fetal cortisol for lung maturation; influences labor timing; increases maternal cortisol. Produced by the syncytiotrophoblast, with levels rising toward term.

Relaxin: Softens pelvic ligaments and cervix; maintains uterine quiescence for childbirth. Primarily secreted by the corpus luteum; minor contribution from placenta.

Kisspeptin: Regulates puberty and reproduction (via GnRH); suppresses tumor spread. Central: Hypothalamus (ARC and AVPV); Peripheral: Placenta, pancreas, liver, small intestine.

34
Q

define infertility/ sterility and subfertility. Explain the difference between primary and secondary infertility.

A

infertility is when someone is unable to conceive, even with medical interventions

primary infertility= couple have never been able to conceive

secondary infertility= couples who, had a baby(/babies) without any difficulty, but cannot get pregnant again or had a miscarriage or ectopic pregnancy

subfertility is delayed/reduced capacity to conceive/ ‘the failure to achieve clinical pregnancy after 12 months or more of regular unprotected sex’

subfertiliy= when someone ca n conceive with medical intervention

1 in 7 couples in UK have fertility problems

35
Q

There are 4 classifications for infertility/subfertility in females. Explain each.

A

1) hypothalamic
-hypothalamic amenorrhea
-anorexia nervosa (decreased weight+ increased exercise= decrease leptin= leptin stims GnRH release. Consider pulsatile GnRH to induce ovulation

2) pituitary
-hyperprolactinaemia (decreases LH + FSH. Give dopamine agonist to inhibit prolactin which increases LH and FSH level e.g. bromocriptine, cabergoline)

3) ovarian
-premature ovarian failure (primary ovarian insufficiency) if under 40 yrs of age; consider donor eggs or alternative parenting options

4) polycystic ovary syndrome (PCOS) (very common endocrine disorder)

36
Q

What is Polycystic ovary syndrome (PCOS) ; explain Rotterdam criteria for diagnosis + pathophysiology of disease

A
  • 33% prevalence in UK
  • numerous small cysts (fluid-filled sacs form in the ovaries
    -linked to diabetes
    -easily diagnosed with ultrasound as well as you can see cysts on ovaries
    -insulin resistance, high BMI

Rotterdam criteria (2 out of 3 of these gives PCOS diagnosis):
1) Hyperandrogenism (increased levels of male hormones) = hirsutism (excess body hair), acne
2) Oligomenorrhoea (<6-9 menses/year)= anovulation (absence of ovulation) or oligovulation (infrequent ovulation)
3)Polycystic ovaries on ultrasound (12+ follicles larger than 9mm)

pathophysiology of PCOS:
- increase in anti-mullerian growth factor (AMH)
- insulin resistance and obesity causes higher androgen levels
-LH hypersecretion due to increased pituitary sensitivity to GnRH
- increase LH, normal FSH= increased free testosterone
- increase angrogen: exclude congenital adrenal hyperplasia (CAH), hyperprolactinaemia, androgen-secreting tumours
- thyroid disorders are more common

37
Q

what are fibroids?

A

fibroids are non-cancerous smooth muscle growths of uterus= leiomyoma

v common 60% of women have them

only cause infertility if they are very large

more common in black women

-surgery can remove fibroids and restore fertility

38
Q

how many miscarriages does a patient need to have to be diagnosed with fetal loss syndrome/ fetal wastage syndrome

A

fetal loss syndrome/ fetal wastage syndrome= more than 3 miscarriages

prevalence is 1% of population

39
Q

which prostaglandin causes contractions of uterus to deliver baby?

A

prostaglandin E2 causes contractions of uterus to deliver baby

40
Q

what is the medical term for undescended testes

A

cryptorchidism

41
Q

what is clomiphene citrate drug used for?

A

Clomiphene citrate is used to induce ovulation (egg production) in women who do not produce ova (eggs) but wish to become pregnant (infertility).

Clomiphene citrate is:
-non-steroidal antagonist at hypothalamic oestrogen receptors
-first line treatment for PCOS
-binds to oestradiol (E2) receptor in hypothalamus
-inhibits E2 negative feedback and activate GnRH secretion, correct the imbalance levels of FSH + LH
-start dose 50mg/day for 5 days during folicular phase; if ovulation doesn’t occur dose is increased

side effects; multiple gestation (mainly twins) + ectopic pregnancy

42
Q

what is a gonadotrophin hormone?

A

any of a group of hormones secreted by the pituitary which stimulate the activity of the gonads.

43
Q

what medications can effect semen; explain how?

A
  • alpha-1 receptor blockers effect transport of spermatozoa because the transport of spermatozoa from the epididymis to the urethra depends on the activation of alpha-1 receptors in smooth muscle cells in the vas deferens

-SSRIs can inhibit vas deferens motility and accessory sex gland emptying

-anabolic steroids mimic testosterone, leading to feedback inhibition of the hypothalamus + pituitary. This suppresses the release of GnRH, LH and FSH.
N.B. FSH + LH stimulate testes to produce sperm= suppression of them leads to decrease in spermatogenesis= low sperm count (oligospermia) or absence of sperm (azoospermia)

the use of anabolic steroids is called androgen abuse as anabolic-androgenic steroids are synthetic derivatives of testosterone

44
Q

what is mumps related orchitis?

A

orchitis= refers to infection or swelling and irritation, called inflammation, of one or both testicles.

Mumps-related orchitis is a condition where the testicles become inflamed due to a viral infection caused by the mumps virus. Orchitis is a recognized complication of mumps, particularly in post-pubertal males.

Cause: The mumps virus, which primarily affects the parotid glands (salivary glands), can spread to other parts of the body, including the testes.
Age group affected: Most common in males who contract mumps after puberty, though it can theoretically occur at any age.

Symptoms:
Pain and swelling: In one or both testicles.
Fever and malaise: Often associated with the systemic effects of mumps.
Tenderness: The testicles may become very sensitive to touch.
Erythema (redness): Overlying the scrotum.
Nausea or vomiting: As a systemic response to the infection.

45
Q

infertility can be caused by MTHFR mutation, explain why ?

A

A gene mutation C677T in methylene tetrahydrofolate reductase (MTHFR) means body does not convert folic acid to folate. Folate deficiency causes fertility problems in men and women

Impact of Deficiency in Men: Folate deficiency can lead to decreased sperm count and motility, as well as increased DNA fragmentation in sperm, reducing fertility.

Impact of Deficiency in Women: Inadequate folate levels can impair egg quality and disrupt ovulation, making conception more difficult.

46
Q

what is the anatomical landmark for pudendal nerve block

A

the anatomical landmark for pudendal nerve block is ischial spine