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Year 1 (PCS & Cases 1-6) > Case 2 > Flashcards

Case 2 Flashcards

1
Q

What does the presence of Leukocytes in the urine indicate?

A

UTI

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2
Q

What does the presence of Nitrites in the urine indicate?

A

Infection.

Bacteria convert nitrates to nitrites indicating infection.

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3
Q

What does the presence of H+ ions in the urine indicate?

A

Kidney stones

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4
Q

What does the presence of Glucose in the urine indicate?

A

Diabetes

Pregnancy

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5
Q

What does the presence of Ketones in the urine indicate?

A

Excess breakdown of fats. Could be due to starvation or fasting.

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6
Q

What day is ovulation in the menstrual cycle and what hormone causes it?

A

Day 14

Surge in LH (stimulated by high levels of oestrogen)

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7
Q

At what stage of development is an egg in during ovulation?

A

Secondary oocyte (passed puberty but not at fertilisation yet where it would turn into an ovum)

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8
Q

What are hormone levels of oestrogen, FSH and LH in a post-menopausal women?

A

Low oestrogen so no negative feedback therefore … High FSH & LH.

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9
Q

What is the difference between

Gonadotrophin Independent precocious puberty vs. Gonadotrophin dependent precocious puberty?

A

Early onset puberty without / with gonadotrophin influence

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10
Q

What part of the ANS is responsible for producing an erection?

A

Parasympathetic.

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11
Q

What part of the ANS is responsible for producing an ejaculation?

A

Sympathetic

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12
Q

Which part of the prostate does Benign Prostatic Hyperplasia (BPH) most affect?

A

Transitional zone as it surrounds the urethra.

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13
Q

What is the pectinate / dentate line?

A

When the epithelia in the rectum changes from simple columnar to stratified squamous.

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14
Q

Hepatitis D can occur only in the presence of the which viral infection?

A

Hepatitis B

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15
Q

What form of male gamete is found in the basal compartment of the seminiferous tubules?

A

Spermatogonia

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16
Q

Fill in :)

Cholesterol –> ____ –> progesterone –> ____ –> oestrogen.

A

Cholesterol, pregnenalone, progesterone, androstenedione, oestrogen

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17
Q

What are the features of Klinefelter’s sydrome?

Type of puberty?

A

Tall, small testes, gynaecomastia (man boobs!!)

Hypergonadotrophic hypogonadism (delayed puberty)

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18
Q

What is Prader-Willi Syndrome?

Features of the condition?

A

A genetic condition (genetic defect on chromosome number 15) resulting in _hypo_gonadotrophic hypogonadism.

Recognised by:

absence of puberty

insatiable appetite

short stature

reduced muscle tone (hypotonia)

learning difficulties

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19
Q

What is Congenital leptin deficiency?

A

A congenital lack of leptin caused by mutations in the LEP gene resulting in _hypo_gonadotropic hypogonadism.

Recognised by:

absence of puberty

insatiable appetite - can result in severe obesity

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20
Q

What is Turner Syndrome?

A

Genetic condition that only affects females.

It is caused by an abnormal sex chromosome. A female with Turner syndrome has part or all of one X chromosome missing.

Recognised by:

short stature

infertility / delayed puberty

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21
Q

What is McCune-Albright syndrome?

A

Gonadotrophin-independent precocious (early onset) puberty

Recognised by:

deformity of the legs, arms

skull pigment patches on the skin

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22
Q

Name the three forms of delayed puberty.

A
  1. Constitutional delay (nothing pathophysiologically wrong)
  2. HYPOgonadotrophic hypogonadism (deficiency in GnRH)
  3. HYPERgonadotrophic hypogonadism (elevated levels of GnRH)
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23
Q

Name two syndromes that are classed as Hypogonadotrophic hypogonadism.

(delayed puberty)

A
  1. Kallmann syndrome
  2. Prader-Willi syndrome
24
Q

Give an example of Gonadotrophin-independent preccocious puberty.

A

McCune-Albright syndrome.

25
Q

How would you treat premature thelarche and adrenarche?

A

No treatment

26
Q

How would you treat secondary preccocious puberty?

A

Treat underlying condition e.g. cerebral tumour.

27
Q

How would you treat gonadotrophin dependent preccocious puberty?

A

LHRH analogue

28
Q

How would you treat gonadotrophin independent preccocious puberty?

A
  1. anti-androgen
  2. acromatase inhibitor
  3. steroid biosynthesis inhibitor
29
Q

Papillomavirus infections can progress into Cervical Intraepithelial Neoplasia (CIN) which is an abnormal and potentially malignant change to the epithelium.

How would you identfy a high grade from a low grade case of CIN through the microscope?

A

HIGH grade:

basal cells are confined to the upper 2/3 of the cells.

LOW grade:

basal cells are confined to the lower 1/3 of the cells.

30
Q

How does the protein synthesis inhibitor Tetracycline work?

A

Binds to 30S (small) subunit.

Prevents aminoacyl-tRNA from binding to the ribosome.

31
Q

How does the protein synthesis inhibitor Erythromycin work?

A

Binds to the 50S (large) subunit.

Inhibits translocation (ribosome can’t move along the mRNA)

32
Q

How does the protein synthesis inhibitor Chloramphenicol work?

A

Inhibits the peptidyl transferase reaction.

Prevents peptide bond formation between amino acids.

33
Q

How does the protein synthesis inhibitor Aminoglycoside work?

A

Binds to the 30S (small) subunit.

Distorts its structure so it interferes with protein synthesis.

The cause the ribosome to misread the codon –> non functional proteins are produced.

34
Q

Go through the steps of oogenesis.

A
  1. oogonia (formed before birth) undergo mitosis to become primary oocytes.
  2. primary oocytes begin meiosis but are arrested in prophase 1 until puberty.
  3. at puberty, primary oocyte completes meiosis 1 to form a haploid secondary oocyte (& polar body).
  4. secondary oocyte is arrested in metaphase 2 of meiosis 2 until the graffian follicle bursts at ovulation.
  5. secondary oocyte is released, binds to sperm and an ovum (& polar body) forms.
35
Q

Go through the steps of spermatogenesis and spermeogensis.

A
  1. spermatogonia (germ cells) divide many times by mitosis to produce primary spermatocytes (diploid)
  2. primary spermatocytes underdo meiosis 1 to form secondary spermatocytes (haploid)
  3. secondary spermatocytes undergo meiosis 2 to form spermatids (halpoid)
  4. spermatids differentiate into spermatozoa.

Spermatogenesis is from s.gonia –> sec.sperm.

Spermeogenesis is from (spermatids –> sperm.zoa)

36
Q

Explain the effects of the pill using this diagram. How does it affect the hypothalamus? Cervical Mucus? Endometrial Lining?

A

Boxes 1&2: Oestrogen is inhibiting FSH –> no follicle development.

Progesterone is inhibiting LH –> no ovulation.

Box 3: Progesterone is thickening cervical mucus making it a barrier to sperm.

Box 4: Lining is thinner and less hospitable for sperm / implanation of the embryo.

37
Q

What are the Fraser guidlines?

A

A doctor can give contraceptive advice and treatment on this criteria:

  1. that the girl (although under 16) understands the advice.
  2. she is likely to continue having sex with or without the pill.
  3. unless she recieves the pll, her physical and mental health may suffer.
  4. he is unable to persuade her to inform her parents.
38
Q

What goes through the pudendal canal?

A

Pudendal nerve

Nerve to obturatur internus

Internal pudendal artery

39
Q

What goes through the greater sciatic foramen (above piriformis)?

A

Superior gluteal nerve, artery and vein

40
Q

Name some things that go through the greater sciatic foramen (below piriformis)?

A

Sciatic nerve

Inferior gluteal nerve, artery, vein

41
Q

Name some things that go through the lesser sciatic foramen?

A

Obturator internus muscle tendon

Pudendal nerve and internal pudendal artery (from gluteal region to perineum)

42
Q

Name the layers of the spermatic cord.

A

Skin

Dartos … originates from scarpa’s fascia.

External spermatic fascia… originates from external oblique aponeurosis.

Cremasteric muscle … originates from internal oblique muscle.

Internal spermatic fascia… originates from transversalis fascia.

Tunica vaginalis (parietal layer)

Tunica vaginalis (visceral layer)… both originate from parietal peritoneum.

Tunica albuginea

43
Q

Name two drugs that can be used to treat precoccious puberty.

Name two things that can be used to treat delayed puberty.

A

Aromatase inhibitors and GnRH analogues are used to treat precocious puberty.

  • Ethinyl estradiol* is used to treat delayed puberty in females.
  • Testosterone* is used to treat delayed puberty in males.
44
Q

Give four examples of hypogonadism?

A

Klinefelter’s syndrome (hyper Hypog)

Turner’s syndrome (hyper Hypog)

Kallman’s syndrome (hypO Hypog)

Prader-Wili syndrome (hypO Hypog)

45
Q

What prostaglandin can be given to INDUCE uterine contraction for labour?

What can be given to INDUCE regular myometrial contraction for labour?

A

1. PGE-analogues

e.g. dinoprost / misoprotosol

Used to induce co-oridinated uterine muscle contractions. Given intravginally.

2. OXYTOCIN

Slow IV infusion

This stimulates release of PGF2a.

46
Q

In terms of granulosa and thecal cells, what is the action of FSH and LH

a) before ovulation?
b) after ovulation?

A

a) FSH - on granulosa cells (androgens –> oestrogen via aromatase)

LH - on theca interna cells (androgens)

b) Just before ovulation, FSH induces expression of LH receptors on the granulosa cells (=respond to LH surge) –> CL develops.

Due to the influence of LH, granulosa cells secrete progesterone & theca cells secrete oestrogen.

47
Q

What is the action of mifepristone when there is no endogenous progesterone present i.e. before ovulation?

A

Acts as a progesterone receptor agonist.

Activates progesterone which inhibits FSH or LH =

no ovulation.

**emergency contraception**

48
Q

What is the action of Mifepristone when progesterone is already present i.e. after ovulation / already pregnant?

A

acts as a progesterone receptor antagonist.

Inhibits progesterone receptors - causes:

[1] endometrium to shed

[2] inhospitable environment for embryo

[3] sensitises myometrium to prostaglandins

When used with gemeprost (PGE analogue –> stimulates uterine contraction), it is an **abortifacient**

49
Q

What drug can lead to grey baby syndrome?

A

Chloramphenicol

e.g. a premature baby will have an immature liver which can lead to reduced breakdown of drugs –> toxicity.

50
Q

What is the action of co trimxazole?

A

Trimethoprim/sulfamethoxazole (synergism)

Inhibits folate synthesis.

Folate is an important building block for synthesis of amino acids and nucleotides.

51
Q

Name some drugs that have an inhibitory effect on breakdown of drugs in the liver.

Name a drug that activates the breakdown of drugs in the liver.

A
52
Q

Name some targets that are difficult for drugs

A

CSF

Prostate

Eye

Intracellular bacteria

53
Q

Intracellular bacteria e.g. mycobacteria / chlamydia can be difficult targets for drugs.

What antibiotics are used here and why?

A

e.g. Macrolides (clarithromycin, azithromycin)

They are lipid soluble (polar) –> can get into the cell.

Pencillins* are lipid insoluble so *can’t get into the cell but can be used to break down the cell wall.

54
Q

What is the action of b-lactasmase and what problem does it cause?

How is this problem overcome?

A

It cleaves the B-lactam ring in B-lactam antibiotics e.g. pencillins. Pencillins lose their antimicrobial activity.

Overcome by B-lactamase inhibitors e.g. calvulanic acid which contain a B-lactam ring. They bind to and inactivate the B-lactamase inhibitor :)

55
Q

Name the three main macrolides.

A

Clarithromycin

Azithromycin

Erythromycin

(target 50S - inhibit translocation)

56
Q

A ‘painless ulcer’ is characteristic of which STI?

A

Syphylis (ulcer - in the primary stage)

Treponema pallidum

Year 1 (PCS & Cases 1-6) (13 decks)

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