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BRS/POM MOCKS > BRS MOCK 6 - Ions, rheumatology1, reproductive1 > Flashcards

BRS MOCK 6 - Ions, rheumatology1, reproductive1 Flashcards

1
Q

How are channel proteins different to carrier proteins?

A

Channel proteins transport solute faster than carrier proteins. Carrier proteins have a solute binding site while channel proteins have selective filter in aqueous pore.

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2
Q

What is secondary active transport?

A

Movement of solute against concentration gradient which is driven by another solute moving down an electrochemical gradient.

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3
Q

Key points about facilitated diffusion?

A

Increases the rate at which a substance can flow down its concentration gradient. Requires a channel or carrier protein. Does not require energy.

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4
Q

Why can fructose be transported via facilitated diffusion instead of active transport?

A

Low levels of fructose in enterocyte and plasma. Fructose can diffuse across basolateral membrane of enterocyte down a concentration gradient.

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5
Q

GLUT2 key points?

A

High capacity, low affinity facilitative transporter.

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6
Q

How is water absorbed in the GI tract?

A

Osmotic flow of water through tight junctions into intercellular space due to hypertonic solution present in intercellular space (high concentration of ions).

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7
Q

Where is the greatest amount of water absorbed?

A

Jejunum (small intestine).

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8
Q

What is the main ion that drives water absorption? How does it happen?

A

Na+ is transported from lumen into enterocytes.

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9
Q

How is sodium absorbed in the duodenum?

A

Counter transport in exchange of H+ ions.

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10
Q

How is sodium absorbed in the jejenum?

A

Co-transport with amino acids and monosaccharides.

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11
Q

How is sodium absorbed in the ileum?

A

Secondary active transport. Co-transport with chloride ions.

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12
Q

How is sodium absorbed in colon?

A

Restricted movement through ion channels.

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13
Q

How is chloride absorbed in the colon?

A

Secondary active transport. Exchanged with bicarbonate.

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14
Q

How is potassium absorbed in the small intestine?

A

Diffusion via paracellular junctions.

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15
Q

How is sodium in enterocytes transported into the lateral intercellular spaces?

A

Active transport by Na+K+ATPase in lateral plasma membrane.

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16
Q

How is chloride and bicarbonate in enterocytes transported into lateral intercellular spaces?

A

Diffusion due to electrical potential gradient caused by sodium in lateral intercellular space.

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17
Q

Where is calcium absorbed?

A

Duodenum and ileum.

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18
Q

When is calcium absorption increased?

A

If someone follows a low calcium diet.

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19
Q

How is calcium absorbed into the blood?

A

Via ion channels in paracellular junctions. Via enterocytes.

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20
Q

Explain calcium absorption via enterocytes

A

Calcium enters enterocyte via TRPV6. To prevent calcium intracellular signalling effects, calbindin binds to calcium to inactivate it. Calcium is then excreted on basolateral side via PMCA or sodium calcium exchange transporter.

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21
Q

How does calcitriol upregulate calcium absorption in enterocytes?

A

Alters gene expression and increases transcription of TRPV6 and PMCA. Allowing more calcium to be absorbed into the enterocytes and excreted into the blood. It also increases levels of calbindin.

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22
Q

Key points about PMCA transporter?

A

Plasma membrane Ca2+ATPase. Has high affinity but low capacity for calcium.

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23
Q

Why is the PMCA transporter important?

A

Maintains low intracellular calcium as pumps calcium across basolateral membrane against concentration gradient using ATP. Important as high intracellular calcium can cause unwanted signalling effects within the cell.

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24
Q

Key points about sodium calcium exchanger?

A

Low affinity for calcium but high capacity. Pumps calcium against concentration gradient across basolateral membrane.

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25
Q

What is the best absorbed form of iron?

A

Heme iron.

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26
Q

What transporter allows for absorption of heme iron?

A

Heme carrier protein 1.

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27
Q

What transporter allows for absorption of non heme iron?

A

DMT1 (Divalent metal transporter 1)

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28
Q

Why is ferritin binding to intracellular iron important?

A

Prevents iron from promoting oxidative stress.

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29
Q

What happens to iron that binds to ferritin?

A

Irreversibly bound to ferritin (can’t be unbound). Oxidised to ferric form. Stores iron which is eventually lost by shedding of enterocytes into faeces.

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30
Q

What converts ferric iron to ferrous iron so it can be absorbed by DMT1?

A

Duodenal cytochrome B.

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31
Q

Explain iron absorption

A

Heme iron enters via HCP1 and non heme iron is reduced by duodenal cytochrome B and enters cells via DMT1. Most iron binds to ferritin and excreted into faeces. Some of the iron moves across basolateral side into blood via ferroportin 1 and subsequently oxidized to ferric form by hephaestin and transferred to the carrier protein apotransferrin and travels as transferrin in blood.

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32
Q

What vitamin helps with absorption of non heme iron?

A

Vitamin C (acts as a reducing agent).

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33
Q

Two ways in which heme iron is absorbed?

A

Via HCP1 and receptor mediated endocytosis.

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34
Q

What does hepcidin act on to regulate iron absorption?

A

Suppresses ferroportin function. Less iron absorbed into blood.

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35
Q

What increases ferritin synthesis?

A

Increase iron concentration in cytosol.

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36
Q

Why is haptocorrin important for B12 absorption?

A

B12 is easily denatured by HCL in the stomach. Haptocorrin prevents this by binding to B12.

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37
Q

Where is haptocorrin released from?

A

From salivary glands and stomach.

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38
Q

Explain B12 absorption

A

Haptocorrin binds to B12. Parietal cells in stomach secrete intrinsic factor which binds to B12. B12 intrisic factor complex binds to cubilin receptor and taken up in distal ileum. B12 intrinsic factor complex broken down in enterocyte and b12 binds to transcobalamin II (TCII) where it then crosses basolateral membrane into blood. Taken to liver where TCII is broken down.

39
Q

What transports b12 in the blood once it leaves enterocytes in distal ileum?

A

Transcobalamin II.

40
Q

What oxidises iron before it is transported into the blood?

A

Hephaestin.

41
Q

Two types of secondary joint inflammation?

A

Infection and crystal arthritis.

42
Q

Type of primary joint inflammation?

A

Immune mediated.

43
Q

Example of non sterile inflammation of joint?

A

Infection of joint.

44
Q

Example of sterile inflammation of joint?

A

Crystal arthritis and immune mediated arthritis.

45
Q

Symptoms of septic arthritis?

A

Acute onset. Inflammation symptoms of joint. Monoarthritis. Fever.

46
Q

How do you diagnose septic arthritis?

A

Joint aspiration to get bacteria sample. Gram stain and culture done.

47
Q

Treatment of septic arthritis?

A

Surgical washout and iv antibiotics.

48
Q

Risk factors of septic arthritis?

A

Immunosupressed and IV drug use.

49
Q

What is an exception for septic arthritis that displays different symptoms?

A

Gonococcal septic arthritis causes polyarthritis.

50
Q

What causes gout?

A

Deposition of monosodium urate crystals around joints. This results in inflammation.

51
Q

What is a key risk factor for gout?

A

High uric acid levels.

52
Q

What causes hyperuricemia?

A

Genetic tendency, increase intake of high purine foods and reduced excretion due to kidney failure.

53
Q

What causes pseudogout?

A

Deposition of calcium pyrophosphate dihydrate crystals around joints which results in inflammation.

54
Q

What are the symptoms of gout?

A

Acute onset, monoarthritis and formation of tophi.

55
Q

Gout biomarkers?

A

High CRP and high serum urate.

56
Q

What is a definitive test for crystal arthritis?

A

Synovial fluid analysis.,

57
Q

Shape of gout crystal?

A

Needle shaped.

58
Q

Shape of pseudogout crystal?

A

Brick shaped.

59
Q

Birefringerence test result for gout?

A

Negative.

60
Q

Birefringerence test result for pseudogout?

A

Positive.

61
Q

What may you administer to treat gout?

A

Non steroidal anti inflammatory drugs. Use of glucocorticoids.

62
Q

What may you prescribe to treat chronic gout?

A

Xanthine oxidase inhibitor.

63
Q

Lifestyle changes for chronic gout?

A

Avoid purine rich foods.

64
Q

How does a xanthine oxidase inhibitor help treat chronic gout?

A

Reduces serum urate levels by inhibiting purine metabolism.

65
Q

How are osteoarthritis different to rheumatoid arthritis?

A

Osteoarthritis is a gradual onset. OA worsens with movement. There is joint enlargement in OA but no swelling. RA has morning stiffness.

66
Q

How is OA different on an Xray to rheumatoid arthritis?

A

OA has osteophytes and has subchondral sclerosis (increased whiteness at joint). RA can have osteopenia and bony erosions.

67
Q

What is subchondral sclerosis?

A

Thickening of bone below cartilage surface.

68
Q

How are fallopian tubes adapted?

A

Contain cilia and spiral muscle. Waft egg.

69
Q

What causes endometrium to shed?

A

Vasoconstriction of arteries supplying it due to drop in progesterone.

70
Q

Where is sperm produced in the testes?

A

Seminiferous tubules.

71
Q

What are the two main cells in the seminiferous tubules?

A

Leydig cells (between seminiferous tubules) and sertoli cells.

72
Q

What receptors do sertoli cells contain?

A

FSH receptors.

73
Q

What do sertoli cells do? How do they do it?

A

Support developing germ cells.

  • Assist movement of germ cells to tubular lumen
  • Transfer nutrients from capillaries to developing germ cells
  • Phagocytosis of damaged germ cells
74
Q

What hormones do sertoli cells produce?

A

Inhibin and activin. Anti-mullerian hormone. Androgen binding hormone.

75
Q

What receptors do leydig cells contain?

A

LH receptors.

76
Q

What is the function of leydig cells?

A

Hormone synthesis.

77
Q

What stimulates hormone synthesis in leydig cells?

A

LH binding to leydig cells.

78
Q

What are polar bodies?

A

Cytoplasmic structures shed during meiotic division during oogenesis.

79
Q

When does 2nd meiosis division and differentiation of oocytes occur?

A

After sperm fusion.

80
Q

Describe folliculogenesis?

A

Primordial follicle to primary follicle. Primary follicle contains layers of granulosa and theca cells. Development of secondary follicle; contains fluid filling cavity, FSH and LH receptors. Surge of LH results in development of mature follicle. Follicle ruptures allowing ovum to leave. Formation of corpus luteum which produces progesterone and oestrogen.

81
Q

What is secreted after fertilisation to keep corpus luteum alive?

A

hCG.

82
Q

What does the female hormome relaxin do?

A

Relaxes muscles during pregnancy.

83
Q

What do theca cells do?

A

Provides structural support of growing follicle. Androgen synthesis.

84
Q

What stimulates theca cells?

A

LH stimulates theca cells to produce androgens.

85
Q

What do overactive theca cells result in?

A

High androgen.

86
Q

What occurs in granulosa cells?

A

Aromatisation.

87
Q

What stimulates granulosa cells?

A

FSH.

88
Q

How do granulosa cells regulate FSH?

A

Secretion of inhibin and activin.

89
Q

What occurs to granulosa cells after ovulation?

A

Formation of corpus luteum. Granulosa lutein cells inside the corpus luteum produce the hormone progesterone which maintains the endometrium. They also produce relaxin.

90
Q

What happens to the Hypothalamic-Pituitary-Gonadal (HPG) Axis during ovulation?

A

Switch to positive feedback due to rise in oestrogen.

91
Q

Describe Hypothalamic-Pituitary-Gonadal (HPG) Axis

A

Kisspeptin stimulates GnRH release; this occur in the hypothalamus. GnRH acts on gonadotrophs in anterior pituitary gland to produce LH and FSH. LH and FSH target gonads. Gonads produce oestrogen, progesterone and androgens; inhibit LH/FSH and GnRH release.

92
Q

Explain Hypothalamic-Pituitary-Gonadal (HPG) Axis in hyperprolactinaemia.

A

Prolactin inhibits kisspeptin. Decrease in downstream hormones - GnRH, FSH, LH, Testosterone, oestrogen.

93
Q

Symptoms of hyperprolactinaemia

A

Amenorrhoea, low libido and osteoporosis.

BRS/POM MOCKS (23 decks)

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