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PPD > SEM4 > Flashcards

SEM4 Flashcards

1
Q

Magnocellular (large) neurosecretory cells

A

release oxytocin + vasopressin

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2
Q

Parvicellular (small) neurosecretory cells

A

Hormone secretions transported via portal veins to anterior pituitary gland

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3
Q

Outer glomerulosa:

A

Produces mineralocorticoids, such as aldosterone (controls salt and water balance)

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4
Q

Middle fasiculata:

A

Produces glucocorticoids, such as cortisol (regulates metabolic and anti-inflammatory actions)

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5
Q

Inner reticularis:

A

Produces androgens, such as DHEA (contributes to gonadal steroid secretions)

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6
Q

ANP

A

increases Na+ and water excretion from kidneys

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7
Q

Androgen antagonists

A

Cyproterone, cetrorelix, ganirelix, danazol, flutamide

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8
Q

GnRH analogues

A

Gonadorelin, buserelin, goserelin

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9
Q

Capacitation:

A

Biochemical alteration of sperm plasma membrane, initiates hyperactivated motility (occurs in presence of uterine/uterine tube fluid)

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10
Q

Primary binding:

A

Sperm penetrates cumulus cell layer + sperm head binds to ZP

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11
Q

Acrosome reaction is initiated:

A

outer acrosomal membrane fuses with plasma membrane of sperm head, forming pores through which hydrolytic enzymes are released

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12
Q

Secondary binding:

A

inner acrosomal membrane binds to ZP, causing proteolysis + formation of a slit

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13
Q

Fusion:

A

sperm fuses with egg’s plasma membrane

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14
Q

Activation and fertilisation:

A

sperm head taken up into egg cytoplasm by a process similar to phagocytosis

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15
Q

why formation of a slit?

A

allows sperm to pass into perivitelline space + hyperactivated motility generates forward thrust necessary to penetrate ZP

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16
Q

Hyperthyroidism

A 
weight loss, tachycardia, irritability, tiredness
audible bruit 
diffuse goitre 
low [TSH]serum 
high thyroid hormones
17
Q

why audible bruit in hyperthyroidism?

A

from increased blood flow of gland

18
Q

why diffuse goitre in hyperthyroidism?

A

from excessive TSH stimulation causing increased growth

19
Q

Grave’s disease

A

1° hyperthyroidism from activating autoantibodies to TSH receptor

20
Q

Hypothyroidism

A

lack growth + development

lethargy + cold

21
Q

Hashimoto’s

A

1° hypothyroidism
low thyroid hormones
high TSH
goitre

22
Q

2° hypothyroidism

A

low TSH + T4

23
Q

why high TSH in 1° hypothyroidism

A

circulating autoantibodies have destroyed thyroid gland, affecting iodine uptake

24
Q

why goitre in 1° hypothyroidism

A

from diffuse lymphocytic infiltration + TSH stimulated growth of surviving tissue

25
Q

Insulin release

A
  • glucose diffuses into β-pancreatic cells
  • increase [ATP]
  • closes K+ channel
  • K+ cannot leave
  • depolarisation
  • opens VDCC
  • Ca2+ enter cell
  • exocytosis of insulin

PPD (8 decks)

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