Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

VSCI200 NSF > export_endocrinology > Flashcards

export_endocrinology Flashcards

1
Q

What factors stimulate insulin secretion?

A
  • plasma aa
  • GI hormones (CCK, gastrin etc) feed forward effect
  • psymp activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What % of insulin secretion is due to ‘feed forward;’effect

A

80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Name 4 catabolc hormones

A
  1. glucagon
  2. GH
  3. cortisol
  4. catecholamines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What effect does insulin have?

A

increased:

  • glucose oxidation
  • lipogenesis
  • glycogensis
  • protein synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does glucagon do?

A

Increases:

  • gluconeogenesis
  • glycogenolysis
  • ketogenesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What glucose transporter is req in skeletal muscle?

A

GLUT 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is adipocytes response to insulin?

A

insert GLUT4 trans into membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is glucose transformed to in the cell?

A

G-6-P
Glycogen
Fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What glucose transporter ispresent in the liver?

A

GLUT 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what does insulin stimulate in the hepatocyte?

A

hexokinase which converts –> G6P

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why is constant blood glucose vital for neurone?

A

they cannot regulate amount of glucose in CSF and the transport of glucose in/out is steady.

If CSF = plasma and glucose v high - dehydrate; if v low - starve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Are neurones sensitive to insulin?

A

NO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What efect does insulin have on K+?

A

inc K+ uptake into cells by providing ATP. It activates NaKATPase pump

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What type of insulin is identical to dogs?

A

Pigs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is cow insulin similar to?

A

Cats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does insuln react with cells?

A

Binds to tyrosine kinase receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Where is insulin metabolised?

A

Liver and kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Which species often metabolises insulin fastest?

A

cats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is crystalline zinc insulin?

A

recomb DNA
phosphate buffer
VERY RAPID ACTION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is lente insulin?

A

insoluble - in acetate

No protamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What type of insulin is found in canisulin

A

Lente insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the purpose of protamine zinc insulin?

A

Slow absorption and action. Large zinc crystals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is insulin glargine?

A

v large precipitate. human. pos in cats.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

From fastest to slowest name insulin formulations

A
  1. soluble
  2. semilente
  3. isophane
  4. lente
  5. protamine zinc
  6. glargine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What lifestyle factor need careful control in diabetic patients?

A

diet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

State 2 pos adverse effects of insulin tx?

A
  1. hypoglycaemia
  2. insulin resistance
    - antibodies attack exo insulin
    - stress response (inc cortisol etc)
    - receptor desensitisation/down-reg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Tx for OD of insulin?

A

feed
IV glucose
glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is Glipizide?

A

stim insulin secretion. Pos OD –> hypoglycaemia BUT less severe than insulin OD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is Metformin?

A

decrease glucose absorption in GIT and dec liver glucose output and increase receptor sensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How does glucose stimulate B-cells to secrete insulin?

A
  1. glucose uptake by GLUT2
  2. ATP prod
  3. BLOCK K+ channels which depol vgated Ca++
  4. Ca++ influx
  5. Insulin released
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is an insulinoma?

A

functional tumour, over-prod insulin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Name a drug t treat hypERinsulinism

A

DIAZOXIDE

- activate K+channels and therefore Ca++ channels = no insulin!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Why is a clinical sign of diabetes 1PU/2PD?

A

++b glucose –> renal threshold. osmotic diuresis and glucose lost in urine (glycosuria).

  • ## thirst centre, ADH etc..
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What other effect can the loss of glucose in urine casue?

A

bdown of fat and protein –> ketone bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the Kreb cycle?

A

acetyl coA, product of FA and glucose catabolism is recyled and ATP made.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How are ketones formed?

A

XS acetyl coA.

if other parts of Kreb cycle are used for glucose production (oxaloacetate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the main contributor of acetyl coA in starvation?

A

B-oxidation of Fats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Which type of thyroid hormone is most active?

A

T3 (free)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Name 5 functions of Thyroid hormones?

A
  1. Stim GH secretions
  2. Inc BMR
  3. CV stim
  4. Inc CHO use/lipolysis
  5. Inc milk prod
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the signs of hypOthyroidism?

A
  • Kg-gain, same appetite
  • cold
  • excercise intol
  • alopecia (hair growth phase NOT activated)
  • bradycardia
  • dullness
  • inc cholesterol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What % of T3 is from T4 metab?

A

80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What parameters can be measured to detect thyroid disease?

A
  • FT3/ 4 or TT3/4 4 is prefered
  • endo TSH
  • TSH stim
  • Thyroglobulin Ab
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Describe the TSH stim test?

A

basal T4, inj TSH and repeat. Normal = 1.5x increase in T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What causes sick euthyroid syndrome

A

concurrent illness, supressing T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What type of TH is Levothyroxine?

A

T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What type of TH is Liothyronine?

A

T3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

During starvation (etc)how is T4 preserved/inactivated?

A

de-iodinated to rT3

48
Q

Where is T4 converted to T3/rT3?

A

liver, muscle and kidney

49
Q

What is the significance of amount of TBG and pharmocokinetics?

A

++ TBG = long half-life

50
Q

Which has the lowest conc of TBG, cats or dogs?

A

Cats

51
Q

Name signs of HypERthyroid?

A
  • inc appetite but kg-loss
  • tachycardia
  • excitable/difficult to handle!
52
Q

Name 2 ways for testing for hypERthyroidism?

A
  1. TT4 levels

2. T3 suppression

53
Q

Desc the T3 supression test

A

record basal TT4
oral T3, 3d

normal = 50%+ dec in T4

54
Q

What is the main 2 anti-thyroid agents?

A

Methimazole

radioactive Iodide

55
Q

What is the role of Methimazole?

A
  • inhibit synth of T3/4
  • metab by liver p450 & conjugation w/ GLUCORONIDE (not in cats!)
  • affects of ++TH will mask renal failure, Tx may ‘unmask’ it
56
Q

HOw does Radioactive I work?

A

iodine vital in T3/4 synth; will destroy rI containing cells. Alt to thyroidectomy.
radioactive for 3wks

57
Q

What is the consequence of low dietary iodine?

A

Cant make TH

TSH remains high, stimulating follicular growth! No ned fb = goitre.

58
Q

What can prevent iodine uptake?

A

Brassicas

59
Q

Decsribe the HPA axis

A
  • Higher centers stim hypothalamic neurones to release ACTHRH
  • hormone travels through 2 x cap beds ( portal system)
  • endocrine cells release ACTH from ant pit
  • Adrenal G releases g-cort or androgens
  • long and short loop neg fb from cortex and ant pit
60
Q

Name the layers of the adrenal cortex

A
  1. zona glomerulosa (m-cort)
  2. zone fasiculata (g-cort)
  3. zona reticularis (androgen)
61
Q

What percentage of the adrenal gland = cortex?

A

90%

62
Q

What is the base structure of steroids?

A

cholesterol

63
Q

What part of steroid synthesis does ACTH act on?

A
  • rate limiting step (chol –> pregnenolone )

* only stimulates production of g-cort and androgens!

64
Q

Desc the mech of action of g-corticoids

A
  • inc mRNA synth of R and enzymes needed in gluconeogenesis.
  • dec synth of cytokines and Rs
65
Q

Desc regulation of aldosterone release

A
  • dec BP –> RAAS
  • inc in K+
  • ad cortex prod aldosterone
  • Principle cells (coll duct)
  • inc Na+ reabs and K+ secretion
66
Q

What is the significance of cortisol fluctuation and circadian variation in animals?

A

SMALL

67
Q

What is the main stimulus for CRH?

A

Stress:
- infection

  • trauma
68
Q

Signs of hypERadrenocorticism

A
    • hyperglycaemia
    • 1PU/2PD
    • DI
    • skin pigment
    • cachexia
    • pot belly
69
Q

Why is skin pigment changes seen in hypERadrenocorticism?

A

Synth of ACTH from ACTHRH makes POMC. in other tissues POMC makes MSH which inc melanin prod and skin darkening

70
Q

Decs the stress leukogram

A

neutrophilia
lymphocytopenia

eosinopenia

71
Q

HyperAC can be iatrogenic or spontaneous. Name the 2 forms of spontaneous HyperAC?

A
  1. pit-dependant hyperAC

2. adrenal-dependant hyperAC

72
Q

Descr PDH?

A

pit tumour = inc ACTH –> inc cortisol

73
Q

Descr adreno-hyperAC

A

adrenal tumour = inc cortisol and therefore LOW ACTH (due to neg fback)

74
Q

What is hyper-AC known as?

A

cushings

75
Q

what is hypoAC known as?

A

addisons

76
Q

What is primary hypoAC

A

atrophy(?) or ad cortex
defic in mineral and gluco-corticoids

ACTH +++

mineralo defic signs (acute)!

77
Q

What is 2rd hypoAC

A

ACTH defic
impaire g-cort secretion

will LEAD to atrophy

mineralo- usually not affected!

78
Q

Name 4 diag tests for AC disease

A
  1. ACTH stim
  2. ACTH endo measure
  3. Dexamethazone supression test
  4. urine cortisol measure (cort:creatinine)
79
Q

Desc the ACTH stim test

A
  • take basal cortisol, inj with ACTH
  • cortisol (3om) after
  • normal = compare to chart, should be normal stimulation

hypER (higher) and hypO (lower)

80
Q

descr the dexamethazone test

A

basal cortisol, inj dex, new cortisol (5hrs)

suppression should be clear

81
Q

steroids can be mineralocorticoid-like or g-corticoid-like. And this gives then 2 main properties, name them

A

anti-inflam AND/OR Na+ retaining

82
Q

Name a short acting steroid with equal anti-inflam and Na+ retaining prop

A

Hydrocortisone and cortisone

83
Q

Why is Fludrocortisone inportant?

A

Only pharm steroid which has ++++ Na+ retaining prop

mineralocorticoid effects

84
Q

How long is T1/2 to be classed as intermediate acting?

A

12-36hrs

85
Q

What is interesting about the properties of the long acting steroids?

A

ONLY has g-corticoid effects, but VV+++ strong!

86
Q

Why should steroid be withdrawn slowly?

A

exog cortisol suppresses pit prod of ACTH = when exo removed, no endo replaces

87
Q

Adverse effects of long-term c-steroid

A

poor healing
myopathy

osteoporosis

oedema

laminitis

abortion

88
Q

Name 2 adrenal steroid inhib

A
  1. Mitotane

2. Trilostane

89
Q

Descr the function of mitotane

A

cytotox to z. fasic and z. retic NOT z. glom!

90
Q

What are the main side effects of mitotane?

A

long T1/2
hypo AC

V+D

= req supplementary steroids to balance!

91
Q

What is the mech of action of Trilostane?

A
  • steroid analogue

* inhib of enzyme involved in corticosteroid synth

92
Q

Why is Trilostane CI in preg animals?

A

inhib prog synth..

93
Q

What type of calcium in metab active?

A

ionised ca++

94
Q

What makes up serum calcium, as measured?

A

ionised and p-bound

95
Q

What are the effects of inc PTH?

A
  • inc osteoclastic activity
  • inc absorption (vitd3)
  • inc renal reabs
96
Q

How does VitD3 inc Ca++ absorption?

A
  • 2 x hydroxylations (liv, kid)
  • inc Ca++ binding protein synthesis
  • t.f inc transport
97
Q

What is the other name for Vit D3?

A

Calcitriol

98
Q

Name 2 other forms of Vit D used pharmacologically

A
  • Di-hydrotachysterol (DHT) - VitD2 analogue

* Alfacalcidol - active D3 metabolite; 1 x hydroxyl only however

99
Q

What are the effects of calcitonin?

A

dec free Ca++; less important, dec osteoclasts

100
Q

What are the effects of PTH on PO4 levels?

A

inc renal excretion

101
Q

What are the effects of Vit D3 on PO4?

A

Same as on Ca++

102
Q

What are the effects of g-corticoids on Ca++ metab?

A

Inc free Ca++ and inc osteoclasts

103
Q

Sex steroid protect against _____

A

osteoporosis

104
Q

How does Prolactin try and prevent parturient hypocalcaemia?

A

prolactin released at part –> milk prod
it stim Vit D3 synth

Vit D3 in Ca++ (free)

105
Q

Name the 5 different calcium salt formulations

A

calcium. .
1. gluconate

  1. carbonate
  2. chloride
  3. lactate
  4. borogluconate
106
Q

What are the drawbacks of oral calcium admin?

A
  • fibre and phytases interfer with absorption

- Vitd3, PTH and

107
Q

hwat is best treatment of a ‘downer cow’, with hypocalc

A

IV admin of calcium gluconate. Jug of milk v

108
Q

Supplementation with Vit D3 and diet high in Ca++, is advised. What are Vit D adverse effects?

A

narrow Therap index
hypercalc

hyper phosph

nephrocalcinosis

109
Q

Why would half life of Vit D3 be reduced in renal disease?

A

reduced vit d3 binding globulin

110
Q

What cells detect need for EPO?

A

renal interstitial cells’ oxygen sensors

111
Q

What disease state would anti-diuretics be for?

A

Diabetes insipidus

112
Q

Why is desmopressin preferntial than vasopressin?

A

long DOA

no vaso-con effects

113
Q

What are the actions of desmopressin?

A

binds and stim ADH receptors in coll duct

114
Q

What is IGF-1

A

insulin like growth factor -1

115
Q

What is unusual with release of GH?

A

regulated by a GHRH (releasing) and GHIH (inhibition)

116
Q

What does IGF-1 do?

A

mediates action of GH in most tissues. Prod in liver.

117
Q

Can GH deficits be treated?

A

no canine GH avail; bov/porcine only. a-bod will develop

VSCI200 NSF (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions