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(SG) Phase 2A lectures > endo > Flashcards

endo Flashcards

1
Q

define endocrinology

A

study of hormones (and their gland of origin), their receptors, the intracellular signalling pathways, and their associated disease

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2
Q

what do hormones do?

A

excite

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3
Q

what’s the diff btwn endocrine and exocrine?

A

endocrine (within glands - pour secretion into blood stream)

exocrine (outside glands - pour secretions through a duct to site of action)

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4
Q

name some examples of endocrine glands (2)

A

thyroid

adrenal

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5
Q

where are peptides/monoamines stored?

A

in vesicles

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6
Q

how are steroids synthesised?

A

on demand

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7
Q

list the hormone classes

A

peptides
amines
iodothyronines
cholesterol derivatives and steroids

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8
Q

what are the 3 stages of hormone production

A

preprohormone
prohormone
hormone

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9
Q

what response do amines stimulate?

A

sympathetic NS - fight or flight

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10
Q

where are peptide hormones stored

A

in secretory granules

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11
Q

what % of T3 in the circulation is secreted directly by the thyroid?

A

20%

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12
Q

what are T4/T3 cleaved from

A

thryoglobulin

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13
Q

are thyroid hormones water soluble?

A

no, 99% protein-bound

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14
Q

what does vitD stimulate the production of?

A

mRNA

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15
Q

what type of basal secretion involves hormones?

A

continuously or pulsatile

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16
Q

define synergism

A

combined effects of 2 hormones amplified (eg glucagon with epinephrine)

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17
Q

define antagonism

A

when 1 hormone opposes another (eg glucagon antagonises insulin)

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18
Q

what is hormone receptor down regulation?

A

hormone secreted in large quantities cause down regulation of its targets receptors

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19
Q

what do hypothalamic neurone synthesise?

A

oxytocin

ADH

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20
Q

where’s oxytocin/ADH transported to from the hypothalamus?

A

the posterior pituitary

via the hypothalamic-hypophyseal tract

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21
Q

what is somatostatin aka

A

(GHIH) growth hormone inhibiting hormone

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22
Q

what are the direct actions of GH?

A

metabolic
anti-insulin
(fat/carb metabolism)

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23
Q

what are the indirect actions of GH?

A

growth-promoting (skeletal and extraskeletal)

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24
Q

what kinda effect does thyroid hormone overall have?

A

increases!

food metabolism
protein synthesis
carbohydrate metabolism
fat metabolism
ventilation rate
CO and HR
growth rate
brain development
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25
Q

where are mineralocorticoids produced?

A

zona glomerulosa

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26
Q

where are glucocorticoids produced?

A

zona fasciculata

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27
Q

where are androgens produced?

A

zona reticularis

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28
Q

name a mineralocorticoid

A

aldosterone

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29
Q

name a glucocorticoid

A

cortisol androgens

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30
Q

which cell is FSH produced in?

A

granulosa cell

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31
Q

which cell is LH produced in?

A

theca cell

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32
Q

which hormone is produced in the heart?

A

ANP (atrial natriuretic peptide)

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33
Q

which hormone is produced in the liver?

A

IGF-I (insulin-like growth factor I)

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34
Q

which hormone is produced in the kidney?

A

erythropoetin

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35
Q

which hormones are produced in the GI tract? (2)

A

gastrin

incretin

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36
Q

which hormones are produced in blood vessels?

A

prostanoids
NO
endothelin

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37
Q

how do alcohol and caffeine impact ADH release?

A

inhibits

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38
Q

how does a lack of ADH influence urine

A

u urinate more

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39
Q

what are the 3 diff presentations of pituitary dysfunctions?

A

tumour mass effects
hormone excess
hormone deficiency

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40
Q

what are the investigations for hormone abnormalities? (2)

A

hormonal tests

if hormonal tests abnormal or tumour mass effects, perform MRI pituitary!

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41
Q

define appetite

A

desire to eat food

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42
Q

define hunger

A

need to eat

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43
Q

define anorexia

A

lack/loss of appetite

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44
Q

define satiety

A

feeling of fullness (disappearance of appetite after a meal)

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45
Q

define BMI

A

weight (kg)
_________
height (metre squared)

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46
Q

what is a bmi of under 18.5?

A

underweight

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47
Q

what is a bmi btwn 18.5 - 24.9

A

normal weight

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48
Q

what is a bmi btwn 25.0 - 29.9?

A

overweight

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49
Q

what is a bmi of 30.0 - 39.9?

A

obese

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50
Q

what is a bmi of >40?

A

morbidly obese

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51
Q

list 7 risks of obesity

A 
t2 diabetes
hypertension
coronary artery disease
stroke
osteoarthritis
obstructive sleep apnoea
carcinoma (breast, endometrium, prostate, colon)
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52
Q

what type of fat is obesity?

A

abdominal (visceral) rather than subcutaneous

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53
Q

how does sleeping out of phase contribute to obesity?

A

sleeping out of phase

  • -> lower leptin levels
  • -> eat more
  • -> cortisol levels higher than they should be
  • -> high cortisol levels at night
  • -> metabolic issues
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54
Q

what are the opposing forces in appetite regulation?

A

energy expenditure vs energy intake

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55
Q

why do we eat? (3)

A

internal physiological drive
feelings that prompt thoughts of food
external psychological drive

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56
Q

what does highly refined sugar lead to?

A

quick and short satiety

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57
Q

what kinda foods are better?

A

low glycemic index food

also high protein - prolonged satiety

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58
Q

where is the hunger centre?

A

lateral hypothalamus

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59
Q

where is the satiety centre?

A

ventromedial hypothalamic nucleus

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60
Q

which part of the brain plays a central role in appetite regulation?

A

hypothalamus

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61
Q

what are the main players in appetite regulation?

A 
peripheral factors (leptin, insulin)
gut peptides (ghrelin, GLP1, CKK)
centra areas, hypothalamus (NPY, POMC, serotonin)
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62
Q

where is leptin expressed?

A

white fat

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63
Q

what does leptin do?

A

switches off appetite

immunostimulatory

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64
Q

after a meal, how do leptin levels change?

A

increase

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65
Q

where are CCK (cholecystokinin) receptors?

A

pyloric sphincter

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66
Q

what does CCK do? (4ish)

A

delays gastric emptying
initiates gall bladder contraction
stim insulin release

via vagus - satiety

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67
Q

where is ghrelin expressed?

A

stomach

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68
Q

how do blood levels of ghrelin change after meal?

A

high

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69
Q

what are the net effects of leptin and insulin?

A

increased satiety and decreased appetite

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70
Q

what is the net effect of ghrelin?

A

increased appetite

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71
Q

what do stretch receptors in the stomach do?

A

increase satiety

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72
Q

define obesity (WHO definition)

A

abnormal or excessive fat accumulation that may impair health

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73
Q

what are the 4 tiers of obesity care pathway at an individual level?

A

tier 1 - universal prevention
tier 2 - lifestyle intervention
tier 3 - specialist services
tier 4 - surgery

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74
Q

why is diabetes a PH issue? (4)

A

mortality
disability
co-morbidity
reduces QOL

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75
Q

what does the obesogenic environment involve?

A 
physical env (car culture)
economic env (expensive fruit n veg)
sociocultural env (family eating patterns)
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76
Q

what is a physical mechanism that maintains being overweight?

A

more weight = more difficult to exercise (arthritis, stress incontinence) and dieting –> metabolic response

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77
Q

what is a psychological mechanism that maintains being overweight?

A

low self-esteem and guilt, comfort eating

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78
Q

what is a socioeconomic mechanism that maintains being overweight?

A

reduced opportunities, employment, relationships, social mobility

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79
Q

what are risk factors for obesity?

A

age, sex, ethnicity, FH, weight, BMI, waist circumference, hypertension, vascular disease, impaired glucose tolerance (IGT) or impaired fasting glucose

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80
Q

what is IGT

A

impaired glucose tolerance

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81
Q

what is IFG

A

impaired fasting glucose

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82
Q

list 5 screening tests for obesity

A 
HbA1c
random capillary blood glucose
random venous blood glucose
fasting venous blood glucose
oral glucose tolerance test (OGTT)
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83
Q

what does OGTT involve

A

venous blood glucose 2 hrs after oral glucose load

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84
Q

what is the diagnostic range for IGT?

A

7.8 - 11.0 mmol/l

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85
Q

what is the diagnostic range for IFG?

A

6.1 - 6.9 mmol/l

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86
Q

how can society reduce the impact of t2 diabetes? (4)

A

identifying ppl at risk
early prevention in those at risk
diagnosing diabetes earlier
effective management and supporting self-management

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87
Q

what does the pituitary gland regulate?

A

growth and development
fertility
metabolism
body composition

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88
Q

does the anterior pituitary gland have a blood supply?

A

no but receives blood through a portal venous circulation from the hypothalamus

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89
Q

where is prolactin released from?

A

the anterior pituitary gland

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90
Q

what is prolactin under neg control by?

A

dopamine

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91
Q

if anything damages the pituitary stalk and thus delivery of dopamine, WHAT levels increase?

A

prolactin

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92
Q

what hormone can tumours secrete?

A

prolactin!

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93
Q

what is the most common disease of the pituitary gland?

A

benign pituitary adenoma

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94
Q

which disease of the pituitary tends to be in younger ppl?

A

craniopharyngioma

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95
Q

what do a lot of endocrine organs get?

A

adenomas

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96
Q

what are most adenomas like?

A

benign

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97
Q

define adenoma

A

benign tumour formed from glandular structures in epithelial tissue

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98
Q

what are the 3 VITAL points of tumour presentation?

A

can cause:
pressure on local structures (eg optic nerves)
pressure on normal pituitary (hypopituitarism)
functioning tumour

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99
Q

what is prolactinoma?

A

too much prolactin

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100
Q

what is acromegaly?

A

too much GH

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101
Q

what is Cushing’s disease?

A

too much ACTH

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102
Q

what can pituitary adenoma pressure cause?

A

headaches

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103
Q

which vision do u lose first?

A

colour!

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104
Q

what is the field defect u get with a pituitary tumour?

A

bitemporal hemianopia starting upper quadrantic

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105
Q

pituitary tumours can go through the bottom of the pituitary fossa and drain the nose …. what is a clue to an important diagnosis to make?

A

CSF has sugar

snot doesn’t

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106
Q

what is the most common prolactinoma?

A

prolactin microadenoma

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107
Q

prolactin causes suppression of what?

A

gonadotrophins

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108
Q

as prolactin causes suppression of gonadotrophin, what tends to happen to females? (2)

A

lose periods

get milk into breasts

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109
Q

how do prolactin levels change during pregnancy?

A

increase

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110
Q

if somebody checks with period loss/infertility issues… check what?

A

prolactin (ngl this always seems to be the answer, but maybe bc I’ve only covered this lecture LOL @ future me, come back to this)

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111
Q

how difficult is it to treat hyperprolactin?

A

87% ppl respond to dopamine agonist!

80% women got pregnant within 3m of starting this

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112
Q

prolactinomas are more common in who?

A

women

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113
Q

what can be a symptom of prolactinoma?

A

libido loss, infertility, amenorrhoea

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114
Q

how can a tumour result in gigantism?

A

tumour presses on pituitary gland, increases GH - don’t go through puberty as bones don’t fuse

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115
Q

what are signs of acromegaly?

A

thick skin
greasy
sweating
frontal bossing

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116
Q

too much steroid/cortisol can result in which syndrome?

A

cushing’s

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117
Q

what is the commonest cause of too much steroid?

A

anti inflammatory drugs

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118
Q

if u have a patient with a pituitary tumour, what are the 3 questions to ask?

A

is it pressing on the optic chasm?
are they hypopituitary?
do they have a functioning tumour?

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119
Q

cortisol deficiency can result in death - why?

A

due to an adrenal crisis

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120
Q

what is the HPA axis a classic example of?

A

negative feedback loop

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121
Q

what does HPA (axis) stand for

A

hypothalamic-pituitary-adrenal

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122
Q

if deficient with cortisol, what to replace it with?

A

hydrocortisone

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123
Q

what is hydrocortisone?

A

the pharmacological name for cortisol

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124
Q

what is the distinct circadian rhythm of cortisol?

A

rises in the early hours of morning (3am, peaks shortly after waking, declines during the day)

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125
Q

what do cortisol levels parallel?

A

energy levels

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126
Q

what is the primary zeitgeber?

A

light

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127
Q

what is a primary disease of adrenal insufficiency?

A

addison’s disease

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128
Q

what is a secondary disease of adrenal insufficiency?

A

hypopituitarism

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129
Q

if u ever see low Na and high K - think of what?

A

addison’s

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130
Q

what is cortisol important for retaining/getting rid of?

A

retaining Na

getting rid of K

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131
Q

when looking at circadian rhythm & deficiency - look when it’s at its…… ?

A

highest

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132
Q

when looking at circadian rhythm & excess - look when it’s at its…… ?

A

lowest

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133
Q

how to treat cortisol deficiency?

A

2/3x daily hydrocortisone 15-25mg

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134
Q

in primary adrenal insufficiency, replace aldosterone with what?

A

fludrocortisone

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135
Q

what is a common presentation of adrenal insufficiency?

A

adrenal crisis

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136
Q

what does an adrenal crisis involve?

A 
hypotension and CV collapse
fatigue
fever
hypoglycaemia
hyponatraemia and hyperkalaemia
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137
Q

how would u manage an adrenal crisis?

A

take bloods (for cortisol and ACTH)
immediate hydrocortisone 100mg IV, IM
fluid resuscitation (1L saline 1 hr)
hydrocortisone 50-100mg IV/IM 6 hourly

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138
Q

what does TDS stand for in pharmacology

A

3x a day

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139
Q

for adrenal insufficiency, always consider what?

A

recent steroid use

check cortisol and ACTH

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140
Q

describe the regulation of HPA axis

A

circadian rhythm controlled by central clock

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141
Q

describe causes of adrenal insufficiency

A

primary (Addison’s and CAH)

secondary (pituitary)

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142
Q

what is the diff btwn gigantism and acromegaly?

A

gigantism = before puberty

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143
Q

what are the commonest endocrine disorders?

A

thyroid diseases

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144
Q

FHx of t1 diabetes is a strong association w what?

A

thyroid disease ;/

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145
Q

what is found in almost all patients with autoimmune hypothyroidism

A

thyroglobulin and thyroid peroxidase (TPO) antibodies

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146
Q

what is the mechanism of thyroid cell destruction?

A

cytotoxic (CD8+) T cell mediated

thryglobulin and TPO antibodies may cause 2ndary damage, but alone have no effect

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147
Q

what are some symptoms of Graves’ disease?

A

retracted eyelids
bulging eyes
redness

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148
Q

what does Graves’ disease cause

A

hyperthyroidism

often an enlarged thyroid

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149
Q

what is the cause of Graves’ disease?

A

thyroid stimulating antibodies

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150
Q

what is Graves’ disease aka

A

hyperthyroidism

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151
Q

what is myxoedema aka

A

hypothyroidism

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152
Q

what is the biggest risk factor to thyroid disease?

A

being female

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153
Q

what are some autoimmune diseases associated w thyroid autoimmunity?

A

t1 DM
addison’s disease
pernicious anaemia
vitiligo

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154
Q

what is swelling in extra ocular muscles?

A

thyroid associated opthalmopathy

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155
Q

how can graves disease occur in pregnancy

A

caused by thyroid stimulating antibodies that may cross the placenta

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156
Q

what is goitre?

A

palpable and visible thyroid enlargement

endemic in iodine deficient areas

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157
Q

what is sporadic non-toxic goitre?

A

commonest endocrine disorder

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158
Q

define hyperthyroidism

A

excess of thyroid hormones in blood

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159
Q

what are 3 mechanisms for increased levels of thyroid hormone?

A

overproduction of thyroid hormone
leakage of preformed hormone from thyroid
ingestion of excess thyroid hormone

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160
Q

what is pituitary adenoma aka

A

TSHoma

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161
Q

list some clinical features of hyperthyroidism

A 
weight loss
tachycardia
hyperphagia
anxiety
heat intolerance
sweating
diarrhoea
menstrual disturbance
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162
Q

what are thionamides?

A

anti thyroid drugs

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163
Q

what is essential for thyroid hormone production?

A

iodine

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164
Q

how is iodine actively transported into thyroid follicular cells?

A

via Na/I symporter

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165
Q

what are some causes of hypothyroidism

A 
Hashimoto's thyroiditis
thyroidectomy
iodine deficiency
thyroid hormone deficiency
pituitary/hypothalamic disease
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166
Q

list some clinical features of hypothyroidism

A 
fatigue
weight gain
cold intolerance
constipation
dry, rough skin
delayed muscle reflexes
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167
Q

what can u see in the investigation of primary hypothyroidism

A 
increased TSH (most sensitive marker)
usually decreased free T4/T3
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168
Q

what is the most sensitive marker of hypothyroidism

A

TSH

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169
Q

amiodarone (iodine rich) often used to treat what?

A

atrial fibrillation

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170
Q

many drugs can affect the thyroid, particularly what?

A

amiodarone

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171
Q

what are the 2 most important hormones in calcium homeostasis?

A

PTH and calcitriol

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172
Q

what is calcitriol aka

A

1,25 dihydroxy vit D

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173
Q

what is 1,25 dihydroxy vitD aka?

A

calcitriol

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174
Q

PTH release is increased in response to what?

A

low serum ionised calcium

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175
Q

what are the 3 ways in which PTH works to increase serum calcium?

A

-CONFUSED-
decreasing renal calcium excretion
increasing bone resorption
enhancing dietary calcium absorption (by stimulating prod of calcitriol in kidney)

?
increased calcium absorption
increased one resorption
increased calcium reabsorption
?
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176
Q

what can abnormal circulating calcium levels result in?

A

impaired muscle and nerve function

cardiac dysrhymias

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177
Q

abnormalities of which hormone levels can be an appropriate response to calcium imbalance OR can be the primary cause of calcium imbalance?

A

PTH

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178
Q

In secondary hyperparathyroidism, how do PTH levels change?

A

increase

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179
Q

In secondary hyperparathyroidism, how do calcium levels change?

A

decrease

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180
Q

In secondary hyperparathyroidism, how do phosphate levels change?

A

decrease

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181
Q

is PTH appropriate or inappropriate in secondary hyperparathyroidism?

A

appropriate

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182
Q

In hypoparathyroidism, how do PTH levels change?

A

decrease

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183
Q

In hypoparathyroidism, how do calcium levels change?

A

decrease

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184
Q

In hypoparathyroidism, how do phosphate levels change?

A

increase

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185
Q

what is pseudohypoparathyroidism aka?

A

PTH resistance

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186
Q

what is another way to say a disorder of PTH resistance?

A

pseudohypoparathyroidism

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187
Q

in pseudohypoparathyroidism, how do PTH levels change?

A

increase

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188
Q

in pseudohypoparathyroidism, how do calcium levels change?

A

decrease

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189
Q

in pseudohypoparathyroidism, how do phosphate levels change?

A

increase

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190
Q

what kind of feedback is calcium homeostasis?

A

negative

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191
Q

what is the set point of serum ionised calcium?

A

1.1 mol/l ish

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192
Q

If Ca decreased by 10%, how much does PTH increase by?

A

200%

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193
Q

if Ca increases by 10%, how much does PTH decrease by?

A

70%

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194
Q

what is the equation for corrected calcium?

A

total serum calcium + 0.02(40 - serum albumin)

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195
Q

if serum calcium = 2.08 mmol/L
and
serum album = 30 g/L

what is the corrected calcium? (mmol/L)

A

2.28

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196
Q

list 6 consequences of hypocalcaemia

A 
parasthesia (burning/prickling sensation in limbs)
muscle spasm
seizures
basal ganglia calcification
cataracts
ECG abnormalities (long QT interval)
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197
Q

what is a fairly common cause of hypocalcaemia?

A

osteomalacia

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198
Q

how to test chvostek’s sign?

A

tap over facial nerve

look for spasm of facial nerves

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199
Q

how to test trousseau’s sign?

A

inflate BP cuff to 20mmHg above systolic for 5 mins - clawing dinosaury thing

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200
Q

name some syndromes of hypoparathyroidism

A

di george
HDR
kenney-caffey

201
Q

list 4 consequences of hypoparathyroidism

A

decreased renal Ca reasborption
incresed renal phosphate reabsorption
decreased bone resorption
decreased formation of calcitriol

202
Q

what are some symptoms of pseudohypoparathyroidism?

A

short stature
obesity
mild learning difficulties
normal calcium metabolism!

203
Q

list 6 symptoms of hypercalcaemia

A 
thirst, polyuria
nausea
constipation
confusion (--> coma)
renal stones
ECG abnormalties (short QT)
204
Q

define parasthesia

A

burning/prickling sensation in limbs, consequence of hypocalcaemia

205
Q

define polyuria

A

excessive urine prod/passage

above 2.5/3L in 24hrs

206
Q

what are 2 main causes of hypercalcaemia?

A

malignancy (bone mets, myeloma, lymphoma etc)

primary hyperparathyroidism

207
Q

primary hyperparathyroidism can cause what?

A

hypercalcaemia

208
Q

what are consequences of primary hyperparathyroidism?

A

bones, stones, grones, and moans lol

osteoporosis
kidney stones
confusion
constipation/acute pancreatitis

209
Q

what’s the main cause of primary hyperparathyroidism?

A

80% due to single benign adenoma :/

210
Q

what happens in tertiary hyperparathyroidism?

A

renal failure
cant activate vit D§
hypercalcaemia

211
Q

define puberty !

A

physiological, morphological, and behavioural changes as the gonads switch from infantile to adult forms

212
Q

what is the definitive sign of puberty in boys?

A

1st ejaculation, often nocturnal

213
Q

what is the definitive sign of puberty in girls?

A

menarch - 1st menstrual bleeding

214
Q

when do secondary sexual characteristics occur

A

at puberty

215
Q

how does ovarian oestrogen contribute to secondary sexual characteristics?

A

regulate growth of breast and female genitalia

216
Q

how do ovarian and adrenal androgens impact secondary sexual characteristics?

A

pubic and axillary hair

217
Q

how do testicular androgens contribute to secondary sexual characteristics?

A

external genitalia and pubic hair growth

enlargement of larynx/laryngeal muscles (voice deepening)

218
Q

what is a good marker of puberty in boys

A

testicular growth

219
Q

how do tanner stages differ?

A

1 - no pubic hear, testicular vol less than 3ml/elevation of papilla only
5 - adult-type hair spread to medial surface of thighs
- genitalia adult size n shape / classic inverse triangle hair type in females, adult contour breast

220
Q

what is significant about testicular volume in klinefelters?!

A

they hardly ever get testicular vol above 5ml

221
Q

what is testicular size mainly dependant on?

A

number of germ cells

222
Q

what is the diff btwn s1 and s2 of tanner stages in girls

A

s1 - breast bud

s2 - no breast bud

223
Q

what is a good marker of puberty in girls?

A

presence of breast bud - can’t grow without oestrogen

224
Q

define thelarche

A

breast development

225
Q

what is thelarche (breast development) induced by?

A

oestrogen

226
Q

how long does it take for breasts to develop?

A

3 years ish

227
Q

what are the effects of oestrogen on the breast? (3)

A

ductal proliferation
site specific adipose deposition
enlargement of areola and nipple

228
Q

other than oestrogen, what other hormones are involved in breast development?

A

prolactin
glucocorticoids
insulin

229
Q

can both breasts be in diff stages of tanners?

A

yuh

230
Q

what is the (basic) diff btwn prepubertal and postpubertal uterus?

A

pre - tubular shaped, 2-3cm length

post - pear shaped, 5-8cm length

231
Q

what are 3 questiosn to ask during a pelvic ultrasound in girls?

A
  1. are mullerian structures present?
  2. is there morphology of the uterus?
    is there morphology of ovaries?
232
Q

what are the 5 ways in which the external genitalia in females changes under the effect of oestrogens?

A

labia majora/minora increase in size n thickness
rogation/?rotation and change in colour of labia majora
hymen thickens
clitoris slightly enlarges
vestibular glands begin secretion

233
Q

define adrenarche

A

the onset of androgen-dependent body changes eg axillary/pubic hair, body odour and acne!

234
Q

define pubarche

A

1st appearance of pubic hair at puberty

235
Q

what is the most pronounced clinical result of adrenarche

A

pubic hair

236
Q

what is the hpg axis?

A

hypothalamus (tertiary)
pituitary (secondary)
gonads (primary)

237
Q

where is GnRH released

A

hypothalamus

238
Q

what does GnRH result in the formation of

A

LH, FSH from pit gland

239
Q

for males with early puberty, what is it important to rule out?

A

brain tumour

240
Q

“true” precocious puberty - 90% of patients are what?

A

female

241
Q

in true precocious puberty, what is the rise in LH:FSH?

A

above 1

242
Q

which type of puberty is GnRH dependent?

A

true precocious puberty

243
Q

which type of puberty is GnRH independent?

A

precocious pseudo-puberty

244
Q

CNS tumours/disorders can result in what?

A

true precocious puberty

245
Q

increased andorgen secretion and gonadotropin secreting tumours can reuslt in what?

A

precocious pseudopuberty

246
Q

congenital adrenal hyperplasia can result in what?

A

increased androgen secretion

247
Q

3 resaons why puberty may be delayed? (they loooong)

A

idiopathic (constitutional) delay in growth and puberty
hypogonadotropic hypogonadism
hypergonadotropic hypogonadism

248
Q

what is idiopathic (constitutional) delay in growth and puberty?

A

delayed activation of the hypothalamic pulse generator

249
Q

what is hypogonadotropic hypogonadism

A

sexual infantilsm related to gonadotropin deficiency

250
Q

lwhat is sexual infantilism?

A

lack of sexual development after expected puberty or delayed puberty

251
Q

is delayed puberty more common in boys or girls?

A

boys

252
Q

how does delayed puberty impact bone mass?

A

reduces it

253
Q

what are some indications of investigation for delayed puberty in girls?

A

lack of breast development by 13
5+ yrs btwn breast development n period
lack of pubic hair by 14
no period by 15-16

254
Q

what are some indications of investigation for delayed puberty in boys?

A

lack of testicular enlargement by 14
lack of pubic hair by 15
5+ yrs for complete genital enlargement

255
Q

what does CDGP stand for

A

constitutional delay of growth and puberty

256
Q

what are some signs of constitutional delay of growth n puberty (cdgp)

A

shorter for age
delay in bone maturation, adrenarche
FH of late menarche

257
Q

what are lab investigations for puberty? (low conc of any of these)

A

complete RBC count
U&E, renal, LFT, coeliac ab

LH,FSH
testosterone, oestradiol

thyroid function, prolactin
DHEA-S, ACTH, cortisol

258
Q

in ALL girls w short stature and delayed puberty: rule out whAT?

A

turner’s (X0)

259
Q

is skeletal or chronological age more closely correlated with pubertal development?

A

skeletal

260
Q

what are some functional causes of delayed puberty?

A 
chronic renal disease
sickle cell
anorexia
psychological/stress
extreme exercise
drugs
cushing's
hypothyroidism
261
Q

which type of hypogonadism is it if ovary/testis fails?

A

primary

262
Q

what happens in primary hypogonadism

A

ovary/testis fails:
oestrogen/tesotsterone decrease
slack of feedback
LH n FSH increase

263
Q

which type of gonadism is it if hypothalamus/pituitary gland fails?

A

secondary

264
Q

what happens in secondary hypogonadism

A

hypothalamus/pituitary fails:
LH n FSH low
no response to feedback
so oestrogen/testosterone decreases

265
Q

define hyposmia/microsmia

A

reduced ability to smell and detect odours

266
Q

define anosmia

A

when no odours can be detected

267
Q

what is kallman syndrome

A

hypogonadotrophic hypogonadism

268
Q

what is the key symptom of kallman syndrome (hypogonadotrophic hypogonadism)

A

inability to detect odours

269
Q

what is hypergonadotropihc gonaidsm?

A

ripmary gonadal failure (males - klinefelters, females - turners)

270
Q

list some signs of klinefelter

A

primary hypogonadism
reduced 2ndary sexual hair
osteoprosis
tallstature

271
Q

define azoospermia

A

medical cond of a man whose semen contains no sperm

272
Q

define gynaecomastia

A

enlargement of a man’s breast

273
Q

what are 3 diff presentations of klinefelters

A

dont go into puberty
go into puberty but stopped, don’t develop fully
infertile (germ cell failure)

274
Q

list some signs of turners, bitch

A

at birth - oedema of dorsa of hands/feet
webbing of neck
CV malformations
short stature

275
Q

what is a horseshoe kidney

A

fusion of kidney at upper poles

can happen in turner’s

276
Q

what does female replacement therapy involve?

A 
ethinyl estadirol (Tablet)
or oestrogen (tablets, transdermal)
277
Q

what does male replacement therapy involve?

A

testosteronen enthane (IM injection)

278
Q

what is the diff btwn precocious and delayed puberty?

A

precocious - onset of 2ndary sexual characteristics before 8/9yrs
delayed - absence of 2ndary sexual characteristics by 14/16 yrs

279
Q

what is the hypothalamic regulation of GnRH secretion

A

increased stim factors (mostly glutamate and kisspeptin)

280
Q

what % of the human body is fluid?

A

60%

281
Q

what is the distribution of ECF vs ICF?

A

ECF - 1/3 total body water (14L)

ICF - 2/3 total body water (28L)

282
Q

what can ECF be split into?

A

intravascular fluid - 1/4 ECF (3.5L)

interstitial fluid - 3/4 ECF (10.5L)

283
Q

how does osmotic pressure of fluid compartments differ?

A

it doesnt, its approx equal

284
Q

what kinda ions does ECF contain

A

Na, Cl and bicarb

285
Q

what kinda ions does ICF contain?

A

K, Mg and phosphate

286
Q

ECF/plasma osmolarity and what conc should be considered together n why?

A

Na conc - bc Na+ comprise majority of solute in ECF

287
Q

how does the body respond to changes in ECF osmolarity, BP or blood vol?

A

by altering water reabsorbed by kidneys and fluid ingested

288
Q

what happens in conditions of water excess?

A

there’s a fall in plasma osmolality and an influx of water into the cells, increasing the intracellular water content. this reduces thirst, suppresses ADH release thus decreasing water intake and increasing water excretion

289
Q

what does ADH bind to?

A

g-protein coupled 7 transmembrane domain receptors

290
Q

what are the diff g-protein coupled 7 transmembrane domain receptors adh binds to?

A

V1a (vasculature)
V2 (renal collecting tubules)
V1b (pituitary gland)

291
Q

what 2 things is ADH release controlled by?

A

osmoreceptors in thalamus (day to day)

baroreceptors in brainstem/great vessels (emergency)

292
Q

in a day to day situation, what controls ADH release?

A

osmoreceptors in the thalamus

293
Q

in an emergency situation, what controls ADH release?

A

baroreceptors in the brainstem/great vessels

294
Q

which receptor does ADH bind to in the renal collecting duct principle cells?

A

V2 receptors

295
Q

which receptor does ADH bind to in vasculature?

A

V1a

296
Q

which receptor does ADP bind to in the pituitary gland?

A

V1b

297
Q

what is the main driver for fluid intake?

A

thirst

298
Q

what are 2 main drivers of variable water excretion by urine output?

A

GFR

ADH

299
Q

what is omolality

A

concentration per kilo

300
Q

list some exogenous solutes that may affect osmolality

A

alcohol, methanol or mannitol etc

301
Q

urine osmolality should be _______ serum osmolality

A

double

302
Q

what is a normol osmolality?

A

282-295 mOsmol/kg

303
Q

how do u approx calculate plasma osmolality?

A

2xNa+ + glucose + urea

304
Q

where does rine conc by kidney occur

A

along theneprhon

305
Q

vasopressin activates V2 receptors in renal collecting ducts, leading to what?

A

increased reabsorption of water via the kidneys
(aquaporin2 proteins synthesised and inserted into apical membrane, increasing permeability of renal collecting duct - water is reabsorbed and returned to blood)

306
Q

when the stimulus for water reabsorption ends, how is aquaporin 2 removed from apical membrane?

A

endocytosis

307
Q

what is the cause of cranial diabetes insipidus

A

lack of ADH

acquired (idiopathic - tumours, infections, inflammatory. primary - genetics, developmental)

308
Q

how do u manage cranial DI?

A

treat any underlying cond
desmopressin
(tablets 100-1200 mg/day, nasal spray 10-40mg/day, injection 1-2mg/day)

309
Q

what is desmopressin used to treat?

A

cranial DI (or in v high dose, nephrogenic CI)

310
Q

what is nephrogenic DI?

A

resistance to ADH action

311
Q

what are some causes of nephrogenic DI?

A

acquired (osmotic diuresis / DM), drugs eg lithium, chronic renal failure)
familiar (x linked - v2 receptor defect, autosomal recessive(AQP2 defect)

312
Q

how can u manage nephrogenic DI?

A

try and avoid precipitating drugs

313
Q

define hyponatraemia

A

serum sodium < 135 mmol/l

314
Q

what is severe hyponatraemia

A

serum sodium < 125 mmol/l

315
Q

what is normal serum sodium range?

A

137-144 mmol/l

316
Q

what are some causes of hyponatraemia? (4)

A

SIADH
drip arm
sodium deficiency
renal failure

317
Q

what do the signs/symptoms of hyponatraemia depend on?

A

speed of onset!

quicker onset = greater symptoms

318
Q

what are some signs of hyponatraemia (less to more severe)

A 
asymptomatic
headache
lethargy
weakness
confusion
decreased concious level
coma
319
Q

what happens in ECF hypo-osmolality?

A

water moves into the brain
brain oedema
brain expels electrolytes and osmolytes
water loss accompanies loss of solutes, reducing swelling

320
Q

what is the diff btwn acute n chronic hyponatraemia?

A

acute - 48H (rapid correction safer n may be necessary)

chronic - CNS adapts (correction must be slow)

321
Q

what are the tests to do when hyponatrameia presents? (this is important )

A 
plasma osmolality
urine osmolality
plasma glucose
urine sodium
urine diptestfor protein
TSH
cortisol
322
Q

what are 3 causes of hyponatraemia

A

flui doverloaded
normovolaemic
dehydrated

323
Q

what is SIADH

A

syndrome of inappropriate ADH secretion

324
Q

what happens in SIADH

A 
too much ADH when it should not be being secreted
low osmolality
plasma sodium low
urine inappropriately concentrated
water retention
normal thyroid and adrenal function
325
Q

what are some causes of SIADH?

A

CNS disorders (head injury, meningitis, brain tumour)
tumours (carcinoma, lymphoma, leukaemia)
resp causes (pneumonia, tuberculosis, severe asthma)
drugs (carbamazipine, thiazides, MAO inhibitors, vasopressin, desmopressin, SSRIs)

326
Q

what is the treatment of SIADH? (acute and chronic)

A

fluid restriction!
acute - daily U+E in hosp
chronic - weekly-monthly U+E

327
Q

what should be the fluid restriction if SIADH?

A

<1L/24hr

328
Q

what is hypertonic saline for?

A

symptomatic hyponatraemia

329
Q

what are vaptans?

A

selective v2 receptor oral antagonist

competitive to ADH

330
Q

so what can cause DI?

A

lack of ADH

resistance to ADH

331
Q

what kind of tissue is the anterior lobe of the pituitary gland?

A

glandular tissue (75% of total weight)

332
Q

what kind of tissue is the posterior lobe of the pituitary gland?

A

nerve tissue (contains axons that originate in the hypothalamus)

333
Q

what kind of tumours are there in the pituitary gland?

A 
non-functioning pituitary adenomas
endocrine active pituitary adenomas
malignant pituitary tumours
metastases in the pituitary
pituitary cysts
334
Q

where do craniopharyngiomas arise from?

A

squamous epithelial remnants of Rathke’s pouch

335
Q

what happens w craniopharyngioma?

A 
remnants of rathe's pouchraised ICP
visual disturbances
growth failure
PH deficiency
weight increase
336
Q

what do rathke’s cysts derive from?

A

derived from remnants of rathke’s pouch

337
Q

what does rathke’s cyst present with?

A

headache and amenorrhoea, hypopituitarism and hydrocephalus

338
Q

after a pituitary adenoma, what is the commonest tumour there?

A

meningioma

339
Q

what is a meningioma associated with

A

visual disturbance and endocrine dysfunction

340
Q

what is lymphocytic hypophysitis

A

inflammation of the pituitary gland due to an autoimmune reaction

341
Q

what are 3 types of pituitary dysfunction?

A

tumour mass effects
hormone excess
hormone deficiency

342
Q

what are investigations for pituitary dysfunction?

A

hormone tests

if hormone tests abnormal or tumour mass effects, perform MRI pituitary

343
Q

what are local mass effects of the pituitary? (4)

A

cranial nerve palsy and temporal lobe epilepsy
visual field defects
headaches
CSH rhinorrhoea (nasal cavity filled w mucus fluid)

344
Q

a chiasmal compression from the pituitary tumour results in what?

A

bitemporal hemianopia

345
Q

what are the 6 hormones the pituitary gland secretes?

A 
gonadotrophins
growth hormone
prolactin
adrenocorticotropin hormone (ACTH)
melanocyte-stimulating hormone (MSH)
thyroid stimulating hormone (TSH)
346
Q

what should u measure in pituitary disease

A

ft4

347
Q

what does Ft4 stand for?

A

free thyroxine

348
Q

what does Ft3 stand for?

A

free tri-iodothyronine

349
Q

in primary hypothyroidism, what are the hormone levels?

A

raised TSH

low ft4

350
Q

in hypopituitary, what are hormone levels?

A

normal/low TSH

low ft4

351
Q

in graves disease, what are hormone levels?

A

suppressed TSH

high ft4

352
Q

in TSHoma, what are hormone levels?

A

normal/high TSH

high ft4

353
Q

how can u test primary hypogonadism in men

A

low/raised LH/FSH

354
Q

how can u test gonadal diseases in women?

A

before puberty - estradiol low with low LH/FSH

puberty - pulsatile LH and oestradiol ncreases

355
Q

what happens in primary ovarian failure

A

high FSH (with high but slightly lower) LH and low oestradiol

356
Q

how is GH secreted

A

in pulses with greatest at night

GH levels fall w age ad low in obesity

357
Q

why might prolactin be raised?

A

stress
drugs - antipsychotics
stalk pressure
prolactinoma

358
Q

oral glucose GH suppression test can be used for what?

A

acromegaly

359
Q

glucagon test can measure what?

A

GH deficiency

360
Q

GnRH stimulation test measures what?

A

gonadotrophindeficiency

361
Q

what is the preferred imaging for the pituitary?

A

MRI

362
Q

what are symptoms of low GH?

A

short stature
abnormal body composition
reduced muscle mass

363
Q

what do u prescribe someone w low GH?

A

GH

364
Q

what are the symptoms of low LH/FSH?

A

hypogonadism
reduced sperm count
infertility
menstruation issues

365
Q

what do u prescribe someone w low LH/FSH?

A

tester one in males

oestradiol +/- progesterone in females

366
Q

what is the symptom of low TSH ?

A

hypothyroidsim

367
Q

what is the prescription for someone w low TSH (hypothyroidism)?

A

levothyroxine

368
Q

what are the symptoms of low ACTH?

A

adrenal failure

decreased pigment

369
Q

what is the treatment for low ACTH?

A

hydrocortisone

370
Q

what are the symptoms of low ADH?

A

DI (ADH deficiency - polyuria)

371
Q

oestrogen replacement can reduce the risk of what?

A

cardiovascular disease and osteoporosis

372
Q

what is the definition of diabetes (measurementS)?

A

fasting plasma glucose ≥7mmol/l
OGTT fasting ≥7
HbA1c >48mmol/mol

373
Q

HbA1c measurement >? indicates diabetes?

A

48 mmol/mol

374
Q

what are suggestive features of T1 diabetes?

A

big 3 symptoms:

constant thirst
frequent urination
rapid weight loss

375
Q

what are T1 diabetics prone to?

A

ketoacidosis

376
Q

what are suggestive features of t2 diabetes?

A

gradual onset

FH positive

377
Q

T1 or T2?

A

can be difficult
T1 in younger patients
T2 can be obese
if in doubt: treat w insulin

378
Q

what happens if t1 diabetes diagnosis is missed?

A

formation of ketone bodies

reduced insulin leads to fat breakdowna nd formation of glycerol and FFA

379
Q

what do FFAs do

A

impair glucose uptake
transported to liver, providing energy for gluconeogenesis
oxidised to form ketone bodies

380
Q

define ketoacidosis

A

absence of insulin and rising counter-regulatory hormones which leads to increasing hyperglycaemia and rising ketones

381
Q

what can ketones cause

A

anorexia and vomiting- vicious circle of increased dehydration

382
Q

define hyperglycaemia

A

plasma glucose above 50 mmol/l

383
Q

define raised plasma ketones

A

urine ketones >2+

384
Q

define metabolic acidosis

A

plasma bicarb <15mmol/l

385
Q

what are the causes of DKA?

A

unknown in half

intercurrent illness

386
Q

what is DKA a triad of?

A

hyperglycaemia
ketones
acidosis

387
Q

what are symptoms of DKA

A 
develops over days
polyuria/polydipsia
nausea n vomiting
weiht loss
weakness
abdominal pain
drowsiness
confusion
388
Q

define polydipsia

A

excessive thirst

389
Q

what are some signs of DKA

A 
hyperventilation
dehydration
hypotension
tachycardia
coma
390
Q

what is the biochemical diagnosis of DKA?

A

hyperglycaemia (<50mmol/l)
K+ high on press despite total K+ deficit
urea and creatinine raised due to pre-rena failure
urinary ketones dipstick >2+ ketones
blood ketones >3

391
Q

what do u do to manage DKA?

A

rehydration (3L in first 3hrs)
insulin
electrolyte (K+) replacement
treat underlying cause

392
Q

what are some complications of DKA?

A

cerebral oedema
adult resp distress syndrome
thromboembolism
death:/

393
Q

what are the aims of treatment in t1 diabetes

A

relieve symptoms
prevent ketoacidosis
prevent vascular complications

394
Q

what are some microvascular complications of t1 diabetes

A

diabetic nephropathy (tend to develop retinopathy)

395
Q

what does the treatment of t1 diabetes aim to achieve

A

restoration of beta cell physiology

396
Q

inappropriately high insulin levels confer a high risk of what?

A

hypoglycaemia

397
Q

what are some physiological defences of hypoglycaemia

A

symptoms of sweating, tremor, palpitations

loss of conc, hunger

398
Q

what is the dilemma for t1 diabetics?

A

setting higher glucose targets reduces risk of hypoglycaemia but increases risk of diabetic complications

n vice versa

399
Q

what is HbA1c?

A

avg blood glucose levels for the last 2-3m

400
Q

what is the commonest type of monogenic diabetes

A

MODY (maturity onset disease of the young)

it’s non insulin dependant

401
Q

what are some endocrine causes of diabetes?

A

acromegaly

cushing’s syndrome

402
Q

how is acromegaly an endocrine cause of diabetes

A

excessive GH secretion
similar to T2
insulin resistance rises, impairing insulin action in liver n peripheral tissues

403
Q

how is Cushing’s syndrome an endocrine cause of diabetes

A

increased insulin resistance, reduced glucose uptake into peripheral tissues
hepatic glucose prod incr through stimulating of gluconeogenesis via increased substrates

404
Q

do glucocorticoids increase or decrease insulin resistance

A

increase

405
Q

what are the 3 main microvascular diabetes complications

A

neuropathy
retinopathy
nephropathy

406
Q

how can DM cause mortality

A

acute hyperglycaemia - if untreated leads to a cute met emergencies, DKA
chronic hyperglycaemia - leads to tissue complications

407
Q

what are some clinical consequences of diabetic neuropathy

A

pain (burning, paraesthesia)
autonomic (cardiac AN, diarrhoea)
insensitivity (foot ulceration, amputation)

408
Q

what are some risk factors for diabetic neuropathy

A 
hypertension
smoking
hba1c change
diabetes duration
BMI
total cholesterol
409
Q

what involves the treatment of diabetic neuropathy

A

good glycaemic control
TCAs/SSRIs
anticonvulsants
opioids

410
Q

what are some consequences of peripheral neuropathy in diabetes

A

diabetic foot ulceration

peripheral vascular disease

411
Q

what are some symptoms of PVD

A

intermittent claudication

rest pain

412
Q

what is claudication

A

limping lol

413
Q

what are some signs of PVD?

A

diminished/absent pedal pulses
coolness of feet n toes
poor skin n nails

414
Q

what is the treatment of PVD?

A

quit smoking
walk through the pain
surgical intervention

415
Q

what is the journey to diabetic amputation?

A 
neuropathy or vascular
trauma
ulcer
failure to heal
infection
amputation
416
Q

what is the hallmark for diabetic nephropathy

A

development of proteinuria
followed by progressive decline in renal function
major risk factor for CVD

417
Q

what is the pathophysiology journey of diabetic nephropathy

A

glomerulus changes
increase of glomerular injury
filtration of proteins
diabetic nephropathy

418
Q

what does treatment for diabetic nephropathy involve

A

BP control
glycemic control
ARB/ACEi
proteinuria and cholesterol control

419
Q

what is the most common cause of kidney failure/end stage renal disease?

A

diabetic nephropathy

420
Q

in the fasting state, where does most glucose come from?

A

liver (a bit from the kidney)

421
Q

in the fasting state, where does glucose come from?

A

gluconeogenesis (utilises 3 C precursors to synthesise glucose inc lactate, alanine n glycerol)

422
Q

in the fasting state, where is glucose delivered to?

A

insulin independent tissues, brain and RBC

423
Q

what are insulin levels like in the fasting state?

A

low

424
Q

what do the muscles use for fuel in the fasting state?

A

FFA

425
Q

post prandial is aka?

A

?post prandial

426
Q

what happens after feeding?

A

physiological need to dispose of nutrient load

427
Q

what stimulates insulin secretion and suppresses glucagon after eating, and when?

A

rising glucose levels

5-10min after eating

428
Q

after feeding, where does glucose ingested go?

A

40% - liver

60% - periphery, mostly muscle

429
Q

what suppresses lipolysis after feeding

A

high insulin and glucose levels

levels of FFA fall

430
Q

ingested glucose helps to replenish what?

A

glycogen stores both in liver n in muscle

431
Q

what is the site of insulin and glucagon secretion in the endocrine pancreas?

A

islet of langerhans

432
Q

which cells in the islet of langerhans secrete insulin?

A

beta cells

433
Q

which cells in the islet of langerhans secrete glucagon?

A

alpha cells

434
Q

which effect (paracrine ‘crosstalk’) is lost in diabetes?

A

paracrine ‘crosstalk’ btwn alpha n beta cells is physiological
ie local insulin release inhibits glucagon. an effect lost in diabetes

435
Q

what is the transporter for glucose to enter beta cell?

A

GLUT2 glucose transporter

436
Q

???how does glucose go to insulin in muscle n fat cells

A

??confused?glucose enters cell via GLUT4 (glucose transporter 4)
GLUT4 vesicle mobilisation to plasma membrane
intracellular GLUT4 vesicles
intracellular signalling cascades
insulin receptor
insulin

437
Q

how does insulin impact hepatic glucose output

A

suppresses

decreases glycogenolysis and gluconeogenesis

438
Q

how does glucagon impact hepatic glucose output

A

increases glucogeolysis n gluconeogenesis

439
Q

how do insulin n glucagon differ in peripheral glucose uptake

A

insulin - increases into insulin sensitive tissues eg muscle, fat
glucagon reduces

440
Q

does insulin suppress or stimulate lipolysis n muscle breakdown?

A

suppresses

441
Q

does glucagon suppress or stimulate lipolysis n muscle breakdown?

A

stimulates

442
Q

counterregulatory hormones such as adrenaline, cortisol and GH have similar effects to what???

A

glucagon

they become relevant inc certain disease states inc diabetes

443
Q

what does insipid mean?

A

dilute n odourless

hence in DI, kidneys pass abnormally large amt of insipid urine

444
Q

what is the diff btwn diabetes insipid n mellitus

A

insipidus - normal blood glucose levels; kidneys cannot balance fluid in the body
mellitus - high blood glucose

445
Q

how would u describe t1 diabetes?

A

an insulin deficiency disease characterised by loss of beta cells due to autoimmune destruction

446
Q

what does failure of insulin secretion lead to?

A

continued breakdown of liver glycogen
unrestrained lipolysis n skeletal muscle breakdown providing gluconeogeneic precursors
inappropriate increase in hepatic glucose output n suppression of peripheral glucose uptake

447
Q

rising glucose conc results in increased urinary glucose _____?

A

losses …as renal threshold (10mM) is exceeded

448
Q

failure to treat with insulin leads to WHAT?(3)

A

increase in circulating glucagon, further increasing glucose
perceived ‘stress’ leads to increased cortisol and adrenaline
progressive catabolic state and increasing levels of ketones

449
Q

how does ketoacidosis happen?

A

absence of insulin and rising counter regulatory hormones leads to increasing hyperglycaemia and rising ketones

450
Q

what do ketones cause?

A

anorexia n vomiting

451
Q

what is IGT?

A

impaired glucose tolerance

pre-diabetic state of hyperglycaemia (associated with insulin resistance an increased risk of CV pathology)

452
Q

impaired insulin action leads to what?

A

reduced muscle/fat uptake after eating
failure to suppress lipolysis n high circulating FFAs
abnormally high glucose output after a meal

453
Q

what’s the diff btwn t1/t2 diabetes????

A

t1 - severe insulin deficiency due to autoimmune destruction of beta cell, initiated by genetic susceptibility n env triggers
t2 - insulin resistance n impaired insulin secretion due to a combo of genetic predisposition and env factors

454
Q

why doesn’t DKA happening t2 diabetes?

A

low insulin levels r sufficient to suppress catabolism and prevent ketogenesis

can happen if hormones such as adrenaline rise to high levels

455
Q

why does obesity cause t2 diabetes?

A

obesity impairs insulin action. in those already insulin resistant/predisposed, this brings out diabetes at an early stage

456
Q

in t1d, what should basal insulin control?

A

blood glucose in btwn meals n particularly during night

457
Q

basal insulin is adjusted to maintain fasting glucose btwn what?

A

5-7 mmol/L

458
Q

how does insulin differ in t1dm vs t2dm?

A

t1 - insulin deficiency

t2 - insulin resistance

459
Q

what’s the diff btwn basal n prandial insulin?

A

basal - long-acting

prandial - rapid-acting/meal time

460
Q

prandial insulins mimic meal-time insulin secretion and their faster action allows for what?

A

greater flexibility at meal times

461
Q

what are the adv of basal insulin in t2 diabetes?

A

simple for patient, adjust insulin themselves, based on fasting glucose measurements
carries on w oral therapy
less risk of hypoglycaemia at night

462
Q

what are the disadvantages of basal insulin in t2 diabetes?

A

doesn’t cover meals

best used with long-acting insulin analogues which are considered exp

463
Q

what are the adv of pre-mixed insulin?

A

both basal n prandial components in a single insulin prep

can cover insulin requirements through most of the day

464
Q

what are the disadvantages of pre-mixed insulin today?

A

not physiological
requires consistent meal n exercise pattern
increased risk for nocturnal hypoglycaemia

465
Q

what is the definition of hypoglycaemia

A

low plasma glucose causing impaired brain function neuroglycopenia 3mmol/l

466
Q

what is mild hypoglycaemia vs severe

A

mild - self-treated (many epodes asymptomatic)

severe - requiring help for recovery (excepting children)

467
Q

what are the 3 types of hypoglycaemia symptoms n some examples of each?

A

autonomic: trembling, palpitations, sweating, anxiety, hunger
neuroglycopenic: difficult concentration, confusion, weakness, dizziness, vision changes, difficulty speaking
non-specific: nausea, headache

468
Q

what is neuroglycopenia?

A

shortage of glucose (glycopenia) in the brain, usually due to hypoglycemia.

glycopenia affects the function of neurons, and alters brain function and behaviour

469
Q

in most patients, what prevents severe hypoglycaemia/

A

counter regulatory n symptomatic defences

470
Q

in t1dm, what are some risk factors for severe hypoglycaemia

A 
history of severe episodes
HbA1c < 6.5% (48mmol/mol)
long duration of diabetes
renal impairment
extremities of age
471
Q

in t2dm, what are some risk factors for severe hypoglycaemia

A 
advancing age
cog impairment
depression
aggressive glycaemia treatment
duration of MDI insulin therapy
renal impairment n other comorbidities
472
Q

what are some consequences of hypoglycaemia?

A 
accidents
fear
QOL
prevents desirable glucose targets
CV risk
seizures
coma
cog dysfunction
473
Q

what are glucose targets like in t1dm/t2dm?

A

aim for lowest hba1c not associated w freq hypoglycaemia
it may sometimes be appropriate to relax targets in patients w advanced disease, complications or limited life expectancy

474
Q

a target of hba1c < 7.5% (58 mmol/mol) is good 4 what?

A

few comorbidities
good physical function
preserved cog function

475
Q

a target of hba1c < 8% (64 mmol/mol) is good 4 what?

A

multiple chronic illnesses
mild cog impairment
risk of falls n hypoglycaemia

476
Q

a target of hba1c < 8.5% (69 mmol/mol) is good 4 what?

A

end-stage chronic illness
moderate-to-severe cog impairment
in long-term care

477
Q

what are some strategies to prevent hypoglycaemia?

A

discuss risk factors w patients on insulin
educate patients n caregivers on how to recognise n treat it
instruct patients to report episodes to doctor

478
Q

what are the 5 steps to treating hypoglycaemia?

A
  1. recognise symptoms so they can be treated asap
  2. confirm need for treatment (blood glucose <3.9mmol/mol is the alert value)
  3. treat w 15g fast-acting carb to relieve symptoms
  4. retest in 15mins to ensure blood glucose >4.0 mmol/mol n retreat if needed
  5. eat long-acting carb to prevent recurrence
479
Q

what is the alert value for hypoglycaemia in treatment?

A

<3.9mmol/mol

480
Q

what is an inevitable side effect of diabetes treatment

A

hypolycaemia

481
Q

why does hypoglycaemia occur?

A

due to inability of insulin therapy to mimic physiology of beta cell

482
Q

what does metformin help?

A

liver

inhibition of glucose prod and increase in hepatic insulin sensitivity

483
Q

nocturia

A

excessive nighttime urination

484
Q

what does NAD stand for? (2)

A

no abnormality detected
OR
no apparent distress

485
Q

what are incretins

A

hormones secreted by intestinal endocrine cells in response to nutrient uptake

486
Q

how do incretins influence glucose homeostasis

A 
via multiple actions
including:
glucose-dependant insulin secretion
postprandial glucagon suppression
slowing of gastric emptying
487
Q

when are incretins secreted

A

by the gut, into circulation in response to food

488
Q

name 3 antihyperglycaemics

A

metformin
SUs (sulfonylureas)
TZDs (thiazolidinediones)

489
Q

what are SUs

A

sulfonylureas, antihyperglycaemics

490
Q

what are TZDs

A

thiazolidinediones, antihyperglycaemics

491
Q

what are the benefits of using metformin as an anti hyperglycaemic?

A

low risk of hypoglycaemia
BP reduction
cardioprotective benefits

492
Q

what are the drawbacks of using metformin as an anti hyperglycaemic?

A 
lactic acidosis (rare)
caution indicated in older patients w CHF
493
Q

how does metformin affect weight?

A

weight neutral or slight weight loss

494
Q

what are the benefits of using SUs (sulfonylureas) as an anti hyperglycaemic?

A

newer class entrants may have reduced CV risk

495
Q

what are the drawbacks of using SUs (sulfonylureas) as an anti hyperglycaemic?

A

may increase risk of CV events

hypoglycaemia

496
Q

how do SUs affect weight?

A

weight gain

497
Q

what are the benefits of using TZDs (thiazolodinediones) as an anti hyperglycaemic?

A

low risk of hypoglycaemia

positive effects on biomarkers

498
Q

what are the drawbacks of TZDs as an antihyperglycaemic?

A

increased CV risk

lipid abnormalities

499
Q

how do TZDs affect weight?

A

weight gain

(SG) Phase 2A lectures (14 decks)

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