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BRS Y2 > endocrinology > Flashcards

endocrinology Flashcards

1
Q

what are the anterior pituitary hormones

A

GH
FSH/LH
TSH
prolactin
ACTH

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2
Q

what happens in primary hypothyroidism

A

T3 and T4 decrease
TSH increase

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3
Q

what happens in secondary hypothyroidism

A

TSH decrease
T3 and T4 decrease

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4
Q

what happens in primary hypoadrenalism

A

cortisol decrease
ACTH increase

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5
Q

what happens in secondary hypoadrenalism

A

ACTH decrease
cortisol decrease

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6
Q

suggest a cause of secondary hypoadrenalism

A

pituitary tumor damage corticotrophs, cannot make ACTH

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7
Q

suggest a cause of primary hypoadrenalism

A

desrtcution fo adrenal cortex (eg autoimmune)

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8
Q

suggest a cause of secondary hypothyroidism

A

pituitary tumor damage thyrotrophs

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9
Q

suggest a cause of primary hypothyroidism

A

autoimmune destruction of thyroid gland

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10
Q

what happens in primary hypogonadism

A

decrease oestrogen/testosterone
increase FSH and LH

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11
Q

what happens in secondary hypogonadism

A

decrease FSH/LH
decrease oestrogen/testosterone

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12
Q

suggest a cause of primary hypogonadism

A

destruction of testis (mumps) or ovaries (chemo)

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13
Q

suggest a cause of secondary hypogonadism

A

pituitary tumor damage gonadotrophs

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14
Q

congenital causes of hypopituitarism

A

mutations of transcirption factor
deficient in GH and at least 1more anterior pituitary hormone

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15
Q

acquired causes of hypopituitarism

A

tumors, radiation, paituitary surgery, infection, traumatic brain injury

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16
Q

what is the name of total loss f anterior and posterior pituitary function

A

panhypopituitarism

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17
Q

why radiotherapy can cause radiotherapy induced hypopituitarism

A

pituitary and hypothalamus are both sensitive to radiation

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18
Q

which hormones are most sensitive to radiotherapy

A

GH and gonadotrophins

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19
Q

what is sheehan’s syndrome

A

post-partum hypopituitarism secondary to hypotension
may lead to pituitary infarction

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20
Q

symptoms of Sheehan’s syndrome

A

lethargy, anorexia, weight loss, failure of lactation (PRL deficiency), posterior pituitary usually not affected, failure to resume menses post delivery, TSH/ ACTH/ GH deficiency

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21
Q

how to radiologically visualise pituitary gland

A

MRI

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22
Q

what is pituitary apoplexy

A

bleeding into pituitary
may be first presentation of pituitary adenoma

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23
Q

symptoms of pituitary apoplexy

A

sudden onset headache
visual field detected
bitemporal hemianopia
diplopia (double vision)
ptosis(drop eyelid)

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24
Q

what are biochemical ways to diagnosis hypopituitarism

A

9am cortisol
T4
FSH/LH
GH/ACTH

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25
Q

how to test ACTH and GH for hypopituitarism

A

insulin induced hypoglycaemia, cause GH and ACTH release (measure cortisol)
TRH stimulates TSH release
GnRH stimulates FSH and LH release

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26
Q

which anterior hormone cannot be replaced

A

PRL

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27
Q

what is the treatment for GH deficiency

A

daily injection (no oral option)
measure response by improvement in QoL and plasma IGF-1

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28
Q

what treatment for TSH deficiency for both primary and secondary hypopituitarism

A

daily T4 (levothyroxine) once
aim for fT4 above middle of reference range
cannot use this to adjust dose in secodnary hypopituitarism as TSH is low

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29
Q

what treatment for ACTH deficiency

A

replace cortisol rather than ACTh
prednisolone or hydrocortisone (replacement steroids)

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30
Q

which group of patients are at risk of adrenal crisis

A

pt with priamry adrenal failure (Addison’s) or secodnary adrenal failure (ACTH defiicency)

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31
Q

features of adrenal crisis

A

dizzy
hypotension
vomit
weakness
collapse and death can be resulted

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32
Q

what are sick day roles for pt who take replacement steroid

A

steroid alert bracelet
double glucocorticoid dose if fever
unable to take tablets, inject or go A&E

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33
Q

treatment for FSH/LH deficiency in men with no fertility required

A

replace testosterone (as this does not restore sperm production, which is dependent on LH and FSH)
measure plasma testosterone

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34
Q

treatment for FSH/LH deficiency in men with fertility required

A

introduction of spermatogenesis by gonadotrophin injections
best response if secondary hypogonadism occurs after puberty
measure testosterone and semen analysis

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35
Q

treatment for FSH/LH deficiency in women with no fertility required

A

replace oestrogen (oral or topical)
need additional progestogen if intact
uterus to prevent endometrial hyperplasia)

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36
Q

treatment for FSH/LH deficiency in women with fertility required

A

induce ovulation by carefully timed gonadotrophin injections (IVF)

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37
Q

what are posterior pituitary hormones

A

oxytocin
AVP

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38
Q

function of AVP

A

stimulate water reabsorption
vasoconstrictor via V1 receptor
stimulates ACTH release from anterior pituitary

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39
Q

which receptor does AVP act on to stimulate water reabsorption

A

V2 receptor in kidney

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40
Q

how to visualise posterior pituitary

A

MRI
posterior bright spot

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41
Q

what are the 2 problems with AVP not working

A

AVP-D
AVP-R

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42
Q

what is AVP-D

A

cranial diabetes insipidus
problem with hypothalamus/posterior pituitary
unable to make AVP

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43
Q

what is AVP-R

A

nephrogenic diabetes insipidus
can make AVP normally but kidney/collecting duct not responding

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44
Q

what are the presentations of AVP-R or AVP-D

A

polyuria
nocturia
thirst
polydipsia

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45
Q

how can AVP-D / AVP-R cause death

A

polydipsia then dehydration then death

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46
Q

causes of AVP-D

A

acquired:
traumatic brain injury
pituitary surgery
pituitary tumors
inflammation of pituitary stalk eg TB
autoimmune
congenital rarer than acquired

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47
Q

causes of AVP-R

A

congenital:
mutation in gene encoding V2 receptor
acquired:
drugs (eg lithium)

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48
Q

what are the plasma presentations for AVP-R / AVP-D

A

increased concentration as pt becomes dehydrated
increase sodium
glucose normal

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49
Q

how psychogenic polydipsia mimic AVP -D or AVP-R

A

also have polydipsia, polyuria, nocturia
but not problem with AVP
symptoms arise from drinking too much

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50
Q

how to distinguish between psychogenic polydipsia and AVP-R AVP-D

A

water deprivation test
over time measure urine vol and conc and plasma conc

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51
Q

why do we needa weigh in water deprivation test

A

if lose >3% body weight it is a marker for AVP-R or AVP-D

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52
Q

how to distinguish AVP-D and AVP-R

A

give desmopressin
(works similar to AVP)
AVP-D responses to desmopressin so urine concentrates but AVP-R no increase in urine osmolarity as kidney don’t respond

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53
Q

treatment for AVP-D

A

replace AVP using desmopressin selective for V2 receptor
(tablets or intranasal)

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54
Q

what is syndrome of Inappropriate ADH (SIADH)

A

too much AVP, reduced urine output

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55
Q

presentations of SIADH

A

high urine osmolarity
low plasma osmolarity
low plasma sodium

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56
Q

causes of SIADH

A

CNS (head injury, stroke, tumor)
lung infections pneumonia)
malignancy (lung cancer small cell)
drug related (anti-depressants, anti-epileptics)
idiopathic

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57
Q

management of SIADH

A

fluid restrict
use vasopressin receptor antagonist (but expensive)

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58
Q

which 2 hormones increase serum calcium

A

PTH
Vitamin D

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59
Q

which hormone reduce serum calcium

A

calcitonin

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60
Q

steps for Vit D metabolism

A

7-dehydrocholesterol -> pre vitamin D3 -> Vit D3 -> 25(OH)cholecalciferol via 25 hydroxtlase -> 1,25(OH)2 cholecalciferol via 1 alpha hydroxylase -> calcitriol (Vit D)`

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61
Q

effect of Calcitriol

A

bones: increase Ca2+ and PO4 3- reabsorption
kidney: increase Ca2+ and PO4 3- reabsorption
gut: increase Ca2+ and PO4 3- absorption

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62
Q

effect of PTH

A

bones: binds to osteoblast to signal osteoclast to cause bone resoprtion to increase Ca2+ resorption from bone to bloodstream
kidney: increase Ca2+ reabsorption, increase PO4 3- excretion thru urine, increase 1 alpha hydroxylase activity to increase Calcitriol
gut: increase Ca2+ and PO4 3- absorption

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63
Q

effect of FGF23 to regulate serum phosphate

A

FGF23 inhibit phosphate transporter / reabsorption in kidney
reduce phosphate reabsorption thru gut
PTH also inhibits reabsorption of Phosphate thru blocking Na+/PO4 3- co-transporter

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64
Q

symptoms of hypocalcaemia

A

sensities excitable tissues
muslce cramps
tetany
tingling
paraesthesia
convulsions
arrhythmias

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65
Q

what are the 2 signs caused by hypocalcemia

A

chvosteks’ sign (facial paresthesia, twitch infacial msucle when gently tapping on patient’s cheek bone))
trousseau’s sign (carpopedal spasm, contract without relaxing)

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66
Q

causes of hypocalcaemia

A

hypoparathyroidism - low PTH level(surgical neck surgery, auto-immune, congenital)
low Vit D (deficiency, lack UV, impaired production due to renal failure)

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67
Q

symptoms of hypercalcaemia

A

CNS, GI, Psych effects
reduced neuronal excitability (atonal muscle), stones, abdominal moans, psychic groans

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68
Q

causes of hypercalcaemia

A

hyperparathyroidism
malignancy
XS Vit D

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69
Q

what happens in primary hyperparathyroidism

A

Ca increase, but PTH still high, so low phosphate as well
(no negative feedback)
due to parathyroid adenoma producing too much PTH

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70
Q

treatment for primary hyperparathyroidism

A

parathyroidectomy

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71
Q

risks of parathyroidectomy

A

osteoporosis (cause reduce BMD, increase risk of fractures)
renal calculi (stones)
psychological impact(mood, mental function)

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72
Q

what happens in secondary hyperparathyroidism

A

normal physiological response to hypocalcaemia
low Ca, high PTH

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73
Q

causes of secondary hyperthyroidism

A

Vit D deficiency
renal failure -> cannot make calcitriol

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74
Q

treatment for secondary hyperparathyroidism in normal patients

A

Vit D replacement
- ergocalciferol
- cholecalciferol
can give as patient can convert this to calcitriol via 1 alpha hydroxylase

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75
Q

treatment for secondary hyperparathyroidism in renal failure patients

A

give alfacalcitriol (active Vit D) as patients hv inadequate 1 alpha hydroxylase, cannot activate 25 hydroxy Vit D preparations

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76
Q

what happens in tertiary hyperparathyroidism

A

initially Ca falls and PTH rises, but overtime high PTH drives enlarged parathyroid gland to increase Ca
chronic renal failure
chronic Vit D deficiency
cammot make calcitriol, PTH increases
Parathyroid gland enlarge

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77
Q

treatment for tertiary hyperparathyroidism

A

parathyroidectomy

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78
Q

how to diagnose hypercalcaemia

A

check PTH

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79
Q

what happens in hypercalcaemia malignancy

A

high Ca
suppressed PTH

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80
Q

how to diagnose Vit D deficiency

A

low calcium
high PTH (secondary to low Ca)

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81
Q

how do we measure Vit D

A

measure 25 (OH) cholecalciferol (as calcitriol is difficult to measure)

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82
Q

does PTH stimulate osteoblast or osteoclast

A

osteoblast

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83
Q

what are some osteoclast activating factor

A

RANKL, receptor activator of nuclear factor kappa-B ligand

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84
Q

what inhibits bone resportion in osteoclast

A

bisphosphonates

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85
Q

what is crytorchidism

A

failure of one or both testes to descend into the scrotum
most stay in inguinal canal

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86
Q

what is endometriosis

A

presence of functioning endometrial tissue outside of uterus

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87
Q

symptoms of endometriosis

A

increase menstrual pain
menstrual irregularities
deep dyspareunia (pain before/during/after sex)
infertility

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88
Q

what is fibroids

A

benign myometrium tumors

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89
Q

symptoms of fibroids

A

usually asymptomatic
increase menstrual pain
menstrual irregularities
deep dyspareunia
infertility

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90
Q

causes of endocrine male infertility in hypothalamus (3)

A

congenital hypogonadotrophic hypogonadism
acquired hypogonadotrophic hypogonadism
hyperlactinaemia

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91
Q

what happens in hypogonadotrophic hypogonadism in hypothalamus

A

decrease GnRH
decrease LH & FSH
decrease T / E2

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92
Q

causes of endocrine male infertility in pituitary

A

hypopituitarism (tumor, infiltration, apoplexy, surgery, radiation)

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93
Q

what happens in hypogonadotrophic hypogonadism in anterior pituitary gland

A

decrease LH & FSH
decrease T / E2

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94
Q

causes of endocrine male infertility in gonads

A

congenital pituitary hypogonadism
(Klinefelters)
acquired pituitary hypogonadism (cryptorchidism, trauma, chemo,radiation)

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95
Q

what happens in hypergonadotrophic hypogonadism in gonads

A

increase LH &FSH
decrease T / E2

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96
Q

what is Kallmann Syndrome

A

failure of migration of GnRH neurons with olfactory fibres, accompanied with failure of puberty and infertility

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97
Q

how hyperprolactinaemia affect HPA

A

prolactin binds to prolactin receptors on kisspeptin neurones
inhibit kisspeptin release
decrease GnRH, LH, FSH, Tor O
inferitility, oligo, amenorrjea

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98
Q

symptoms of klinefelters syndrome

A

tall stature
decrease facial hair
breast development
small penis and testes
mildly impaired IQ
narrow shoulders
reduced chest hair
wide hips
low bone density
infertility

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99
Q

what are the key hx for male infetility

A

duration
previous children
pubertal milestones
associated symptoms

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100
Q

what are the key examination of male infertility

A

BMI
sexual characteristics
testicular vol
anosmia

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101
Q

key investigations of male infertility

A

semen analysis
blood tests
imaging

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102
Q

treatment for male infertility

A

dopamine agonist for hyperPRL
gonadotrophin treatment for fertility
testosterone
surgery
optimise BMI
smoking cessation
alcohol reduction/cessation

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103
Q

what pattern will u see in premature ovarian insufficiency for FSH LH and oestradiol

A

increase FSH & LH
decrease oestradiol

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104
Q

causes of premature ovarian insufficiency

A

autoimme
turner’s syndrome (genetic)
cancer therapy

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105
Q

what pattern will u see in anorexia nervosa induced amenorrhea for FSH LH and oestradiol

A

all decrease

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106
Q

what is PCOS

A

irregular periods
XS androgen in female
polycystic ovaries enlarged with lots of fluid filled sac surrounding egg

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107
Q

PCOS treatment for infertility

A

ovulation induction (IVF)

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108
Q

PCOS treatment for irregular menses/amenorrhoea

A

oral contraceptive pill
metformin

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109
Q

PCOS treatment for increase insulin resistance

A

metformin
diet/lfiestyle changes

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110
Q

PCOS treatment for endometrial cancer risk

A

progesterone courses

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111
Q

PCOS treatment for hirsutism

A

anti-androgens
creams, laser, waxing

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112
Q

Symptoms of Turners Syndrome

A

short stature
low hairline
shield chest
wide spaced nipples
coarctation of aorta
poor breast development
amenorrhoea
underdeveloped reproductive tract
small fingernails

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113
Q

female infertility key hx

A

duration, previous children, pubertal milestones, menstrual hx, medications

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114
Q

female infertility key exams

A

BMI
sexual characteristics
hyperandrogenism signs
anosmia

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115
Q

key investigations for female infertility

A

blood test
pregnancy test
imaging

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116
Q

why in testosterone replacement need at least 2 fasting measurements of serum testosterone in morning

A

food can decrease testosterone temporarily

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117
Q

what are some testosterone replacement safety monitorings

A

increased Hct (as testosterone increase blood cells)
risk of hyperviscosity and stroke
prostate (prostate specific antigen level)

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118
Q

what is secondary hypogonadism

A

deficiency of gonadotrophins (LH/FSH) –> hypogonadotrophic hypogonadism

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119
Q

importance of gonadotrophins (LH, FSH)

A

induce spermatogenesis

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120
Q

function of LH in sperm induction

A

LH stimualtes leydig cells to increase intratesticular testosterone levels

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121
Q

function of FSH in sperm induction

A

stimulates seminiferous tubule development and spermatogenesis

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122
Q

why we should not give testosterone to men desiring fertility

A

testosterone can further reduce LH/FSH and worsen spermatogenesis

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123
Q

what are some treatments for inducing spermatogenesis

A

hcG injections (act on LH receptors to increase LH)
if no response then FSH injections

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124
Q

how letrozole triggers ovulation

A

letrozole acts on aromatase, cause low oestradiol, decreased -ve feedback , cause higher GnRH and hence increase FSH/LH to induce ovulation

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125
Q

where does clomiphene act on to induce ovulation

A

oestrogen receptor to reduce negative feedback of oestradiol

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126
Q

how does oral contraceptive pills work on HPG axis

A

contains and aim to increase oestrogen and progesterone
1. reduce ovulation in ovaries
2. progesterone cause thickening of cervical mucus
3. cause thinning of endometrial lining to reduce implantation

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127
Q

what are some non contraceptive uses for combined oral contraceptive pills

A
  1. make periods lighter and less painful
  2. regular withdrawal bleeds or no bleeds
  3. reduce LH and hyperandrogenism (acne/hirsutism)
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128
Q

what are some long acting reversible contraceptives

A
  1. coils
  2. intra-uterine device (copper coil)
  3. itranuterine systems to secrete progesterone
    progesterone - only injectable contraceptives or subdermal implants
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129
Q

what are some emergency contraceptives

A

copper intrauterine device (IUD)
ulipristal acetate (stops progesterone and prevent ovulation)
levonorgestrel (prevents ovulation)

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130
Q

benefits of HRT (menopause hormone treatment)

A
  1. relief symptoms due to low oestrogen (low mood, flushing, disturbed sleep etc)
  2. reduction in osteoporosis related fractures
  3. transdermal reduce risk of VTE and stroke
  4. lower risk of CVD in ypunger
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131
Q

risks of HRT

A
  1. venous thrombo embolism
  2. pulmonary embolism
  3. Hormone sensitive cancer (breast, ovarian)
  4. endometrial cancer (must prescribe progesterone in women with endometrium)
  5. CVD, stroke
    oral will increase clotting factor
    transdermal oestrgens are safer for VTE than oral
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132
Q

what is precurosr of steroid

A

cholesterol

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133
Q

which part secretes corticosteroids

A

adrenal cortex

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134
Q

example of corticosteroids

A

mineralcorticoids (aldosterone)
glucocorticoids (cortisol)
sex steroids (androgens, oestrogens)

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135
Q

effect of angiotensin ll on adrenals

A

activate metabolic enzymes to increase corticosteroids production

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136
Q

effect of aldosterone

A

controls BP and sodium
lowers potassium

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137
Q

activation of enzymes ti form aldosterone

A

side chain cleavage
3 hydrosteroid dehydrogenase, 21,11,18 hydroxylase

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138
Q

activation of enzymes to form cortisol

A

3,17,21,11

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139
Q

what rhythm does cortisol have

A

diurnal

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140
Q

what is Addison’s disease

A

primary adrenal failure
autoimmune, immune system destroys adrenal cortex

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141
Q

what happens in Addison’s

A

pituitary secretes lots of ACTh hence MSH , so skin has hyperpigmentation

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142
Q

symptoms of Addison’s

A

hyperpigmentation in skin
low BP
weakness
weight loss
vitiligo
n+v
diarrhea
constipation
abdominal pain

143
Q

what is pro-opio-melanocortin (POMC)

A

POMC is large precursor of protein cleaved to form smaller peptides eg ACTH, MSH, endorphines
high levels of ACTh become tanned in pt

144
Q

causes of adrenocorticoid failure

A

adrenal glands destroyed
missing enzymes in steroid synthetic pathway
tuberculosis addison’s disease
autoimmune addison’s disaese
congential adrenal hyperplasia

145
Q

consequecnes of adrenocorticoid failure

A

BP fall
loss salt in urine, low NA in plasma (hyponatraemia)
increased plasma potassium(less potassium excreted in urine)
low glucose due to glucocorticoid deficiency
high ACTH cause increased pigmentation
death due to severe hypotension

146
Q

tests of addison’s

A

9am cortisol
clincial:fatigue
blood tests: biochem (low Na, high K)
high ACTH
short synACTHen test

147
Q

primary adrenocorticoid failure treatments

A

repalce cortisol and aldosterone
no need to replace adrenal sex steroids (gonads)

148
Q

why use fludrocortisone than aldosterone for primary adrenocortical failure

A

half life of aldosterone too short for safe once daily administration, fludrocortisone longer acting

149
Q

what is congenital hyperplasia

A

21-hydroxylase deficiency
(can be complete or partial)

150
Q

which hormone will be totoally absent in complete 21-hydroxylase deficiency

A

aldsterone and cortisol

151
Q

how long can babies survive in complete 21-hydroxylase deficiency

A

babies present within 1-3 weeks with a salt losing crisis

152
Q

which hormones will be in excess in complete 21-hydroxylase deficiency

A

sex steroids (androgens, estrogens and progestogens.)
and testosterone

153
Q

which hormones will be in deficient in partial 21-hydroxylase deficiency

A

cortisol and aldosterone

154
Q

which hormones will be in excess in partial 21-hydroxylase deficiency

A

sex steroids and testosterone

155
Q

main problem in girls in partial 21-hydroxylase deficiency

A

hirsutism
virilisation

156
Q

what happens in 11 hydroxylase deficiency

A

accumulate of 11-deoxycorticosteroe
not enough cortisol to inhibit ACTH
chronic adrenal overactivity

157
Q

which hormone does 11 deoxycorticosterone behave like

A

mineralocorticoid

158
Q

what happens to excess aldosterone / 11 deoxycorticosterone

A

hypertension
hypokalaemia

159
Q

which hormones will be in deficient in 11-hydroxylase deficiency

A

cortisol
aldosterone

160
Q

which hormones will be in excess in 11-hydroxylase deficiency

A

sex steroids
testosterone
11-deoxycorticosterone

161
Q

what problems are in 11-hydroxylase deficiency

A

virilisation
hypertension
hypokalaemia

162
Q

which hormones will be in deficient in 17-hydroxylase deficiency

A

cortisol
sex steroids

163
Q

which hormones will be in excess in 17-hydroxylase deficiency

A

aldosterone
11 deoxycorticosterone

164
Q

what problems are in 17-hydroxylase deficiency

A

hypertension
hypokalaemia
sex steroids deficiency
cortisold deficiency

165
Q

clinical features of Cushing’s

A

centripetal obesity
moon face
buffalo hump
proximal myopathy
hypertension
hypokaelemia
red striae
thin skin
bruising
osteroporosis
diabetes

166
Q

role of 11B-hydroxysteroid dehydrogenase

A

stops cortisol from activating aldosterone receptors
turns cortisol to cortisone (inactive form)

167
Q

causes of Cushing’s

A

take too many steroids
pituitary dependent (cause Cushing’s disease)
ectopic ACTH from lung cancer
adrenal adenoma secretes cortisol

168
Q

tests to determine cause of Cushinhg’s syndrome

A

24hr urine collection for urinary free cortisol
blood diurnal cortisol levels (highest at 9am and lowest at midnight if asleep)
low dose dexamethasone suppresion test

169
Q

what happens to the rhythm of cortisol in cushings

A

high all the time

170
Q

what is dexamethasone

A

artificial glucocorticoid (steroid)

171
Q

how healthy people and Cushing’s pt respond to dexamethasone

A

healthy: suppress cortisol to 0
Cushing’s : fail to suppress cortisol

172
Q

what are some pharmaclogical manipiulation of steroids

A

enzyme inhibitors
receptor blockign drugs

173
Q

what is metyrapone

A

inhibit steroid biosynthesis
11B-hydroxylase inhibitor

174
Q

what is the mechanism of metyrapone

A

inhibit 11B-hydroxylase
arrest steroid synthesis in zona fasciculata and reticularis at 11-deoxycortisol stage
11-deoxycortisol has no negtaive feedback on hypothalamus and pituitary gland

175
Q

what are the uses of metyrapone

A

control cushing’s syndrome prior to surgery
improve pt symptoms and promote better post-op recovery
control cushing’s symptoms after radiotherapy

176
Q

unwanted side effects on metyrapone

A

hypertension on long term administration
hirsutism

177
Q

mechanism of ketoconazole

A

inhibit 17-hydroxylase
use as antifungal agent
at higher conc inhibits steroidogenesis

178
Q

uses of ketoconazole

A

treatment and control cushing’s symptoms prior surgery
orally active

179
Q

unwanted side effects of ketoconazole

A

liver damage

180
Q

mechanism of osilidrostat

A

inhibit 11&17 hydroxylase
block several enzyme in steroid synthetic pathway

181
Q

what are some surgical treatment of cushing’s

A

pituitary surgery
bilateral adrenalectomy
unilateral adrenalectomy for adrenal mass (for single adrenal tumor)

182
Q

medical treatment for cushing’s

A

metyrapone
ketoconazole
osilidrostat

183
Q

what is conn’s syndrome

A

benign adrenal cortical tumor
aldosterone in XS
hypertension and hypokalaemia

184
Q

what are the action of aldosterone

A

increase renal sodium and potassium reabsorption
increase BP (sodium and water retention)

185
Q

how to diagnose Conn’s syndrome

A

primary hyperaldosteronism
RA system should be suppressed

186
Q

what are medixal treatments for Conn’s Syndrome

A

Mineralocorticoid antagonist
spironolactone
epleronone

187
Q

mechanism of spironolactone

A

competitive antagonist of mineralocorticoid receptor
blocks Na+ reabsorption and K+ excretion in kidney tubules

188
Q

unwanted side effects of spironolactone

A

gynaecomastia (androgenr eceptor)

189
Q

mechanism of epleronone

A

MR antagonist
similar affinity to MR compared to spironolactone
less binding to androgen and receptors compared to spironolactone, better tolerated

190
Q

what are phaeochromocytomas

A

adrenal tumors in medulla to secrete catecholamines

191
Q

clinical features of phaeochromocytomas

A

hypertension in young ppl
episodic severe hypertension, cause stroke or MI
more common in certain inherited conditions
high adrenaline may cause ventricular fibrillation and death

192
Q

treatment of phaeochromocytomas

A

alpha blocker
pt may need IV fluid as alpha blockade commences
beta blockade to prevent tachycardia

193
Q

what are the anterior pituitary cells and their respective hormones (5)

A

somatotrophs– GH
lactotrophs – prolactin
Thyrotrophs – TSH
gonadotrophs – FSH/LH
corticotrophs – Adrenocorticotrophic hormone (ACTH, corticotrophin)

194
Q

what are the anterior pituitary tumors (5)

A

somatotrophs – acromegaly
lactotrophs – prolactinoma
thyrotrophs – TSHoma
Gonadotrophs – gonadotrophinoma
corticotrophs – cushing’s disease (corticotroph adenoma)

195
Q

how to classify pituitary tumor (3)

A

radiological (MRI)
function
benign or malignant

196
Q

how to classify pituitary tumor in terms of radiological MRI

A

size (microadenoma < 1cm and macroadenoma)
sellar or suprasellar
compress optic chiasm or not
invade cavernous sinus or not

197
Q

how to classify pituitary tumor in terms of function

A

excess secretion of specific pituitary hormone or not
if no excretion – non functioning adenoma

198
Q

what is the most common functioning pituitary adenoma

A

prolactinoma
serum of prolactinoma con proportional to tumor size

199
Q

presentations of prolactinoma

A

menstrual disturbance
erectile dysfunction
reduced libido
galactorrhoea
subfertility

200
Q

physiological causes of elevated prolactin

A

pregnancy
breastfeeding
streess
venepuncture
nipple stimulation

201
Q

pathological causes of elevated prolactin

A

primary hypothyroidism
PCOS
chronic renal failure

202
Q

iatrogenic causes of elevated prolactin

A

antypsychotics
SSRIs
anti emetics
high dose oestrogen
opiates

203
Q

treatment of prolactinoma

A

first line: medical
doopamine receptor agonists
cabergoline

204
Q

how does dopamine receptor agonists work

A

dopamine from hypothalamic dopaminergic neurones/ D2 receptor agonists bind to D2 receptors on anterior pituitary lactotrophs
inhibit release of prolactin

205
Q

mechanisms of GH action

A

somatotrophs release GH–> stimulate body tissues / stimulate liver to release IGF-1 and IGF-2 to stimulate body tissues –> stimualte growth and development

206
Q

how to diagnose acromegaly

A

elevated serum IGF-1
oral glucose tolerance test – failed suppression of GH following oral glucose load
once confirmed GH XS, use MRI to confirm pituitary tumor

207
Q

what risk is associated with untreated acromegaly

A

cardiovascular risk

208
Q

treatment for acromegaly

A

first line: surgical (trans-sphenoidal pitutiary surgery)
use medical (somatostatin analogues, dopamine agonists) prior to surgery to shrink tumor or if surgical resection incomplete

209
Q

what is pattern of GH secretion

A

pulsatile – random measurement unhelpful to diagnose acromegaly

210
Q

Cushing’s syndrome symptoms

A

osteoporosis
red cheeks
moon face
impaired glucose tolerance
proximal myopathy
easy bruising\thin skin
mental changes

211
Q

what is ACTH dependent Cushing’s disease

A

pituitry corticotroph adenoma

212
Q

what is ACTH independent Cushing’s syndrome

A

taking steroids by mouth
adrenal adenoma or carcinoma

213
Q

what are non functioning pituitary adenomas

A

don’t secrete any specific hormone

214
Q

which symptom is often present in non functioning pituitary adenomas

A

visual disturbance
bitemporal hemianopia

215
Q

why serum prolactin will raise in non functioning pituitary adenomas

A

dopamine cannot travel down pituitary stalk from hypothalamus

216
Q

in primary hypothyroidism, what is the level of TSH

A

high, because lack thyroxine to suppress

217
Q

what is Graves’ Disease

A

autoimmune, hyperthyroidism
Ab binds and stimulate TSH receptor
cause goitre

218
Q

what symptoms seen in Graves’ Disease

A

goitre
exophthalmos cuz other Ab bind to muscles behind the eyes
pretibial myxoedema

219
Q

why goitre in Graves’ Disease

A

Ab binds to and stimulate TSH receptor in thyroid

220
Q

is toxic nodular thyroid disease autoimmune

A

No

221
Q

what is toxic nodular thyroid disease

A

single / mulyiple toxic nodules (multinodular goitre)
benign adenomas overactive at making thyroxine

222
Q

what are the symptoms difference in Graves’ and toxic nodular thyroid disease

A

in toxic nodular thyroid disease there is no pretibial myxoedema and no exophthalmos

223
Q

what are the effects of thyroxine on SNS

A

Sympathetic activation – sensities beta adrenoceptors to ambient levels of adrenaline and Noradrenaline
tachycardia
palpitations
tremor in hands, lid lag

224
Q

symptoms of hyperthyroidism

A

weight loss despite increased appetite
breathlessness
palpitations
tachycardia
sweating
heat intolerance
diarrhoea
lid lag

225
Q

what is thyroid storm

A

when someone with hyperthyroidism has more than 2 below features
hyperpyrexia (> 41 degrees celcius)
accelerated tachycardia
arrhythima
cardiac failure
delirium
frank psychosis
hepatocellular dysfunction
jaundice

226
Q

treatment options for hyperthyroidism

A

surgery (thyroidectomy)
drugs
radioiodine

227
Q

what are the drug classes for treatment in hyperthyroidism

A

thionamides (anti thyroid drugs)
potassium iodide
radioiodine
B-blockers (help w symptoms)

228
Q

mechanism of thionamides

A

inhibit thyroid peroxidase and hence reduce T3/T4 synthesis and secretion

229
Q

unwanted effects of thionamides

A

agranulocytosis
rashes

230
Q

follow up actions after using thionamides

A

aim to stop anti thyroid drug after 18 months
need review periodically including thyroid function tests for remission or relapse

231
Q

what is the role of B blockers in thyrotoxicosis

A

reduce tremor, slower HR, less anxiety

232
Q

mechanism of KI in hyperthyroidism

A

inhibits iodination of thyroglobulin
inhibits peroxide generation and thyoperoxidase

233
Q

problems with thyroidectomy

A

risk of voice change (recurret laryngeal nerve)
risk of losing parathyroid glands
scar
anaesthetic

234
Q

examples of Beta blockers for hyperthyroidism

A

propranolol

235
Q

examples of anti thyroid drug

A

carbimazole
propylthiouracil

236
Q

what is viral (de Quervain’s) thyroiditis

A

painful dysphagia
hyperthyroidism
pyrexia (fever)
thyroid inflammation

237
Q

pathology of viral thyroiditis

A

virus attack thyroid gland
causing pain and tenderness
thyroid stops making thyroxine and makes virus instead
thus no iodine uptake
causing stored thyroxine released
4 weeks later stored thyroxine exhausted
hypothyroid

238
Q

what is T1DM

A

autoimmune
partial or complete deficiency of insulin production

239
Q

which type of DM can present in later life

A

autoimmune diabetes
latent autoimmune diabetes

240
Q

which type of DM can present in childhood

A

T2DM

241
Q

why T1DM may present later

A

orig may hv fully functioning B cells to secrete insulin until autoimmune attack
–> ketoacidosis

242
Q

what is C-peptide

A

product when proinsulin cleaved to insulin

243
Q

symptoms of diabetes

A

polyuria
nocturia
polydypsia
blurring of vision
recurrent infections
weight loss
fatigue

244
Q

signs of diabetes

A

dehydration
hyperventilation
smell of ketones
glycosuria
ketonuria

245
Q

what are the effects of insulin deficiency metabolically

A

proteinolysis
increase hepatic glucose output
lipolysis to increase glycerol and NEFA

246
Q

acute complication of hyperglycaemia

A

diabetic ketoacidosis

247
Q

chronic complication of hyperglycaemia

A

microvascular (retinopathy, neuropathy, nephropathy)
macrovascular (ischaemia heart disease, cerebrovascular disease, peripheral vascular disease)

248
Q

management of T1DM

A

insulin
dietary support
educations
technologies
transplantation

249
Q

why insulin level never drops to 0

A

need insulin to prevent cascade of breaking down fat, to prevent ketoacidosis

250
Q

what are types of short acting insulin

A

human insulin (exact molecular replicate of human insulin)
insulin analogue

251
Q

what are types of long acting insulin

A

bound to zinc or protamine
insulin analogue

252
Q
A
253
Q

relationship between cortisol and insulin

A

cortisol levels become elevated and you become insulin resistant

254
Q

what are transplantation options of T1DM

A

islet cell transplants
simultaneous pancreas and kidney transplants
(both requires life-long immunosuppression)

255
Q

what is HbA1c

A

glycated Hb

256
Q

what can HbA1c reflect

A

reflect last 3 months of glycaemia
biased to the 30 days preceding measurement
irreversible reaction

257
Q

acute complication from T1DM

A

diabetic ketoacidosis
uncontrolled hyperglycaemia
hypoglycaemia (from treatment)

258
Q

is diabetic ketoacidosis a life threatening complication

A

yes

259
Q

risks of hypoglycaemia

A

seizure
coma
death
impacts on day to day function, cognition and driving

260
Q

risk factors of hypoglycaemia

A

exercise
missed meals
inappropriate insulin regime
alcohol intake
lower HbA1c
lack training ard dose adjustment for meals

261
Q

how to support problematic hypoglycaemia

A

insulin pump therapy
try diff insulin analogues
education
transplantation

262
Q

acute management for hypoglycaemia for alert and orientated patients

A

oral carbs
rapid acting (eg juice, sweet)
longer acting (sandwich)

263
Q

acute management for hypoglycaemia for drowsy/confused but swallow intact patients

A

buccal glucose
glucogel
comple carbs

264
Q

acute management for hypoglycaemia for unconscious or concerned abt swallow patients

A

IV access
20% glucose IV

265
Q

what is T2DM

A

combination of insulin resistance and beta cell failure

266
Q

when can T2DM present

A

young / young adult

267
Q

what is the normal bgl in fasting state

A

4-5.9, under 7.8

268
Q

what is the normal bgl in 2hrs of eating

A

4-7.8

269
Q

what is the normal bgl in random

A

below 6.9

270
Q

what is relative deficiency of insulin in T2DM

A

insulin produced by pancreatic beta cells but not enough to overcome insulin resistance

271
Q

when does ketones form

A

when there’s no insulin

272
Q

why there is no ketosis in T2DM

A

there’s still insulin, but may still hv DKA when unwell eg infection/sepsis

273
Q

what happens in long duration of T2DM

A

beta cell failure progress to complete insulin deficiency

274
Q

why in T2DM there is high bgl (2 reasons metabolically)

A
  1. reduced insulin action causes less uptake of glucose into skeletal muscle
  2. increase Hepatic glucose production as there is reduced insulin action and increase in glucagon action
275
Q

consequences of insulin resistance in liver

A

increase hepatic glucose output

276
Q

consequences of insulin resistance in myocytes

A

less glucose uptake by muscle

277
Q

consequences of insulin resistance in adipocytes

A

increase fatty acid uptake from gut
increase fatty acid production
triglyceride from unhealthy types of lipid

278
Q

what is a major risk for T2DM

A

obesity

279
Q

T2DM presentations

A

hyperglycaemia
overweight
dyslipidaemia
fewer osmotic symptoms
insulin resistance
later insulin deficiency

280
Q

risk factors for T2DM

A

age
BMI
PCOS
family Hx
inactivity
ethnicity

281
Q

association with T2DM and gut microbiota

A

bacterial lipopolysaccharides fermentation to short chain FA, bacterial modulation bile acids
inflammation, signalling metabolic pathways

282
Q

first line diagnosis of T2DM

A

HbA1c+1 symotoms
or with 2 x HbA1c >/= 48mmol/mol

283
Q

acute presentation of complication of T2DM

A

hyperosmolar hyperglycaemic state

284
Q

chronic presentation of complication of T2DM

A

ischaemic heart disease
retinopathy

285
Q

what is hyperosmolar hyperglycaemic state

A

presents commonly with renal failure
insufficient insulin for prevention of hyperglycaemia but sufficient insulin for suppression of lipolysis and ketogenesis

286
Q

management for hyperosmolar hyperglycaemic state

A

give gluids slowly

287
Q

risk of hyperosmolar hyperglycaemic state

A

slowly get very hyperglycaemic
super dehydrated

288
Q

management of T1DM

A

exogenous insulin
self monitoring of glucose
education

289
Q

management of T2Dm

A

diet
oral meds
education
may need insulin later

290
Q

prevention diabetes - related complications and their risk factor

A

retinopathy
neuropathy
nephropathy
cardiovascular

291
Q

what are prinicples of T2DM consultation

A

HbA1c
weight
cholesterol level
BP
screen for complications (foot check, retinal screening)

292
Q

which drug helps to address XS hepatic glucose production
(and the drug’s strategy)

A

metformin
helps reduce hepatic glucose production

293
Q

which drug helps to address resistance to action of circulating insulin
(and the drug’s strategy)

A

metformin
Thiozolidinediones
(improve insulin sensitivity)

294
Q

which drug helps to address inadequate insulin production for extent of insulin resistance
(and the drug’s strategy)

A

Sulphonylureas
DPPG4-inhibitors
GLP-1 agonsits
(boost insulin secretion)

295
Q

which drug helps to addressXS glucose in circultion
(and the drug’s strategy)

A

alpha glucosidase inhibitor
SGLT-2 inhibitor
(inhibit carbohydrate gut absorption and renal glucose resorption)

296
Q

what is metformin’s mechanism of action

A

insulin sensitiser, oral
reduce insulin resistance
reduce HGO
increase peripheral glucose disposal

297
Q

side effects of metformin

A

GI side effects
contraindicated in severe liver, cardiac or renal failure

298
Q

what is sulphonylureas’ mechanism of action

A

bind to ATP sensitive potassium channel and close it
boost insulin production of B-cells
independent of glucose or ATP which both are needed for normal insulin production

299
Q

what is pioglitazone’s mechanism of action

A

insulin sensitiser mainly peripheral

300
Q

side effects of pioglitazone

A

HF
hepatitis

301
Q

GLP-1 mechanism of action

A

stimulates insulin
suppress glucagon
increase satiety

302
Q

what is GLP-1, where is it secreted

A

gut hormone
secreted in response to nutrients in gut
transcription product of pro-glucagon gene mostly from L-cell

303
Q

example of GLP-1 agonist

A

liraglutide
semaglutide

304
Q

function of GLP-1 agonist

A

decrease conc of glucagon and glucose
weight loss

305
Q

example of DPPG-4 inhibitor

A

gliptins

306
Q

function of DPPG-4 inhibitor

A

increase half life of exogenous GLP-1
increase conc of GLP-1
decrease conc of glucagon and glucose
neutral on weight

307
Q

mechanism of SGLT-2 inibitor

A

inhibits Na-Glu transporter
increase glycosuria
lower HbA1c

308
Q

what are some microvascular complications for DM

A

retinopathy
nephropathy
neuropathy

309
Q

what are some macrovascular complications for DM

A

cerebrovascular disease
ischaemic heart disease
peripheral vascular disease

310
Q

which complication is associated with HbA1c and BP

A

microvascular
positive correlation

311
Q

factors related to microvascular complications

A

duration of diabetes
smoking ( endothelia dysfunction)
genetics
hyperlipidaemia
hyperglycaemic memory (inadquate glucose control earlier can result in higher risk)

312
Q

what are the mechanism leading to microvascular complication

A

activation of inflammatory pathways –> damage endothelium –> leaky capillaries, ischaemia

313
Q

what are the 4 types of retinopathy and maculopathy

A

background retinopathy
pre-proliferative retinopathy
proliferative retinopathy
diabetic maculopathy

314
Q

what happens in background retinopathy

A

hard exudates (yellow spots)
microaneurysm
blot haemorrhages

315
Q

what happens in pre-polferative retinopathy

A

cotton wool spots / soft exudates
represent retinal ischaemia

316
Q

what happens in proliferative retinopathy

A

visible new vessels on disc or elsewhere in retina
these new vessels will bleed v. early, lead to haemorrhage

317
Q

what happens in maculopathy

A

hard exudates / oedema near macula
same as background retinopathy but nearer to macula
can threaten vision

318
Q

treatment for background retinopathy

A

continue annual surveillance

319
Q

treatment for pre-proliferative retinopathy

A

early panretinal photocoagulation

320
Q

treatment for proliferative retinopathy

A

panretinal photocoagulation

321
Q

treatment for maculopathy

A

if oedema: anti-VEGF injections directly into eye
frid photocoagulation

322
Q

what are we looking at when doing annual urine sample for diabetics

A

albumin:creatinine ration (ACR)

323
Q

what false positives may hv in urine ACR

A

fever
urine infection

324
Q

mechanism of diabetic nephropathy

A

diabetes –> hyperglycaemia and hypertension –> glomerular hypertension increase –> proteinuria -> glomerular ad intestinal fibrosis -> glomerular filtration rate decline -> renal failure

325
Q

mechanism of renin angiotensin system

A

liver release angiotensinogen - renin from kidney change angiotensinogen to angiotensin l -> ACE change it to angiotensin ll

326
Q

effects of angiotensin ll

A

vasoconstrictor
stimulate aldosterone to release in adrenal cortex
lead to hypertension

327
Q

how to block RAS to reduce BP and progression of diabetic nephropathy

A

block with ACE inhibitor or angiotensin 2 receptor blocker

328
Q

management of diabetic nephropathy

A

optimise glycaemic control and BP (HbA1c and BP)
start SGLT-2 inhibitor if T2DM
stop smoking

329
Q

what happens in diabetic neuropathy

A

small vessels supplyign nerves are called vasa nervorum
vasa nervorum blocked -> lower limb amputation

330
Q

why diabetic neropathy more common in feet

A

longest nerve supply feet
peripheral neuropathy (gloves and stocking distribution)
can be painful
but patients may not sense an injury to the foot

331
Q

risk of diabetic foot ulceration

A

reduced sensation to feet (peripheral neuropathy)
foot deformity
poor vascular supply to feet (peripheral vascular disease)

332
Q

management for peripheral neuropathy

A

regular inspection of foot
good footwear
avoid barefoot walking

333
Q

management for peripheral neuropathy with ulceration

A

offloading
revascularisation if concomitant PVD
orthotic footwear
Antibiotics if infected

334
Q

what is mononeuropathy

A

sudden motor loss (wrist drop or foot drop)
cranial nerve palsy (double vision due to oculomotor nerve palsy)

335
Q

what is autonomic neuropathy

A

damage to SNS and PNS nerves (innervating GI tract, bladderm cardiovascualr system)

336
Q

symptoms of autonomic neuropathy

A

GI: delayed gastric emptying, nausea, vomiting, constipation, nocturnal diarrhoea
cardiovascular: postural hypotension, collapsing on standing, sudden cardiac death

337
Q

how to treat obesity

A

diet

338
Q

what happens in leptin deficiency

A

infertility
stunted linear growth
decreased body temp
decreased energy expenditure
decreased immune function

339
Q

importance of leptin

A

help reduce appetite
control metabolism and energy homeostasis
regulate synthesis of thyroid hormones
decrease glucose-stimulated insulin secretion
increase HR
regulate bone mass and menstrual cycle
activation of immune cells

340
Q

how leptin administration help leptin deficiency children

A

restore LH pulsatility
increase LH FSH
can go thru normal puberty and reproductive cycle

341
Q

what happens in leptin resistance

A

fail to signal CNS that we have sufficient fat reserves for normal functioning

342
Q

drugs to treat obesity

A

orlistat
liraglutide/ Saxenda

343
Q

side effects of orlistat

A

fatty n oily stool
faecal urgency
faecal incontinence

344
Q

function of GLP-1

A

reduce appetite and increase satiety
increase insulin reduce glucagon
reduce liver fat and inflammation
reduce insulin resistance
increase NA excretion and diuresis
increase endothelial function
reduce arterial stiffness and inflammation
increase myocardial contractility ad ishcaemic preconditioning
reduce glucose uptake

345
Q

where is GLP-1 from

A

released from GI tract
a gut hormone

346
Q

what is liraglutide / saxenda

A

long acting GLP-1 receptor agonist

347
Q

how to administer liraglutide / saxenda

A

daily injection
double dose for T2DM

348
Q

when to consider bariatric surgery for obese pt

A

BMI > 40
BMI 35-40 + other comobidities
BMI 30-34.9 for newly diagnosed T2DM

349
Q

what are the common types of bariatric surgery (3)

A

gastric bypass (top of stomach joined to small intestine, can feel fuller sooner and don’t absorb that much calories from food)
gastric band (band placed ard stomach, so don’t eat much to feel full)
sleeve gastrectomy (part of stomach removed, cannot eat as much as u could)

350
Q

what is semaglutide and how it works

A

long acting GLP-1 receptor agonist
cause weight loss

351
Q

what is tirzepatide and how it works

A

long acting GLP-1 receptor and glucose dependent insulinotropic polypeptide (GIP) receptor co-agonist

352
Q

what is cagrilintide and how it works

A

long acting amylin analogue
given in combo with semaglutide

353
Q

what is retaturtide and how it works

A

triple agonist of GIP, GLP-1 and glucagon receptors

354
Q
A

BRS Y2 (5 decks)

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