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BRS 1b > endocrinology > Flashcards

endocrinology Flashcards

1
Q

mechanism of action of thionamides

A

stop TPO production so stop T3/4 secretion

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2
Q

mechanism of action of KI

A

presumed autoregulatory effect - wolff chaikoff effect
stops iodination of TG
stop TPOH2O2 production so stop thyroid hormone secretion

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3
Q

how long does it take for biochemical and for clinical effects of thionamides to show

A

biochemical effects: hours
clinical effects: weeks

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4
Q

2 side effects of thionamides

A

agranulocytosis
rashes

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5
Q

which hyperthyoid conditions present with pain in gland area

A

viral thyroiditis
toxic nodular goitre (plummers)

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6
Q

which cells produce calcitonin

A

thyroid parafollicular cells

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7
Q

which hormone in the Vitamin D pathway regulates its own synthesis and how does it do it

A

1,25 (OH)2 cholecalciferol
regulates its own synthesis by decreasing transcription of 1 alpha hydroxylase

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8
Q

what effect does vitamin D have on bones

A

increases osteoBlast activity

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9
Q

what effect does PTH have on bones

A

increases osteoClast activity - increases calcium mobilisation

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10
Q

what effects does PTH have on the kidney

A

1) increases calcium reabsorption
2) increases phosphate excretion –> by inhibiting the Na+/PO4 3- co transporter
3) increases 1 alpha hydroxylase production
–> increases 1,25 (OH)2 cholecalciferol production
–> acts on gut to increase calcium and phosphate absorption

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11
Q

what is the role of the Na+/PO4 3- co transporter and which part of the nephron is it

A

increases sodium and phosphate reabsorption / decreases excretion
found in proximal convoluted tubule

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12
Q

how does FGF23 regulate phosphate levels

A

inhibits sodium phosphate co transport in the proximal convoluted tubule –> increases phosphate (and sodium) excretion
inhibits calcitriol/vit D –> decreases phosphate absorption in gut

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13
Q

give 4 causes of low vitamin D

A

diet
malabsorption
lack of UV light
production issues - renal failure

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14
Q

4 causes of low PTH

A

surgical
autoimmune
congenital
Magnesium deficiency

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15
Q

what effect does hyeprcalcaemia have on muscles and why

A

atonal muscles
due to reduced neuronal excitability

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16
Q

causes of hypercalcaemia

A

1) primary hyperparathyroidism eg parathyroid adenoma
2) malignancy
- bony metastases: factors released activate osteoclasts
- certain cancers eg squamous cell carcinoma release PTH-related peptide
3) vitamin D excess - rare

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17
Q

primary hyperparathyroidism

A

parathyroid adenoma - high PTH
calcium rises as a result
but no negative feedback as parathyroid gland is just autonomously secreting high levels of PTH

so end up with high PTH and high Calcium

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18
Q

secondary hyperparathyroidism

A

low calcium (usually due to vitamin D deficiency - diet, UV, malabsorption, renal failure) and so PTH levels rise as a result

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19
Q

treatment for secondary hypoparathyroidism for someone with and without renal failure

A

without renal failure:

ergocalciferol - 25 hydroxy vitamin D2
cholecalciferol - 25 hydroxy vitamin D3

with renal failure (can’t produce 1 alpha hydroxylase so have to just give them active from of vitamin D):

Alfacalcidol - 1 alpha hydroxycholecalciferol (active vit D analogue)

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20
Q

treatment of primary hyperparathyrodism

A

parathyroidectomy

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21
Q

treatment of tertiary hyperparathyrodism

A

parathyroidectomy

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22
Q

what is tertiary hyperpararthyoidism

A

happens in chronic renal failure
get chronic vitamin D deficiency therefore low calcium
as a result, parathyroid gland secretes more and more PTH, enlarging as a result
the gland hyperplasia causes autonomous PTH secretion, causing hypercalcaemia

(initial part is like secondary hyperparathyroidism, but then get autonomous secretion from gland and high calcium)

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23
Q

a patient is suffering from severe vomiting as a result of hypercalcaemia of malignancy, what is the initial treatment plan

A

1) rehydrate with IV fluids - for the vomiting
2) give bisphosphontaes - for the hypercalcaemia

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24
Q

what is the diagnosis if PTH is low and calcium is high

A

hypercalcaemia of malignancy

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24
Q

what is the diagnosis if PTH is low and calcium is high

A

hypercalcaemia of malignancy

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25
Q

what is the diagnosis if PTH is high, calcium is high and renal function is normal

A

primary hyperparathyroidism

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26
Q

what is the diagnosis if PTH is high, calcium is high and renal function is abnormal

A

tertiary hyperparathyroidism

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27
Q

a patient presents with pain passing urine, haematuria, high PTH, high calcium, normal vit D, low phosphate
what is diagnosis

A

primary hypoparathyroidism

bc have high PTH and high calcium
–> if vit D was low would have been tertiary hypoparathyroidism

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28
Q

what is the name of the neurones carrying AVP and oxytocin to the posterior pituitary, and where do they originate

A

magnocellular neurones
originate in supraoptic and paraventricular nuclei hypothalamic nuclei

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29
Q

contrast the actions of vasopressin when it works on V1 vs V2 receptor

A

V1: vasoconstriction
V2: increases water reabsorption from collecting duct

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30
Q

describe how a haemorrhage would result in less inhibition of VAP

A

haemorrhage = loss of blood volume
therefore less stretch of/pressure in right atrium
therefore less stimulation of stretch receptors
therefore less inhibition of AVP release via vagal afferents by stretch receptors

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31
Q

describe why AVP needs to be released after a haemorrhage

A

acts on V1 to cause vasoconstriction - increase bp
acts on V2 to increase water reabsorption 0 increase bp

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32
Q

what are the two types of stimuli for AVP release

A

osmotic and non osmotic

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33
Q

describe osmotic simulation of AVP release

A

subfornical organ and organum vasculosum are osmoreceptors
–>they are circumventricular structures meaning that they are highly vascularised, lie around the 3rd ventricle, and do not have a BBB - so can respond to changes in systemic circulation
when there is an increase in extracellular osmolarity/sodium, water leaves the osmoreceptors causing them to shrink
this causes their firing rate to increase
their neurones project to the supraoptic nucleus in the hypothalamic nucleus, so their firing stimulates the release of AVP

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34
Q

describe non osmotic stimulation of AVP release

A

increase in pressure in right atrium is detected by atrial stretch receptors
the atrial stretch receptors inhibit AVP release via vagal afferents to the hypothalamus

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35
Q

is glucose normal or abnormal in diabetes insipidus

A

normal

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36
Q

what should you always check in pateints with polyuria, nocturia, polydipsia and thirst - and why

A

glucose
if its normal it could be diabetes insipidus
if its abnormal it could be diabetes mellitus

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37
Q

why do patients with diabetes insipidus feel thirst

A

they produce large volumes of dilute urine so plasma is hyper osmolar
this is detected by osmoreceptors which stimulate feeling of thirst

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38
Q

congenital and acquired causes of nephrogenic diabetes insipidness

A

congenital: mutations in AVP/AQP2
acquired: drugs - lithium

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39
Q

how to distinguish between pschogenic polydipsia and diabetes insipidus

A

water deprivation test - test osmolarity of urine under water deprivation to see if body is conserving water in body or not

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40
Q

cranial DI treatment

A

desmopressin (like vasopressin but is selective for V2 receptor)

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41
Q

distinguishing between cranial and nephrogenic DI

A

give ddAVP under water deprivation and measure urine osmolarity

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42
Q

pt has a BMI of 19 and low FSH and LH, with amenhorrea, what is the diagnosis and treatment

A

hypogonadotrophic hypogonadism
lifestyle changes

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43
Q

what is the treatment for POI to help with fertility

A

IVF –> stimulates the ovaries using gonadotrophs

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44
Q

why would HRT not help with fertility due to POI

A

HRT is a combination of oestrogen and progesterone
this would help with symptoms but not with infertility as it doesn’t contain gonadotrophs LH/FSH –> so does cause ovulation

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45
Q

treatment for hyperprolactinaemia

A

dopamin agonsit: carbergoline
or
surgery

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46
Q

what is infertility definition

A

inability to achieve clinical pregnancy after 12 months or more of unprotected regular (every 2-3 days) sexual intercourse

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47
Q

list the post testicular causes of male infertility

A

obstructive azoospermia

erectile dysfunction
- mechanical
- retrograde ejaculation
- pscyhological

iatrogenic
- vasectomy

congenital
- absence of vas deferent in cystic fibrosis

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48
Q

what is cyrptorchidism and what kind of infertility does it cause

A

undescended testes - causes acquired primary hypogonadism
(bc it doesn’t cause hypogonadism straight away, only if left untreated)

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49
Q

what is endometriosis and what are the symptoms

A

endometrial tissue found outside the uterus which responds to progesterone

menstrual pain
deep dyspareunia
infertility
menstrual irregularities

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50
Q

what are fibroids

A

benign tumours of the myometrium which respond to oestrogen

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51
Q

list the hypothalamic endocrine causes of male infertility

A

hyperprolactinaemia

congenital hypogonadotrophic hypogonadism
- anosmic (Kallmans syndrome)
- normosmic

acquired hypogonadotrophic hypogonadism
- stress
- low BMI
- XS exercise

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52
Q

give an example of congenital primary hypogonadism in males

A

Klinefelters syndrome (47XXY)

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53
Q

what is the cause of Kallmans syndrome

A

failure of the GnRH neurones to travel with the olfactory fibres from the olfactory placode to the hypothalamus
resulting in anosmia and infertility + failure of puberty

CAN HAPPEN IN MALES AND FEMALES

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54
Q

what is X0 chromosome condition called

A

turners syndrome

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55
Q

symptoms/signs of Klinefelters syndrome

A

reduced facial and chest hair
female pattern of pubic hair
reduced IQ
small penis and testes
gynaecomastia
narrow shoulders
wide hips
reduced bone density
infertility
tall stature

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56
Q

treatment for male infertility

A

dopamine agonist (cabergoline) for high prolactin
testosterone (for symptoms, not fertility)
gonadotrophins (for infertility)
surgery (micro testicular sperm extraction)

lifestyle
- optimise BMI
- smoking and alcohol cessation

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57
Q

blood tests for male infertility

A

PRL
FSH
LH
morning fasting testosterone

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58
Q

POI levels of LH, FSH, oestradiol

A

LH high
FSH high
Oestradiol low

–> as it is primary hypogonadism

59
Q

diagnostic criteria for POI

A

FSH > 25 iU/L, 2 times at least 4 weeks apart

60
Q

causes of POI

A

congenital eg turners syndrome (X0)
autoimmune
cancer treatment

61
Q

anorexia induce amenhorrea levels of FSH , LH, oestradiol

A

all low

62
Q

PCOS diagnostic criteria

A

2/3 of

oligomenorrhoea or amenorrhea

high androgens or signs of high androgens eg hirsutism, acne

cysts found on ovarian USS

63
Q

treatment for the different aspects of PCOS

A

infertility/ irregular menses
- contraceptive pill
- metformin
- IVF

insulin resistance
- lifestyle changes
- metformin

hirsutism
- creams, laser
- anti androgens eg spironolactone

endometrial hyperplasia
- progesterone course

64
Q

hormone levels in PCOS

A

high LH: FSH ratio
normal E2
high E1

65
Q

symptoms of turners syndrome

A

shield chest
brown nevi
small fingernails
amenhorrea
infertility
webbed neck
short stature
short 4th metacarpal
elbow deformity
coarcation of part
poor breast development

66
Q

investigation for female infertility

A

trasnvaginal US
hysterosalpingogram
pituitary MRI
pregnancy test
bloods
- FSH
-LH
-PRL
- mid luteal progesterone
- oestradiol
- androgens

67
Q

what is the name of the tract between the hypothalamus and anterior pituitary

A

hypothalamic hypophyseal tract

68
Q

what is panhypopituitarism

A

total loss of anterior and posterior pituitary

69
Q

which hormone does ACTH regulate

A

cortisol
NOT aldosterone - that is regulated by the renin angiotensin system

70
Q

if a women who has recently delivered a child presents with lethargy, weight loss, inability to breastfeed and her menses haven’t returned since pregnancy, what are the likely diagnoses

A

Sheehans syndrome
anaemia
pituitary tumour

71
Q

what is Sheehans syndrome

A

post partum haemorrhage –> hypotension –> anterior pituitary infraction –> anterior hypopituitarism

the anterior pituitary enlarges during pregnancy (lactotroph hyperplasia) so is the most vulnerable to infarction

presents with weight loss, lethargy, anorexia, inability to lactate or restarts menses

72
Q

what is pituitary apoplexy

A

infarction or haemorrhage of the pituitary
presentation is exacerbated by presence of pituitary adenoma - may even be the first presentation of a pituitary adenoma
presents as
severe sudden onset headache
bitemproal hemianopia
if cavernous sinus is involved: diplopia (cn 4/6), ptosis (cn3)

72
Q

what is pituitary apoplexy

A

infarction or haemorrhage of the pituitary
presentation is exacerbated by presence of pituitary adenoma - may even be the first presentation of a pituitary adenoma
presents as
severe sudden onset headache
bitemproal hemianopia
if cavernous sinus is involved: diaposis (cn 4/6), ptosis (cn 3)

73
Q

how to treat GH deficiency and monitor the response

A

daily injection
monitor response using quality of life assessment and measure IGF1 levels

74
Q

how does GH deficiency present in adults vs children

A

adults: reduced quality of life
children: short stature

75
Q

how does ACTH deficiency present

A

fatigue
NOT salt losing crisis - that do to with the renin angiotensin system and aldosterone

76
Q

how to treat ACTH deficiency

A

give synthetic steroids
prednisolone - 1 x a day in morning, 3mg a day
hydrocortisone - 3 x a day, 10mg 5mg 5mg

(to represent diurnal rhythm)

77
Q

what are the sick day rules for people with ACTH deficiency, and what are they followed in order to avoid

A

wear a steroid alert bracelet/necklace
double steroid dose if have fever/intercurrent illness
if cannot take steroids eg are vomiting, inject intramuscularly or go to A&E

in order to avoid adrenal crisis - hypotension, weakness, collapse, death

78
Q

what is primary hypoadrenalism called

A

Addisons

79
Q

describe radiotherapy induced hypopituitarism

A

can either be direct or indirect - hypopituitarism induced by radiotherapy targeted at the pituitary eg for an adenoma, or near the pituitary eg for a cns tumour
the higher the total radiotherapy dose, the higher the risk of HPA axis damage

80
Q

which parts of the pituitary is most sensitive to damage from radiotherapy

A

GH and gonadotrophin

81
Q

what is the best scan to look at pituitary

A

MRI

82
Q

what medications can precipitate pituitary apoplexy

A

anticoagulants

83
Q

which two hormones are released from pituitary in response to hypoglycaemia

A

GH
ACTH

84
Q

what is the numerical cut off for hypoglycaemia

A

< 2.2 mM

85
Q

what is the difference between a microadenoma and a macroadenoma

A

micro adenoma < 1cm
macro adenoma > 1cm

86
Q

which receptor does dopamine bind to on anterior pituitary lactotrophs

A

D2 receptor

87
Q

what medication is used to treat hyperprolactinaemia

A

cabergoline - dopamine agonist

88
Q

name some drugs which can cause hyperprlocatinaemia

A

anti psychotics
anti emetics
SSRIs
high dose oestrogen
opiates

89
Q

name some pathological causes of hyperprolactinaemia (other than a prolactinoma)

A

PCOS
chronic renal failure
primary hypothyroidism

90
Q

name some physiological causes of hyperprolactinaemia (other than a prolactinoma)

A

stress
pregnancy / breast-feeding
nipple / chest wall stimulation

91
Q

how does GH directly and indirectly stimulate growth

A

direct: acts on muscles directly
indirect: stimulates liver to produce iGF (insulin like growth factor) which acts on muscles

92
Q

treatment for high GH

A

transphenoidal pituitary surgery
somatostatin analogue - octreotide
dopamine agonist - cabergoline (there are D2 receptors on GH secreting pituitary tumours)

93
Q

how to measure if cortisol is high

A

high late night cortisol
high 24 hr urine free cortisol
high cortisol after given oral dexamethasone

94
Q

how to measure if GH is high

A

high IGF 1
or high GH after given oral glucose load

95
Q

what are the ACTH dependent causes of high cortisol

A

pituitary corticotroph adenoma
ectopic ACTH (lung cancer)

96
Q

what are the ACTH independent causes of high cortisol

A

adrenal adenoma
oral steroids

97
Q

difference between cushings disease and syndrome

A

syndrome = high cortisol
disease = high cortisol due to ACTH secreting corticotrophin adenoma

98
Q

what treatment is used for hyperthyroidism due to graves or plummers

A

symptom management:
beta blockers - propanolol

reduce thyroxine:
thianomides - carbimazole (CB2), propylthiouracil (PTU)

if thianamodies don’t work can try
- radioiodine therapy
- surgery –> KI treatment before to reduce the size of the gland

98
Q

what treatment is used for hyperthyroidism due to graves or plummers

A

symptom management:
beta blockers - propanolol

reduce thyroxine:
thianomides - carbimazole (CB2), propylthiouracil (PTU)

if thianamodies don’t work can try
- radioiodine therapy
- surgery –> KI treatment before to reduce the size of the gland

99
Q

what are some side effects of thionamides

A

agranulocytosis –> get a sore throat due to reduction in neutrophils and subsequent infection by commensal streptococci

rashes

100
Q

why do you get palpitations, tachycardia etc in hyperthryoidism

A

you get apparent activation of the sympathetic nervous system
because thyroxine sensitises beta adrenoreceptors to adrenaline and noradrenaline

101
Q

what is plummers

A

hyperthyroidism due to a benign thyroid adenoma –> toxic nodular goitre

102
Q

difference in presentation of graves, plummers and viral thyroiditis on radio iodine uptake scan

A

graves - symmetrical shape, all of gland is dark
plummers - only one dark area (the adenoma), not symmetrical
viral - no uptake on scan (gland stops making thyroxine and makes viruses instead)

103
Q

why do you get hyper thryoidism then hypothyroidism in viral thryoiditis

A

virus attacks gland and uses it to make viruses instead of thyroxine
starts of as hyperthyroidism because gland is over stimulated and releases all of the thyroxine it previously made
then hypo as all the thyroxine stores have been released and its just making viruses now

104
Q

difference in symptoms between graves and plummers

A

in plummers get no smooth symmetrical goitre, exophthalmus or pretibial, myxoedema

105
Q

what are the symptoms of leptin deficiency

A

infertility
short stature
reduced
- immune function
- body temp
- energy expenditure

106
Q

what is orlistat

A

gastric and pancreatic lipase inhibitor

107
Q

side effects of orlistat

A

fatty and oily stool
oily spotting
facial incontinence and urgency
deficiency of fat soluble vitamins

108
Q

what medications other than orlistat can be used for obesity

A

liraglutide/saxenda - GLP 1 receptor agonist
semaglutide - long acting GLP1 receptor agonist
terzapetide: GLP 1 and GIP receptor agonist

GLP 1 = glucagon like peptide
GIP = glucose dependent insulinotropic peptide

109
Q

3 types of bariatric surgery

A

gastric bypass - attach top of stomach to small intestine
gastric band
sleeve gastrectomy - remove part of stomach

110
Q

requirements for being able to get bariatric surgery

A

BMI
> 40 kg/m2
35 - 40 with comorbidities
30 - 34.9 with newly diagnosed T2DM

111
Q

name the 3 autoantibodies that could be found in type 1 diabetes

A

insulin autoantibody (IAA)
glutamic acid decarboxylase autoantibody (GADA)
inculinoma-associated-2-autoantibodies (IA2A) - zinc transporter- 8 (Zn8)

112
Q

name some environmental exposures that could stimulate the genetic predisposition for type 1 dm to become a disease

A

enteroviral infection
cows milk protein exposure
seasonal changes
changes in microbiota

113
Q

which 2 transplants can be done for T1DM

A

islet cell transplant - from dead donor into hepatic portal vein

pancreas and kidney transplant (works better when together)

114
Q

name some metabolic effects of insulin deficiency

A

lipolysis
hepatic glucose output (HGO)
proteinolysis
conversion of fatty acyl coA into ketones (fatty acyl coA–> acetoacetate –> acetone + 3OH-B)

115
Q

what are the treatment options for T1DM

A

insulin pump therapy - short acting insulin, eg novarapid, via a pump, with basal bolus regime

education - DAPHNE course, swap refined carbs for complex carbs

closed loop/artificial pancreas - measures glucose levels of blood and calculates exactly how much insulin is needed

transplant - islet stem cell, kidney and pancreas

116
Q

how is normal insulin release pattern different from the insulin pump therapy release pattern

A

normal release pattern: prandial peaks with 2 phase (1st and 2nd phase insulin release) - helps make sure have the right amount of insulin

insulin pump therapy - basal bolus regime, release continuous amount of short acting insulin (basal) then larger amounts with meals (bolus)

117
Q

give examples of short and long acting insulin

A

short
- human insulin eg act rapid
- insulin analogue eg lispro, aspart, glulisine

long
- insulin bound to protamine or zinc eg NPH - neutral protamine Hagedorn
- insulin analogue - glargine, determiner, degludec

118
Q

what are some problems with using HbA1c for glucose measurements

A

changes with
erythropoiesis
breakdown of erythrocytes
glycation
altered haemoglobin

119
Q

what is the pH, bicarbonate an glucose cut off for diabetic ketoacidosis

A

pH < 7.3
bicarbonate < 15
glucose >11

120
Q

what is the pH, bicarbonate an glucose cut off for diabetic ketoacidosis

A

pH < 7.3
bicarbonate < 15
glucose >11

121
Q

what treatments are immediately needed for diabetic ketoacidosis

A

IV fluids - salien
insulin
anti emetics

122
Q

what are the two types of genetic backgrounds of T2DM

A

monogenic - single gene mutation: MODY, definitely will get diabetes

polygenic: polymorphisms increasing risk of diabetes: high risk of developing, but its dependent on other factors

123
Q

which type of obesity is worse for causing T2DM

A

visceral > subcutaneous

124
Q

name 3 conditions which have associations with T2DM

A

obesity
perturbations in gut microbiota
intra-uterine growth retardation

125
Q

how to diagnose T2DM

A

one HbA1c reading >= 48 , with symptoms
or
two HbA1c readings >= 48 , without symptoms

126
Q

describe the hyperosmolar hyperglycaemic state that can occur in T2DM

A

often presents as renal failure
not enough insulin to prevent hyperglycaemia, but enough to stop lipolysis and ketogenesis

127
Q

why is ketoacidosis rare in T2DM

A

because you still have some insulin, juts not enough to overcome the resistance - have a ‘relative deficiency’ of insulin

128
Q

which drugs solve the problem of excess hepatic glucose production - T2DM

A

metformin, reduces hepatic glucose production

129
Q

which drugs solve the problem of insulin resistance - T2DM

A

metformin + thiozolidinediones, increase insulin sensitivity

130
Q

which drugs solve the problem of insufficient insulin production to counteract the insulin resistance - T2DM

A

sulphonylureas, GLP1 agonist, DPP4 inhibitors, increase insulin secretion

131
Q

which drugs solve the problem of high glucose in blood - T2DM

A

alpha glucosidase inhibitor - inhibit carb absorption from gut
SGLT2 inhibitors - inhibit glucose reabsorption from kidneys

132
Q

which 2 things can induce remission of T2DM

A

sustaining a very low calorie diet
gastric bypass surgery

133
Q

what is metformin contraindicated in

A

severe liver failure
severe heat failure
moderate renal failure

134
Q

how does metformin reduce insulin resistance

A

reduces hepatic glucose output
increases peripheral glucose disposal

135
Q

how do sulphonylureas work for T2DM

A

block the ATP and glucose dependent K+ channel, stimulating insulin release

136
Q

how do SGLT2 inhibitors work for T2DM

A

inhibit sodium glucose transporter, causing glycosuria

137
Q

how do GLP1 work for T2DM

A

stimulates insulin, suppresses glucagon
decreases glucose and glucagon

138
Q

why does GLP1 have a short half life

A

it is rapidly degraded by DPP4 enzyme

139
Q

effects of pioglitazone

A

peripheral insulin sensitisation
modulation of adipocyte proliferation
peripheral weight gain

140
Q

how is GLP1 produced

A

transcription of pro glucagon gene in L cell

141
Q

effects of GLP

A
142
Q

2 enzymes involved in conversion of cholesterol to progesterone

A

side chain cleavage
3 hydroxysteroid dehydrogenase

143
Q

3 main causes if adrenocortical failure

A

TB addisons
autoimmune addisons
congenital adrenal hyperplasia

BRS 1b (10 decks)

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