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Endocrine Flashcards

1
Q

What do the cells of pancreatic islets secrete

A

alpha - glucagon
beta - insulin
gamma - somatostatin
PP - pancreatic polypeptide

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2
Q

Where is insulin synthesised and describe the structure of it before it is cleaved

A

RER of beta cells
called prepoinsulin
alpha and beta chain with C peptide - sulphide bonds

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3
Q

C peptide where does it come from and what does it do

A

prepoinsulin is cleaved and C peptide is a by product of insulin
no known physiological function

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4
Q

how many phases does insulin have? describe them

A

biphasic
rapid phase (5%) lasts 5-10mins
slow phase - lasts 1-2 hours

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5
Q

what is the insulin receptor called

A

tyrosin kinase

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6
Q

what happens when insulin binds to its receptor

A

beta chains of the receptor are phosphorylated which caused insulin substrates to phosphorylate
PK13 -> PKB -> glycogen synthesis
Ras -> MAP kinase activity -> gene expression
PKB -> GLUT4 - allows glucose entry into cells

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7
Q

what is leprechaunism

A

also known as donohue syndrome
autosomal recessive
genetic mutation in the insulin receptor causing severe insulin resistance

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8
Q

what are the symptoms and signs of leprechaunism (4)

A

elfin facial appearance
growth retardation
absence of fat
decrease in muscle mass

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9
Q

What is rabson mendenhall syndrome

A

defect in insulin binding
autosomal recessive
insulin resistance, hyperglycaemia and compensatory hyperinsulinaemia

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10
Q

symtoms and signs of rabson mendenhall syndrome (5)

A

development abnormalities
hyper pigmentation
acanthuses nigricans
DKA

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11
Q

How are amines released
how are peptides and proteins released
how are steroids released

A

pre synthesised and released in response to stimuli by ca dependant exocytosis. hydrophilic
synthesised and released on demand. hydrophobic. transported bound to plasma proteins

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12
Q

Whats is DIDMOAD (wolfram syndrome)

A 
diabetes insipidus 
diabetes mellitus 
optic atrophy 
deafness
neurological abnormalities
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13
Q

Thyroid pathology - draw it out
what does the centre contain
what do C cells secrete

A

draw

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14
Q

What happens when the TSH binds with the TSH receptor on thyroid epithelial cells

A

GTP->GDP which causes cAMP to produced which then further releases T3 and T4

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15
Q

what HLA is involved in hypothyroidism

A

HLA DR3 and DR5

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16
Q

What antibodies are released in hashimotos and other things are released

A

anti thyroid antibodies
CD8 T cells which cause destruction of thyroid epithelium
cytokine mediated cell death

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17
Q

What thyroid carcinoma leads to amyloid deposition

A

medullary (calcitonin)

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18
Q

what two cells is the parathyroid composed off

describe what the first set of cells do and what they look like

A

chief cells - secrete PTH, act on calcium homeostasis, they are round cells with moderate cytoplasm and bland round nuclei
supported by oxyphil cells

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19
Q

subclinical hypothyroidism
secondary hypothyroidism
subclinical hyperthyroidism

A

increase in TSH, normal T3/T4
normal or decrease in TSH, decrease in T3/T4
decrease in TSH and normal T3/T4

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20
Q 
Nodular thyroid disease
who does it happen in 
what kind of onset does it have
what are the thyroid hormone levels
what antibodies are present 
exams and ix
A 
elder population
insidious onset
low TSH high T3/T4
AB negative 
assym goitre
high uptake on scintigraphy
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21
Q

what are the screening tests and the definitive tests for cushings

A

overnight 1mg dex tests 100 abnormal

24 hour urinary cortisol free test

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22
Q

what are the drug treatments for cushings

A

metyprane if treatment failed or waiting for radiotherapy to start working
ketocondzone
pasicreatide (somatostatin analogue)

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23
Q

water deprivation test

A

check 8 hours before and 4 hours after giving IMDDAVP

Ur/serum osmolality ration >2 normal

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24
Q

which of the thyroid homorones is most secreted

A

T4 90%

T3 10%

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25
Q

what is T4 converted to and where

A

T3

liver and kidneys

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26
Q

which thyroid hormone is the more biologically active

A

T3

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27
Q

how do the thyroid hormones travel

A

hydrophobic/lipophillic

bound to plasma proteins

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28
Q

zona glomerular
zona fasciculate
zona reticularis

A

mineralocorticoids - aldosterone
glucocosteroids - cortisol
adrenal androgens

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29
Q

investigation for Conns

A 
measure aldosterone: rennin 
if raised (abnormal) do a 2L saline suppression test
failure to suppress by 50%  diagnostic for Conns
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30
Q

what is CAH (recessive/dom)
what is the investigation for it
treatment

A

21 alpha hydroxyls deficiency
autosomal recessive
base 17 hydroxyprogesterone (17 OH progesterone) levels checked
glucocorticoid and mineralocorticoid replacement

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31
Q

treatment of phaemochromocytoma

A

A before B
alpha blocker phenylbenzamine
BBs propranolol, atenolol

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32
Q

what is anterior pit called and where is it derived from

what is the posterior pit called and where is it derived from

A

adenohypophyisus - derived from rathkes pouch

neurohypophisus - extension of neural tissue

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33
Q

what is a craniopharyngioma derived from
give three symptoms/signs of it
who does it occur in
symptoms

A

remnants of rathkes pouch
slow growing, cystic, may calcify
5-15s, 60s, 70s
headaches, visual disturbances, growth retardation in children

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34
Q

How much do adrenal glands weigh and what are the cells called and what do they secrete

A 
4-5g each
neuroendocrine cells (chromaffin) secrete catecholamines
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35
Q

Causes of pit hyper function

hypofunction

A

adenoma/carcinoma

surgery. haemorrhage. ischaemic necrosis (sheegans syndrome)

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36
Q

Autocrine
Parocrine
Endocrine

A

releases hormones - acts on itself
releases hormone - acts on cells nearby
releases hormone - enters blood and travels

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37
Q

what are the three different types of hormones

A

glycoproteins and peptides - oxytocin, insulin
steroids - cortisol, testosterone
tyrosine and tryptophan derivatives

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38
Q

what are the three types of hormone receptors

A

G coupled - activated by amines and peptides
receptor kinases - activated by proteins (insulin)
nuclear receptors - class 1 activated by steroids - move from cytoplasm to nucleus
-class 2 activated by lipids in nucleus
-class 3 activated by T3

39
Q

what are acinar cells

A

functional unit of the exocrine pancreas

40
Q

what kind of a receptor do KATP channels have

A

a sulphylurea receptor

41
Q

what are the 4 effects of insulin

A

lipolysis and glucagonesis in liver
glucose uptake into adipose and muscles
lipogenesis in adipose and liver
glycogen synthesis in liver and muscle

42
Q

how are ketones formed

A

derived from acetyl coA

43
Q

how are ketone bodies in DM

A

oxaloacetate is low in the liver due to gluconeogenesis excess acetyl CoA enters the krebs cycle leading to ketone body formation

44
Q

give an example of alpha glucose inhibitors

A

arcarbose

45
Q

what do alpha glucose work on and how
effect
side effects

A

alpha glucosidase is a brush border enzyme that breaks down starch to form glucose
inhibitors delay absorption of glucose
prevent post prandial rise in glucose
GI symptoms

46
Q

DPP4 inhibitors - how do they work

A

inhibits DPP4 allowing prolongation of GLP and GLP-1 action

47
Q

what is MODY treated with

A

SU

48
Q 
give rapid acting insulins 
short acting insulins 
intermediate insulins 
long lasting insulins
rapid acting - intermediate mix
short acting - intermediate mix
A 
humolag, apidra, novarapid
humalin S, actrapid, insumen rapid
insulatard, humulin, insumen basal
lantus, levemir
humalog mis 25/50, novomix 30
humulin M3, insumen comb 15, 25, 50
49
Q

HbA1c diabetes and pre diabetes

target

A

48 (6.5%) - diabetes
42-47 (6-6.4%) - pre diabetes
48 but 53 is okay

50
Q

levels of DM foot

A

low - pulses and sensation present
medium - loss of pulse or sensation
high - loss of both or previous ulcers/amputation

51
Q

BP control in DM - when to treat and what is the target

A

lifestyle unless >140/90

target 130/80

52
Q

what is charcots foot and what is the treatment

A

disarticulation of bone and collapse of mid foot

immobilise and cast

53
Q

adrenal hyperplasia diffuse enlargement is ACTH what

adrenal hyperplasia nodular enlargement is ACTH what

A

diffuse ACTH driven

nodular ECTH independent

54
Q

describe an adrenal adenoma

A

well circumsised, encapsulated, small nuclei, yellow, non functional

55
Q

Describe an adrenal carcinoma

A

local invasion to retroperonium and kidney
large haemorrhage and necrosis
frequent and atypical mitosis
lack of clear cells and capsular or vascular invasion

56
Q

what are the two types adrenal medullary tumours and describe the second one

A

pheochromocytoma

neuroblastoma - 40% are in medulla, rest are along the sympathetic chain, might differentiate towards ganglion cells

57
Q

causes of goitrous hypothyroidism
causes of non goitre hypothyroidism
causes of secondary hypothyroidism

A

hashimotos, iodine deficiency, drug induced (amiodarone)
congenital atrophic thyroiditis, post ablative, post radiation
hypothalamic (infection, congenital, malignancy) or pituitary (trauma)

58
Q 
MEN1 autosomal what
what gene 
what does the gene do
how is it activated 
where is the mutation
A 
autosomal dominant 
MEN1 gene 11q
tumour suppressor 
bi-allelic activation
mutations throughout gene
59
Q

MEN2 autosomal what
what gene
what does the gene do
where is the mutation

A

autosomal dominant
RET gene 10q
proto oncogene
mutation in one specific codon

60
Q

what is MEN2 associated with

A

medullary thyroid carcinoma
parathyroid hyperplasia
bilateral phaemochromocytoma

61
Q

give the process of bone remodelling

A

takes place at remodelling sites
osteoclasts absorb old bone
osteoblasts replace them - fill gap with osteoid
osteoid mineralises to form new bone

62
Q

what is oogenesis and when does it restart and end

A

creation of ovum

restarts at puberty and end at menopause

63
Q

what is the earliest female germ cell

A

primordial cell

64
Q

what are oocytes and when are they formed

A

immature ovum and are formed after completion of ion and pre meiotic division

65
Q

what do two polar bodies indicate

A

sperm entry and completion of second meiotic division

66
Q

what is the follicular phase
what is the primary follicle and secondary follicle
how does the follicular phase end and what is it the main hormone

A

maturation of egg
primary oocyte surrounded by single layers of granulosa cells is the primary follicle
oocyte grows and follicle expands and becomes differentiated - secondary follicle
ends with ovulation
main hormone - oestrogen

67
Q

Luteal phase - what happens
main hormone
life span of the copeus leutum - what happens after it died
what happens if fertilised

A

follicular cells undergo luetinisation and transform into CL and reproductive tract
progesterone
14 days - degeneration - new follicular phase
if fertilised CL persists and produces progesterone and oestrogen

68
Q

what are the hormone changes in pregnancy

A

embryo produces hCG to maintain CL

progesterone to support pregnancy and suppress ovulation

69
Q

Kallmans syndrome - what is it
genetics
symptoms/signs

A

loss of GnRH secretion and anosmia
X linked - just males - autosomal dominant
cleft lip palate, missing tooth, delayed puberty

70
Q

male hypogonadism
primary - causes
secondary - causes

A

primary - decreased testosterone increased FSH/LH
klinefines syndrome, undescendent testcles, haemachromatosis
secondary - hypothalamic/pit dysfunction
kallmans, pit dysfunction, sarcoid, HIV/AIDS, meds, obesity, ageing

71
Q 
Klinefelters syndrome - how
symptoms 
what gene 
hormone levels 
treatment
A 
congenital 
decreased testosterone volume, gynacamastea, azoosprenia, infertility 
K7XXY
decreased testosterone, increased FSH/LH
testosterone therapy
72
Q

rubella syndrome - signs

A 
rash at birth
small head
low birth weight 
bulging forehead 
visual problems 
patent ductus arteriosis
73
Q

what changes in the endometrium could lead to infertility

A

anatomical change
dyspareunia
altered peritoneum environment

74
Q

why are there eye changes in Graves

A

fibroblasts etc. express TSH receptors

75
Q

when is octeotride used in acromegaly and why

A

1st line

used post op resolves in 1 hour improves outcome

76
Q

Why are phaemachromocytoma tumours brown/red

A

brown due to catecholamines

red- due to haemorrhagic/necrosis

77
Q

What is MODY

A

defective glucose sensing in pancreas or loss of insulin secretion

78
Q

Normal ion gap

A

10-18

79
Q

What is the normal osmolality

A

285-295

80
Q

How long is the normal menstrual cycle last

A

28-35 days

81
Q

What kind of drug is clementine citrate and why is it given

A

anti androgen

to stimulate FSH

82
Q

What cells in the anterior pit release prolactin

A

lactotroph cells

83
Q

Structure of T3

T4

A

DIT + MIT

DIT + DIT

84
Q

Where is the defect in pseudo hypoparathyroidism

A

GNAS1

85
Q

ACTH level in adrenal cushings
ectopic cushings
pit cushings

A

low
high
high on in between

86
Q

low dose dex suppression test how much over how many hours

A

2mg/24 hours

87
Q

CRH test in cushings

A

increase in cortisol and ACTH - pit not ectopic

88
Q

test done in addisons

A

250mg synching at 0 and 30 mins

30 minute level of 580 diagnostic

89
Q

What is secreted in phaeos

A

catecholamines (metanpehrines)

90
Q

MEN1 (3Ps)

A

pituitary, parathyroid, pancreatic endocrine tumours

91
Q

Conns tests

A

Aldosterone:rennin ratio high >750 then
2L saline suppression test - if fail to suppress over 50%
adrenal CT to confirm adenoma
Adrenal vein sampling in elderly

92
Q 
Thyroid uptake scans
cold nodule
graves
toxic multi nodular
hot nodule
autonomous
thyroiditis
A 
cyst, cancer
butterfly
hot and cold
one bit high uptake
only one side loads
no uptake
93
Q

what is hyperemesis rabidarcom

A

picture of thyrotoxicosis but no symptoms

usually after pregnancy or during preg

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