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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
what is T4 converted to and where
T3 | liver and kidneys
26
which thyroid hormone is the more biologically active
T3
27
how do the thyroid hormones travel
hydrophobic/lipophillic | bound to plasma proteins
28
zona glomerular zona fasciculate zona reticularis
mineralocorticoids - aldosterone glucocosteroids - cortisol adrenal androgens
29
investigation for Conns
``` measure aldosterone: rennin if raised (abnormal) do a 2L saline suppression test failure to suppress by 50% diagnostic for Conns ```
30
what is CAH (recessive/dom) what is the investigation for it treatment
21 alpha hydroxyls deficiency autosomal recessive base 17 hydroxyprogesterone (17 OH progesterone) levels checked glucocorticoid and mineralocorticoid replacement
31
treatment of phaemochromocytoma
A before B alpha blocker phenylbenzamine BBs propranolol, atenolol
32
what is anterior pit called and where is it derived from | what is the posterior pit called and where is it derived from
adenohypophyisus - derived from rathkes pouch | neurohypophisus - extension of neural tissue
33
what is a craniopharyngioma derived from give three symptoms/signs of it who does it occur in symptoms
remnants of rathkes pouch slow growing, cystic, may calcify 5-15s, 60s, 70s headaches, visual disturbances, growth retardation in children
34
How much do adrenal glands weigh and what are the cells called and what do they secrete
``` 4-5g each neuroendocrine cells (chromaffin) secrete catecholamines ```
35
Causes of pit hyper function | hypofunction
adenoma/carcinoma | surgery. haemorrhage. ischaemic necrosis (sheegans syndrome)
36
Autocrine Parocrine Endocrine
releases hormones - acts on itself releases hormone - acts on cells nearby releases hormone - enters blood and travels
37
what are the three different types of hormones
glycoproteins and peptides - oxytocin, insulin steroids - cortisol, testosterone tyrosine and tryptophan derivatives
38
what are the three types of hormone receptors
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
what are acinar cells
functional unit of the exocrine pancreas
40
what kind of a receptor do KATP channels have
a sulphylurea receptor
41
what are the 4 effects of insulin
lipolysis and glucagonesis in liver glucose uptake into adipose and muscles lipogenesis in adipose and liver glycogen synthesis in liver and muscle
42
how are ketones formed
derived from acetyl coA
43
how are ketone bodies in DM
oxaloacetate is low in the liver due to gluconeogenesis excess acetyl CoA enters the krebs cycle leading to ketone body formation
44
give an example of alpha glucose inhibitors
arcarbose
45
what do alpha glucose work on and how effect side effects
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
DPP4 inhibitors - how do they work
inhibits DPP4 allowing prolongation of GLP and GLP-1 action
47
what is MODY treated with
SU
48
``` give rapid acting insulins short acting insulins intermediate insulins long lasting insulins rapid acting - intermediate mix short acting - intermediate mix ```
``` 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
HbA1c diabetes and pre diabetes | target
48 (6.5%) - diabetes 42-47 (6-6.4%) - pre diabetes 48 but 53 is okay
50
levels of DM foot
low - pulses and sensation present medium - loss of pulse or sensation high - loss of both or previous ulcers/amputation
51
BP control in DM - when to treat and what is the target
lifestyle unless >140/90 | target 130/80
52
what is charcots foot and what is the treatment
disarticulation of bone and collapse of mid foot | immobilise and cast
53
adrenal hyperplasia diffuse enlargement is ACTH what | adrenal hyperplasia nodular enlargement is ACTH what
diffuse ACTH driven | nodular ECTH independent
54
describe an adrenal adenoma
well circumsised, encapsulated, small nuclei, yellow, non functional
55
Describe an adrenal carcinoma
local invasion to retroperonium and kidney large haemorrhage and necrosis frequent and atypical mitosis lack of clear cells and capsular or vascular invasion
56
what are the two types adrenal medullary tumours and describe the second one
pheochromocytoma | neuroblastoma - 40% are in medulla, rest are along the sympathetic chain, might differentiate towards ganglion cells
57
causes of goitrous hypothyroidism causes of non goitre hypothyroidism causes of secondary hypothyroidism
hashimotos, iodine deficiency, drug induced (amiodarone) congenital atrophic thyroiditis, post ablative, post radiation hypothalamic (infection, congenital, malignancy) or pituitary (trauma)
58
``` MEN1 autosomal what what gene what does the gene do how is it activated where is the mutation ```
``` autosomal dominant MEN1 gene 11q tumour suppressor bi-allelic activation mutations throughout gene ```
59
MEN2 autosomal what what gene what does the gene do where is the mutation
autosomal dominant RET gene 10q proto oncogene mutation in one specific codon
60
what is MEN2 associated with
medullary thyroid carcinoma parathyroid hyperplasia bilateral phaemochromocytoma
61
give the process of bone remodelling
takes place at remodelling sites osteoclasts absorb old bone osteoblasts replace them - fill gap with osteoid osteoid mineralises to form new bone
62
what is oogenesis and when does it restart and end
creation of ovum | restarts at puberty and end at menopause
63
what is the earliest female germ cell
primordial cell
64
what are oocytes and when are they formed
immature ovum and are formed after completion of ion and pre meiotic division
65
what do two polar bodies indicate
sperm entry and completion of second meiotic division
66
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
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
Luteal phase - what happens main hormone life span of the copeus leutum - what happens after it died what happens if fertilised
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
what are the hormone changes in pregnancy
embryo produces hCG to maintain CL | progesterone to support pregnancy and suppress ovulation
69
Kallmans syndrome - what is it genetics symptoms/signs
loss of GnRH secretion and anosmia X linked - just males - autosomal dominant cleft lip palate, missing tooth, delayed puberty
70
male hypogonadism primary - causes secondary - causes
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
``` Klinefelters syndrome - how symptoms what gene hormone levels treatment ```
``` congenital decreased testosterone volume, gynacamastea, azoosprenia, infertility K7XXY decreased testosterone, increased FSH/LH testosterone therapy ```
72
rubella syndrome - signs
``` rash at birth small head low birth weight bulging forehead visual problems patent ductus arteriosis ```
73
what changes in the endometrium could lead to infertility
anatomical change dyspareunia altered peritoneum environment
74
why are there eye changes in Graves
fibroblasts etc. express TSH receptors
75
when is octeotride used in acromegaly and why
1st line | used post op resolves in 1 hour improves outcome
76
Why are phaemachromocytoma tumours brown/red
brown due to catecholamines | red- due to haemorrhagic/necrosis
77
What is MODY
defective glucose sensing in pancreas or loss of insulin secretion
78
Normal ion gap
10-18
79
What is the normal osmolality
285-295
80
How long is the normal menstrual cycle last
28-35 days
81
What kind of drug is clementine citrate and why is it given
anti androgen | to stimulate FSH
82
What cells in the anterior pit release prolactin
lactotroph cells
83
Structure of T3 | T4
DIT + MIT | DIT + DIT
84
Where is the defect in pseudo hypoparathyroidism
GNAS1
85
ACTH level in adrenal cushings ectopic cushings pit cushings
low high high on in between
86
low dose dex suppression test how much over how many hours
2mg/24 hours
87
CRH test in cushings
increase in cortisol and ACTH - pit not ectopic
88
test done in addisons
250mg synching at 0 and 30 mins | 30 minute level of 580 diagnostic
89
What is secreted in phaeos
catecholamines (metanpehrines)
90
MEN1 (3Ps)
pituitary, parathyroid, pancreatic endocrine tumours
91
Conns tests
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
``` Thyroid uptake scans cold nodule graves toxic multi nodular hot nodule autonomous thyroiditis ```
``` cyst, cancer butterfly hot and cold one bit high uptake only one side loads no uptake ```
93
what is hyperemesis rabidarcom
picture of thyrotoxicosis but no symptoms | usually after pregnancy or during preg

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