Endo Disorders II Flashcards
what mass lesions can cause hypopituitarism
craniopharyngioma
Rathke’s pouch cyst
meningioma
non-functional pituitary macroadenoma
metastasis from lung
intrasella ICA aneurysm
what drug causes lymphocytic hypophysitis
ipilimumab
what hormone deficiency does haemochromatosis cause in pituitary
deficiency in gonadotropin
list infiltrative lesions affecting pituitary
lymphocytic & granulomatous hypopthysitis
haemochromatosis
infection
systemic corticosteroids
genetic
ischaemia causing necrosis & haemorrhage
sudden onset
headache
visual disturbances
vomiting
occular paresis CNIII, disruption to IV and VI
pituitary apoplexy
blood loss during childbirth
postpartum pituitary necrosis / haemorrhage
severe lethargy
norexia, weight loss
failure post partum lactation
amenorrhoea weeks/months post delivery
GH, PRL, GnT deficiency
Sheehan syndrome
obese
female
HTN
defect in diaphragm of sella
excess CSF –> herniate SA space into sella
primary - empty sella syndrome
(2’ regression size pituitary)
(3’ transcription factor abnormality - pituitary differentiation)
mutation KAL1 and FGFR1
failure of migration of neurons
testicular hypotrophy
pubic hair present
hypo/anosmia
Kallman Syndrome (genetic)
Anosmia because migratory neurons arise in olfactory epithelium
posterior pituitary hypofunctino is associated with
arginine vasopressin (ADH) deficiency
central diabetes insipidus
sequence for testing pituitary hormones
test in pairs i.e. cortisol & ACTH
timing
deprivation test i.e. psychogenic DI
stimulatory test - if no increase, there is deficiency
MRI
biopsy
short, obese stature
AR
resistance to GH
abnormalities in GHr
high serum GH
low IGF-1
Laron Syndrome
polydipsia
polyuria
hypernatraemia
dilute urine
confusion
diabetes insipidus
(ADH absense/loss)
name the type of diabetes insipidus:
1) problem with no ADH
2) problem with kidney
3) no problem with function
1) central DI
2) nephrogenic DI
3) psychogenic polydipsia
normal ADH
hypernatraemia
high plasma osmol
low urine osmol
nephrogenic DI
decreased ADH
hypernatraemia
high plasma osmol
low urine osmol
central DI
N/increased ADH
hyponatraemia
low plasma osmol
low urine osmol
primary polydipisa (psychogenic)
water deprivatino test:
- plasma osmol increases
- urine osmol low
desmopressin admin (DDAVP):
- plasma osmol decreases
central DI
water deprivatino test:
- plasma osmol increases
- urine osmol low
desmopressin admin (DDAVP):
- plasma osmol remains high
nephrogenic DI
water deprivatino test:
- plasma osmol increases
- urine osmol increases
desmopressin admin (DDAVP):
- not required
psychogenic polydipsia
hypoosmolality
euvolemic hyponatremia
concentrated urine
high urinary Na+
nausea, muscle cramps
SIADH
causes of SIADH
antidepressant agents - SSRIs
SCLC - paraneoplastic
CNS infection, trauma
drug cause of nephrogenic DI
Lithium
bradycardia, HTN
cold intolerance
constipation
anaemia
carpel tunnel syndrome
dry skin, delayed DTR
myxoedema
hyperthyroidism
TSH high
fT4 low
fT3 low/n
primary hypothyroidism (thyroid gland)
TSH low
fT4 low
T3 low
secondary / tertiary hypothyroidism (pituitary)
TSH normal
T4 normal
T3 decreased
associated with acute illness
Euthyroid sick syndrome
T4 not converted to T3
associated with cytokines; IL-1, IL-6, TNF-a, IFN-b
child
iodine deficiency
thyroid hypoplasia
pale, puffy face
protruding umbilicus
poor brain development
protuberant tongue
pot bellied
congenital hypothyroidism - Cretinism
hashimotos thyroiditis is type ____ hypersensitivity
type 4 HS
What are the 3 phases of hashimitos thyroiditis
thyrotoxic phase
hypothyroid phase
euthyroid phase
damage to follicular cells, release colloid
increased T3, T4
decreased TSH
Thyrotoxic phase - hashimoto thyroiditis
last 2-8 weeks
permanent subacute granulomatous thyroiditis
low T3, T4
high TSH
hypothyroid phase - hashimoto thyroiditis
what antibodies are seen in hashimoto thyroiditis
thyroid peroxidase (TPOAb)
thyroglobulin (TgAb)
antimicrosomal Ab
low T3
high TSH
anti-TPOAb (+)
anti-TgAb (+)
painless diffuse thyroid enlargement
lymphocytic infiltration
Hurthle cells
hashimoto thyroiditis
complications of hashimoto thyroiditis
hashitoxicosis
increased risk B cell lymphoma
myxoedema coma
severe hypothyroidism
Decreased CNS
Hypothermia
Bradycardia
Hyponatraemia
Hypoglycaemia
Hypotension
Precipitating illness
myxoedema coma
(hypothyroidism)
iodine induced hypothyroidism
excess iodine - inhibited organification
normal thyroid function
escape phenomena present
Wolf-Chaikoff effect
iodine induced hyperthyroidism
iodine deficient hypothyroidism
increased iodine exposure - excessive hormone sythesis
not occur in euthyroid individuals
Jod-Basedown phenomenon
tremor, tachycardia, anxiety, HTN, weight loss
hyperdefecation
warm, smooth skin
hyperpigmentation
heat intolerance, normo-anaemia, oligo-amenorrhoea
madarosis (eyebrows)
hyperthyroidism
low/absent
Radioactive iodine uptake seen in:
hasimoto thyroiditis
thyroid drug ingestion
high/normal
radioactive iodine uptake seen in:
Graves disease
toxic adenoma
toxic multinodular goiter
focal, high uptake RIU
toxic adenoma
diffuse high uptake RIU
Graves disease
female
diffuse goitre
exophthalmos
dry eyes, lig lag
myxoedema
graves disease
Graves disease is type ____ hypersensitivity
type 2 HS
what is the pathogenesis of Grave disease
autoimmune
auto-AB (IgG) against TSH receptor
haplotypes HLA-B8 and DR3 associated with
Graves disease
diffuse symmetric
enlarged meaty appearance thyroid gland
Graves disease
pseudopapillary infolding
scalloping of colloid
hyperplastic follicular cells
Graves disease
process behind exophthalmos
activated B/T cell infiltrate –>
TNF-a, IFN-y inflammatory response –>
fibroblast proliferation, adipocyte differentiation –>
production hyaluronic acid & GAG –>
increased volume intraorbital fat & muscle tissue –> exophthalmous
hyperthyroidism
goitre
dysphagia, dyspnoea
multinodular
arely assoc. eye signs
toxic multinodular goitre
female
30-50yo
following viral infection or drug use (lithium/amiodorone)
transient pathcy inflammation of thyroid gland
subacute thyroiditis
2 types of subacute thyroiditis
subacute granulomatous thyroiditis (de Quervains)
subacute lymphocytic thyroidits
treatment of subacute thyroiditis
NSAIDS
steriods if severe
follows viral URTI
CD8 T cells damage follicles
colloid leakage & macropahe infiltrate
severe neck pain - radiate to ear/jaw
inflammatory infiltrate - multinucleated giant cells, disruptive follcies
de Quervains
subacute granulomatous thyroiditis
inherited
HLA-DR3, HLA-DR5
painless, silent
lymphocytic infiltration
sparse germinal centres
subacute lymphocytic thyroiditis
thyroid dysfunction within first year post-partum
post-partum thyroiditis
goitre - iron collar
stony hard fibrosis
tan-grey woody thyroid
fibrosclerotic changes
pathcy lymphocytic & eosinophilic infiltration
Riedel syndrome
what thyroid condition can mimic anaplastic carcinoma
Riedel syndrome
acute onset
aggitation, delirium
fever, coma
diarrhoea, Afib, high output HF
upregulation B1-adrenergic receptors
low TSH, high T3/T4
recent stresor - infection, surgery, withdrawal antithyroid drugs
thyroid storm
life threatening hypermetabolic state
