Endocrinology Flashcards
1
Q
How is T3 and T4 released stimulated
A
- thyrotrophin releasing hormone from hypothal
- TSH anterio rpituitary
- T4, T3 thyroid
- negative feedback to hypothalamus (less TRH)
2
Q
what do T3 and T4 bind to after release to be transported
A
thyroxine binding globulin and albumin
3
Q
how do T3 and T4 become activated
A
- T3 is active on release
- T4 is activated peripherally by losing an iodine molecule
4
Q
what are the function of thyroid hormones and what receptors do they stimulate
A
- increase metabolism
- via nuclear receptors
- growth and mental development
5
Q
What states are thyroid binding globulin increased/reduce din
A
Increased:
- pregnant
- oestrogen therapy
- hepatitis
Decreased- low protein states
- nephrotic syndrome
- chronic liver disease
- acromegaly
6
Q
what does primary hyper/hypothyroidism mean
A
- problem with the thyroid
7
Q
TFT results for primary hyperthyroid
A
low TSH, high T4
8
Q
TFT results for primary hypothyroid
A
hihg TSH , low T4
9
Q
what does central hypo/hyperthyroid mean
A
issue with pituitary or hypothalamus
10
Q
sx of hyperthyroid
A
Sweating Weight loss ****Emotional lability (irritable, psychosis) Appetite increase Tremor/tachycardia (AF) Intolerance to heat/irregular menstruation Nervousness/anxiety Goitre/GI problems (diarrhoea)
11
Q
signs for hyperthyroid
A
- tachycardia/AF (can cause lightheadedness/syncope)
- ****- palmar erythema
- goitre
12
Q
most common cause of hyperthyroidism
A
Grave’s
13
Q
Causes of hyperthyroidism
A
Grave’s
toxic multinod. goitre
toxic adenoma (1x nodule)
***ectopic thyroid tissue (mets, ovarian teratoma)
***pituitary adenoma secreting TSH
exogenous-
- iodine excess
- levothyroxine excess
- *****- amiodarone, lithium
14
Q
tx of hyperthyriodism
A
carbimazole- TFTs and sx guide dose - titrate
- ***propylthiouracil (2nd line)
- ***beta-blockers (AF)
radioiodine
thyroidectomy
15
Q
what are the sx of a thyroid storm
A
life threatening
tachycardia, HTN anxiety/restlessness fever (>40) mental status changed D+V \+- jaundice
16
Q
tx thyroid storm
A
- **antithyroid drug- - carbimazole OR propylthiouracil
- **beta blockers IV
- **steroids- hydrocortisone or dexamethasone - blocks T4 T3 conversion
- fluids, NG if vomiting
- bloods- TFT, cultures
- BP monitoring
- tx any infection
- paracetemol for fever
BB alternatives- diltiazem/verapamil, digoxin (AF)
17
Q
causes of thyroid storm
A
person with thyroid disease and:
- fever, sepsis
- dehydration
- MI
- radioactive iodine
18
Q
what is grave’s disease
A
hyperthyroidism due to circulating autoantibodies
- activate TSH receptors
- also react with orbital autoantigens
19
Q
what genetic mutation is grave’s disease associated with?
what other conditions are also associated with this mutation?
A
HLA-DR3
vitiligo
T1DM
addisons
20
Q
what populaitons is grave’s disease more commonly seen in
A
- females
- pregnant/post-partum
21
Q
sx of Grave’s disease
A
hyperthyroidism- SWEATING
****- pretibial myxedema
- Goitre- smooth thyroid enlargement
eye disease
Ophthalmology
- upper eyelid retraction with lid lag,
- swelling, erythema, conjunctivitis of the eyes
- exophthalmopathy (bulging)
- diplopia
- discomfort, grittiness/tearing
22
Q
what autoantibodies are seen in graves
A
- thyroid stimulating hormone receptor antibodies- gold standard
- thyroid perioxidase antibodies (also in Hashimoto’s)
23
Q
symptoms of hypothyroid
A
BRADYCARDIC
Bradycardia Reflexes slow Ataxia Dry, thin hair and skin Yawning (fatigue) Cold (low temp) ****Ascites and non-pitting oedema ****Round face, obesity Depression **Immobile (proximal weakness), ileus ***Congestive HF, constipation
24
Q
causes of hypothyroidism
A
Iodine deficiency Primary atrophic hypothyroid Hashimoto's thyroiditis thyroidectomy drug induced
25
what is primary atrophic thyroiditis
diffuse lymphocytic infiltration of thyroid
leads to atrophy
no goitre
no autoantibodies
26
tx of hypothyroidism
levothyroxine
27
what is autoimmune/hashimoto's thyroiditis
- lymphocytic and plasma infiltration
- goitre
- autoantibodies
- assoc with other AI conditions and MALT lymphoma
28
autoantibodies found in hashimotos/autoimmune thyroiditis
*****thyroglobin antibodies
| thyroid peroxidase antibodies
29
what is myxoedema coma, sx
- severe hypothyroid state, precedes death
- hypothermia
- hyporeflexia
- low glucose
- bradycardia
- coma, seizures
30
what can cause myxoedema coma
- infection
- MI
- stroke
- Coma
31
management myxoedema coma
* ******- TFT, FBC, UE, cortisol, glucose, cultures
* ******- ABG
- active warming
* ****- correct hypoglycaemia
* ****- tx infection
- IV T3 (Liothyronine) very slowly, sometimes can give levothyroxine
32
what is postpartum thyroiditis
hyper/hypothyroisism within the first year following a birth
33
what is foetal thyrotoxicosis, what can it cause
when TSH- receptor antibodies (Graves) cross the placenta
| - can cause cardiac conditions, IUGR, foetal goitre, hydrops, preterm, miscarriage
34
management of foetal thyrotoxicosis
- anti thyroid meds- carbimazole to mother
35
what is gestational thyrotoxicosis
- 1st 1/2 of pregnancy
| - T4 raised, low TSH
36
tx of gestational thyrotoxicosis
- propanolol
- carbimazole
- surgery
37
mots common type of thyroid cancer
papillary- good prognosis
Paul's Focaccia Most Awarded Loaf- papillary>follicular>medullary>anaplastic>lymphoma
-anaplastic- v bad prog
38
ix for ?thyroid cancer
aspirate large nodule
39
tx thyroid cancer
hemi/total thyroidectomy
40
complications of thyroidectomy
- external superior laryngeal- voice change, loss of high pitch
- recurrent laryngeal- hoarse, weak voice
- BL recurrent laryngeal- lose voice, need tracheostomy
- hypothyroidism
41
what are the 2 tyes of cells in the parathyroid glands
```
chief cells
oxyphil cells (unknown use)
```
42
what do chief cells secrete
PTH
43
what does PTH do
released when Ca levels low
- increases serum Ca
- increased bone resorption
- increased Ca re-absorption in kidneys
- Vit D synthesis- which then acts on the gut to increase Ca absorption
- negative feedback- Ca=less PTH
44
causes of primary hyperparathyroidism
- solitary adenoma
- general hyperplasia
- cancer
45
sx hyperparathyroidism
```
Bones- pain, #, OP
Stones
Groans- abdo pain, constipation
Moans- confusion, delirium, agitation, depression
Thrones- polydipsia, polyuria
```
pancreatitis
weakness
fatigue
46
blood resuts in primary hyperparathyroidism
- hgih Ca
- PTH high
- reduced phosphate
47
what is secondary hyperparathyroidism
high PTH, but being released in an appropriate response to consistently low Ca
48
causes of secondary hyperparathyroidism
- low vit D
- chronic renal failure (increased Ca excretion)
- low Ca intake
- reduced intestinal Ca absorption
49
tx primary hyperparathyroidism
- fluids
- high Ca and vit D intake
- excise adenoma/PT glands
- conservative- cinacalcet- calcimimetic- increases PT cell sensitvity to Ca to increase -ve feedback- if surgery is unsuccessful
- consider bisphos
50
tx secondary hyperparathyroidsm
- correct cause
- phosphate binders
- Vit D
- cinacalcet - a calcimimetic- increases PT sensitivity to Ca
- parathyroidectomy
51
blood results in secondary hyperparathyroidism
low Ca
| high PTH
52
what is tertiary hyperparathyroidism
- very LT secondary hyperparathyroidism
- hyperplasia
- inapp. PTH desensitised to Ca serum levels
53
blood results for tertiary hyperparathyroidism
- high Ca, very high PTH
54
what is primary hypoparathyroidism
failure of the glands- low PTH excretion leading to low Ca
55
causes of primary hypoparathyroidism
autoimmune destruction
- type 1- AIRE mutations
- Type 2- HLA D3+ and HLA D4
congenital eg diGeorge
56
test results for primary hypoparathyroidism
low PTH, low Ca
| high or normal phosphate
57
sx of hypoparathyroidism
```
- petechiae/purpura
tingling around mouth
tetany
muscle spasms
seizures
confusion
cardiac arrest
```
58
tx primary hypoparathyroidism
calcium
calcitriol
synthetic PTH
59
What is and what causes secondary hypoparathyroidism
high calcium level
- malignancy- bony mets, vit D secretion of lymphoma, myeloma, lung, breast
- rapid burn turnover
- renal failure
- thiazides
60
what is pseudohypoparathyroidism
- failure of target cells to reposond to PTH
61
SIGNS of pseudohypoparathyroidism
- short metacarpals
- short stature
- round face
- calcified basal ganglia
62
test results for pseusohypoparathyroidism
- low Ca
- high PTH
- hgih phosphate
63
tx pseudohypoparathyroidism
Ca
64
what are the zones of the adrenal cortex
Glomerulosa
Fasiculata
Reticularia
65
what does the glomerulosa of the adrenal cortex, produce?
mineralocorticoids
| - aldosterone
66
what stimulates the glomerulosa of the adrenals
- kidneys produce renin (low BP)
- angiotensin, thats produced from liver, converted to angiotensin I
- ACEI (lungs) cnoverts angiotensin I to angiotensin II
- aldosterone production from adrenals
67
what does aldosterone do
- increases BP
- increases Na and H2O retention
- increases K excretion
68
what does the fasiculata of the adrenal cortex, produce?
- glucocorticoids
| eg cortisol
69
what is the function of cortisol
- increase glucose in blood
| - increases gluconeogenesis in liver
70
how is cortisol release stimulated
HPA axis
- hypothal produces corticotrop. releasing hormone
- ant pit produces adrenocorticotropic hormones
- adrenals release cortisol
71
what does the reticularis zone of the adrenal cortex secrete
androgens (testosterone precursors)
72
how is androgen release from adrenals stimulated?
HPA axis- CRH hypothal--> ACTH from ant. pituitary--> stimulation of adrenal cortex zona reticularis to prod. androgens (testosterone and others)
ACTH also stimulated cortisol release from adrenals, and to a much lesser extent , aldosterone
NB- production of testosterone does not rely on 21-hydroxylase, yet cortisol and aldosterone does (relevant in CAH)
73
what part of the adrenal glands are responsible for the production of catecholamines eg noradrenaline, adrenaline
medulla
74
when are catecholamines stimulated to be secreted
Adrenaline, norepinephrine, dopamine
Sympathetic innervation
Adrenergic receptors
- alpha (arteries)
- beta-1 (heart- increase HR, contractility)
- beta-2 (bronchioles and arteries of the skeletal muscles)
75
what is Cushing's syndrome
clincial state produced by chronic glucocorticoid excess and loss of normal feedback mechanisms of HPA
76
What is primary Cushing's syndrome
non-ACTH dependent:
- issues with adrenal gland
- increased release of steroid hormones without stimulation by HPA axis
77
blood results of primary Cushing's syndrome
* *cortisol-secreting adenoma in the cortex of the adrenal gland**
- low ACTH (release is activated by CRH)
- high cortisol
- ACTH suppression test will not affect amount of steroid in blood, but suppresses ACTH
78
causes of primary Cushing's syndrome
- adrenal adenoma/cancer
| - adrenal nodular hyperplasia
79
what is secondary Cushing's syndrome
increased ACTH
| causing high steroid serum
80
causes of secondary Cushing's syndrome
- Cushing's disease (ACTH secreting pituitary tumour)
| - Ectopic ACTH- SCC, carcinoid tumours
81
sx of Cushing syndrome
- increased weight (central)
- mood change (depression, psychosis, irritability)
- skin, muscle atrophy
- gonadal dysfunction (irregular menses, hirtuisism, ED)
- acne
- moon face
- bufalo bump
- easy bruising
- purple abdo striae
- OP
- HTN
- hyperglycaemia
- poor healing
82
sx of Cushing's disease/pituitary tumour
- Cushing's syndrome
- bitemporal hemianopia
- headaches
- CN III, IV, VI palsy (eye movements)
- diabetes insipidus (low ADH)- tumour pushes on post. pituitary
- temp/sleep/appetite control issues
- CSF leak through nose
83
what skin changes occur in very high levels of ACTH
- yellow/tanned
seen in ectopic ACTH production and addisons (increased ACTH in response to low adrenal activity)
84
ix for Cushing's syndrome
- plasma cortisol (raised)
- 24hour urinary free cortisol
- midnight cortisol levels
- plasma ACTH
****- low dose dexa methasone suppression test- 1mg
Normal-- dexa- hypothal CRH reduced, ACTH from pituitary reduced , cortisol level supressed
Abnormal- cortisol level not supressed
High dose dex supp (8mg)
- pit adenoma- Cort and ACTH suppressed
- Adrenal adenoma- cortisol not supressed, ACTH suppressed
- Ectopic ACTH - both not suppressed
85
tx of Cushing's syndrome
* **Metyrapone- reduce cortisol prod.
* **Ketoconazole - reduce cortisol prod.
Adrenal adenoma/carcinoma (primary):
- adrenalectomy
Paraneoplastic/Cushing's disease (secondary)
- surgery - removal of tumour
- RT
Iatrogenic
- stop steroids
86
What is Addison's
Primary adrenal Insufficiency
| No negaive feedback to pituitary or hypothal (high ACTH levels, low cortisol/aldotserone/androgens)
87
sx of addison's
- GI- abdo pain/diarrhoea/constipation
- weakness, fatigue
- weight loss
- hyperpigmentation of skin (golden)/vitiligo- high ACTH released from ant. pituitary
- depression, psychosis, low self esteem
- hyponatraemia- N+V, headache, fatigue, weakness/cramps/spasms, confusion, seizures, coma
- hyperkalaemia- abdo pain, diarrhoea, palpitations, weakness, paraesthesia, N+V
- hypercalcaemia- stones, moans, groans, thrones, polyuria/polydipsia
88
causes of Addisons'
primary
- destruction of adrenals
- autoimmune
* **- infective (TB, CMV, HIV)
- adrenal haemorrhage
- malignancy
* **Secondary
- LT steroid use supresses pituitary ACTH production, so adrenals underproduce steroids
89
ix for ?addison's
- low Na and high K- low mineralocorticoids (aldosterone)
- low glucose (low cortisol)
-uraemia, hyperCa, eosinophilia, anaemia
- ACTH response test- cortisol response to ACTH measured- no response in primary/LT secondary
- ACTH- high in primary addison's , low in secondary causes
- 21-hydroxylase autoantibodies for autoimmune (primary) cause
90
tx addisons
- stop exogenous corticosteroid slowly if possible
- hydocortisone (cortisol and mineralocorticoid action)
+- fludrocortisone (mineralocorticoid, replaces aldosterone)
91
what is primary hyperaldosternoism
Conn's
excess production of aldosterone, independent of RAAS
Cause:
- adrenal adenomas
- adrenal hyperplasia
92
what is seondary hyperaldosteronism
ecxess aldosterone due to hgih levels of renin
93
ix for primary hyperaldosteronism (Conn's)
- aldosterone-to-renin ratio- high (ald high, renin levels low)- GOLD STANDARD
- UEs- low K, high HCO3, high Na
- CT abdo- adenoma
94
what is Conn's syndrome
- primary hyperaldosteronism
Causes:
- solitary aldosterone producing adrenal adenoma
- adrenal gland hyperplasia
- adrenal cancer
- familial
95
causes of secondary hyperaldosteronism
```
***Due to excessive RAAS activation****
renal artery stenosis
accelerated HTN
diuretics
cong HF
hepatic failure
```
96
what is Batter's syndrome
- loss of Na and Cl in loop of henle (defect channels)
- sodium loss means volume depletion
- increased renin
97
sx of hyperaldosteronism
asx
Hypernatraemia:
- weakness
- polydipsia, thirst
- confusion
hypokalaemia:
- paraesthsia
- cramps, weakness, paralysis
- polyuria
- polydipsia
- HTN
98
tx of hyperaldosteronism
- Conn's- removal of adenoma
- aldosterone antag- spironolactone, eplerenone
* *- dexamethasone (supresses aldosterone)
99
where is prolactin produced
anterior pituitary
100
what inhibits prolactin secretion
dopamine form hypothal
101
what substances does the posterior pituitary secrete
ADH
- made inhypothal, stored in post, pit
- increase water reabs-- increases osmolality of the urine
- aquaporin 2 in DCT
oxytocin-
- milk
- behaviour
- myometrial contraction
102
Whhat does the hypothal produce? what does this then stimulate production form ant.pit--> what do these then cause the production of?
- TRH-->TSH --> T3/4
- CRH-->ACTH --> cortisol (adrenal zona fasciculata)
- GnRH--> LH/FSH
- dopamine --X-> prolactin (lactotroph cells)
- GHRH--> GH
103
causes of hypopituitarism
HYPOTHAL
- Kallmans (ansomnia, GnRH X)
- tumour
- inflammation
- infection
- ischaemia
PItuitary
- trauma, surgery, radiation
- tumour, mass, meningoma , mets
- carotid artery aneurysm
- ischaemia- eg Sheehans, DIC
- haemochromatoisis, amyloid
- inflammation
- autoimmunity
104
sx and signs of hypopituitarism
TSH
- BRADYCARDIA
GH
- obesity
- atheroscerosis
- dry skin
- weakness, loss of balance
- low CO
FSH, LH
- oligo/amenorrhoea, ED, OP
ACTH
- adrenal insuff/addison's- GI, wt loss, weakness, low mood, confusion, hypotension, electrolytes
- no skin pigment changes
ADH
- polyuria
- polydipsia
- electrlyte
105
tx of hypopituitarism
- hydrocortisone (low ACTH- aldosterone and cortisol replacement)
- thyroxine- (low TSH)
- testosterone/oestrogen (low FSH/LH)
* **- somatotrophin (mimics GH)
106
tx of prolactinoma in pituitary
dopamine agonist (bromocriptine)
- OP prevention
- surgery- to remove tumour
107
what is pituitary apoplexy
rapid pituitary haemorrhage due to tumour
- acute hypopituitarism, cardiac collapse, mass effects, death
- headache, meningism, decreased GCS, LoC
108
tx pituitary apoplexy
hydrocortisone IV ( has mineralocorticoid and glucocorticoid actions- mimics aldosterone (and cortisol) and so prevent ssalt losing crisis)
fluid balance
operate
109
Causes of acromegaly
pituitary tumour
| hyperplasia due to ectopic GHRH from another tumour
110
sx acromegaly
- paraesthesia, carpal tunnel, prox weakness
- headache, - bitemp hemianopia
- sweating
- snoring
- arthralgia
- large hands and feet, gigantism
- diabetes, DKA
- cardiomegaly, arrhythmias
- hepatosplenomegaly
- goitre
- colon cancer
hypopituitarism-
- hypothyroid (TSH)
- polyuria, polydipsia, confusion, low BP (ADH)
- hypotension, N+V, weakness, wt loss (low ACTH)
- low libido, amenorrhoea (LH/FSH)
111
ix for acromegaly
- GH- diurnal so NOT helpful
- glucose, IGF-1, prolactin, cortisol, thyroid, gonadal hormones
- high Ca, phosphate (high bone turnover)
- MRI pituitary
- visual field testing
- ECG
- ECHO (cardiomegaly)
- CT- lung, pancreas, adrenals, ovaries- ectopic GH release
112
tx acromegaly
- somatostatin analogues- oppose GH eg OCREOTIDE
- GH antagonist- PEGVISOMANT
- remove pit tumour
- radiotherapy if large
113
what is diabetes insipidus
- reduced ADH /vassopressin secretion from post. pit or low response to ADH in kidneys
- impaired water resorption
114
sx diabetes insipidus
polyuria
polydipsia
- hypernatraemia- as ADH causes water resorption without assoc electrolyte reabs-- concentrated Na due to water loss--- lethargy, weakness, irritable, myoclonic jerk, seizures
115
ix diabetes inspidus
- UE, Ca, Na
- Glucose- r/o DM
- urine and plasma osmolalities- high in plasma (drinking alot of water), low in urine (dilute urine)
- fluid deprivation test if diagnosis reminas unclear (no fluids for 4-12hours- no change in the water loss)
- desmopressin stimulation test- to distinguish between the two types of diabetes insipidus (central- would reduce water loss- nephrogenic- no change in water loss)
116
tx diabete insipidus
- tx cause (cranial/nephrogenic)
- reduce Na with 0.9% saline at a rate of <12mmol/L/day
- desmopressin IM (man made ADH)-- will help if central cause to DI, if nephrogenic cause, wont help
117
what is SIADH
syndrome of inappropriate ADH
118
sx SIADH
- hyponatraemia- anorexia, nausea, malasia, low GCS, headache, irritability
119
causes of SIADH
- paraneoplastic tumours secreting ADH- SSC, pancreas, prostate, thymus, lymphomas
- CNS issues
- chest- TB , pneumonia, abscess
- thiazide like diuretics, carbamazepine, NSAIDs, opiates, SSRIs
120
ix results in SIADH
- hyponatraemia (diluted blood)
| - highly concentrated urine (high osmolality)
121
tx SIADH
tx cause
restrict fluids
salt
loop diuretics if severe
122
what are cacinoid tumours
slow growing neuroendocrine tumours
secrete neuropeptides- serotonin, histamine and postaglandins
appendix, small intestine
123
tx carcinoid tumours
***ocreotide (somatostatin analogue- inhibits the secretion of other hormones)
resection
124
what is multiple endocrine neoplasia
group of genetic conditions
growth of hormone producing tumours in endocrine organs
MEN 1- 3ps
- parathyroid
- pancreas
- pituitary
```
MEN 2
A
- medullary thyroid
- Pheochromocytoma
- parathyroid hypeprlasia
B
- medullary thyroid
- Pheochromocytoma
- Marfans/neuromas
FMTC- Familial Medullary Thyroid Carcinoma- medullary thyroid Ca is only feature
```
125
what is a phaeochromocytoma, sx
catcecholamine (adrenaline) producing tumours
sx
- anxiety
- sweating
- HTN (crisis= cardiogenic shock)
- palpitations, tachy, AF
- headache
126
how do you tx HTN crisis that may occur due to phaeochromocytoma
- IV alpha blcoker- phentolamine
- then long acting one- phenoxybenzemine
- beta blocker
- surgery on tumour once controlled
127
What does LH do in males
stimulate Leydig cells to produce testosterone
| - negative feedback on hypothal GnRH and ant. pituitary LH production
128
What does FSH do in males
stimulate Sertoli cells to produce androgen binding globulin and inhibin
- inhibin has negative feedback effect on hypothal GnRH and ant. pit. gland
129
What effect does FSH and LH have on the female ovaries
- produce oestrogen and follicular development
- when oestrogen levels peak- FSH inhibited and LH surges
- progesterone prod. by corpus luteum inhibits LH secretion
130
what is the definition of precocious puberty
- breast development <8
- testicular enlargement >3-4ml <9
- more common in girls, more worrying in boys
131
causes of precocious puberty
True/central
- gonadotrophin dependent
- FSH and LH raised
- congenital or hypothalamic tumours
Pseudo
- gonadotrophin independent
- FSH and LH low
- adrenal (tumour, Cushing's, CAH)- build up of precursors
- gonadal- tumour, cyst
- exogenous steroids
132
A 7 year old boy presents with his mother. His mother complains he is already developing secondary sexual characteristics. O/E testicular volume is 4ml. What red flag symptoms should you ask about
Central cause (tumour)- hydrocephalus
- headhaches
- changes in vision
- changes in eye movements
- drowsiness
- N+V
- poor balance and coordination
- seizures
133
ix for precocious puberty
- LH, FSH, estradiol and testosterone
If LH/FSH high (central)
- MRI head
- tumour markers- bHCG, AFP
if LH/FSH low (pseudo)
- adrenals- abdo imaging, urine steroid
- gonadal imaging
134
tx precocious puberty
- radiation
- chemo
- surgery
- steroids for hydrocephalus
135
definition of late puberty
- no breast development by 13yo
- testicles <4ml in boys by age 14
- more common in boys
136
causes of late puberty
Intact hypothalamo-pituitary axis
- consitutional
- chronic illness
- excessive sport
- psychosocial deprivation
- steroids
Impaired hypothal-pit axis (hypogonadotrophic hypogonadism)
Peripheral- hypergonadotrophic hypogonadism
137
name some causes of hypogonadotrophic hypogonadism
- intracranial tumours
- congenital- Kallman's
- irradiation
- trauma- head injury, surgery
- sheehans
138
name some causes of hypergonadotrophic hypogonadism in boys
- BL testicular damage- cryptorchidism, atresia, torsion, infection (mumps), failed orchidoplexy
* **- conditions that cause crytorchidism/gonadal dysgensesis eg Noonan's, prader-willi- klinefelters XXY
* *******- inborn steroids enzyme deficiencies
- damage- surgery, chemo, RT, trauma, autoimmune
139
name some causes of hypergonadotrophic hypogonadism in girls
- dysgenesis- tuner's, prader-willi
- drugs- cyclophosphamide
- intersex- androgen insensitivity, CAH
- inborn steroid enzyme deficiencies
- PCOS
premature failure
- toxicity- galactosaemia (inherited, galactose), thalassaemia (iron)
- damage- surgery, CT, RT, trauma, autoimmune
140
ix for late puberty
- FBC (anaemia), ferritin, UE, coeliac screen, urinanalysis, TFT, bone profile
- bone age- central, hypothyroidism, GH deficiency
- FSH, LH
- Prolactin, insuline like GF
- chromosomal testing
- Girls- pelvis USS
If hgih FSH/LH (peripheral, hypergonadotrophic cause)
- sex chromosome testing
- HCG testing
- sweat sodium testing
Low FSH/LH (central, hypogonadotrophic cause)
- MRI head is sx
- screen for chronic illnesses
- GH, cortisol testing for pituitary functioning
- karyotype
- constitutional?
141
tx for late puberty
- oral oxandrolone
- low dose IM testosterone in boys
- oestradiol in girls
- tx underlying cnodition if necessary
- remove tumours/chemo/RT
142
definition of arrested puberty
- lack of pubertal progression for >2years after spontaneous onset at appropriate age
143
common presenting issues with arrested puberty
- failure to achieve menarche and thelarche (start then stop)
- failure to reach >15ml tetsicular size from 4ml for >5years
- poor breast development
- suboptimal growth spurt
- poor male virilisation (bulk, deep voice, hair)
144
management of arrested puberty
- pathological until proven otherwise
| - urgent referral and ix
145
Pathophysiology of PCOS
- hyperinsulinaemia due to insulin resistance
- causes increased androgen production (theca cells in ovaries)
- reduced available sexhormone binding globulin by liver-- free testosterone raised
146
what is the name of the criteria used for PCOS
Rotterdam
147
What is the rotterdam criteria
2 of the following
- oligo/anovulation/amenorrhoea
- hyperandrogenism (clinically or biochemically)- exclude renal cause
- polycystic ovaries on USS
148
sx of high testosterone in females
hirtuism
male pattern alopecia
- increased muscle mass, deep voice if severe
149
other sx of PCOS not included in rotterdam criteria
- infertility/subfertility
- acne
- mood swings, depression, anxiety, low self-esteem
- sleep apnoea, obesity
- acanthosis nigrans- insluin resistance
- painful iliac fossa if cysts are large (unsual)
150
ddx for hirtuism/high androgen sx
hyperandorgenism:
- PCOS
- CAH
- androgen secreting tumours (adrenal, ovarian)
- androgen therapy
- Cushing's
- Thyroid dysfunction
- hyperprolactinoma
- SE of meds- phenytoin, corticosteroids
- obesity (increased insulin resistance)
151
ix for ?PCOS
- total testosterone and free testosterone
- USS ovaries
* *- sex hormone binding globulin- normal/low
* *- LH- may be elevated, LH:FSH ratio increased
- fasting glucose tolerance test- insulin resistance
- asses CV risk and lipid levels
R/o other causes of hyperandrogenism
- TFT
- 17-hydroxyprogesterone levels (CAH)
- prolactin
- 24hr urinary cortisol
152
tx PCOS
- weight <30 BMI
- COCP , cyclical progesterone
- IUS
Clomiphene or tamoxifen
- For fertility , anti-oestrogen
- restarts GnRH pulse
- makes pit produce more FSH as body thinks you have low oestrogen
- give up to 6x cycles, don't give >12m as risk of ovarian Ca
Metformin- less effective, esp if obese, may help if clomiphene resistant, GI SE
- Laparoscopic ovarian drilling
- Gonadotrophin ovulation induction (gonadotrophin injections)
- Assisted conception tx
153
sx of prolactinoma
- menstrual dysfunction - amenorrhoea, oligomenorrhoea, anolvulation
- delayed puberty, growth failure
- infertility, reduced libido
- galactorrhoea
- OP
- tumour- headache, visual changes
- men - ED, reduced hair growth , gynaecomastia
154
blood tests in prolactinoma
- high prolactin
| * *- low GnRH, FSH, LH (negative feedback on hypothal and ant pit)
155
ix ?prolactinoma
- TFTs
- pregnancy tets
- serum prolactin, GnRH, FSH, LH
- visual field testing
- MRI head
156
causes of azoospermia
- can be primary (hypergonadotrophic) or secondary (hypogonadotrophic)
Hypogonadotrophic (primary):
- chemo/RT
- idiopathic
- genetic
Hypergonadotrophic (secondary):
- obstructive- varioceles, epididymis obstruction, previous inguinal/scrotial injury, hernia repair, vasectomy
157
what is retrograde ejaculation
- semen passes into bladder rather than along urethra
158
causes of retrograde ejaculation
- transurethral resections of the prostate
- bladder neck incisions
* *- psychotrophic meds
* *- alpha adrenergic blockers- doxazosin, prazosin (HTN, BPH)-- smooth muscle/sphincter relaxation
* *- spinal cord lesions
- congenital anatomical cause
159
sx of retrograde ejaculation
- abscence of ejaculate
| - cloudy urine post-organsm
160
ix ?retrograde ejac
- post ejaculatory urine - spermatozoa, seminal fluid, or fructose
161
tx of retrograde ejac
- alpha adrenergic agonists (clonidine)- sympathomimeitc, smooth muscle and BV constriction
- antihistamines
162
WHO classification of female infertility
I
- hypothalamic /pituitary/hypognoadism
- pit tumour
- sheehans
- stress, wt loss, exercise
- hyperprolactinoma
II- normogonadotrophic-- PCOS
III- ovarian failure/hypergonadotrophic
- premature menopause
- chromosomal disorder
- surgery, trauma, RT
163
What level counts as hypocalcaemia
<2.1mmol/L
164
Causes of hypocalcaemia
- low vit D/Ca intake/malabs
- hypoparathyroidism (post thyroidectomy, idiopathic, diGeorge, infiltration)
- meds- bisphos, cisplatin, loop diuretics
- CKD/chronic liver disease
- AKI, rhabdomyolysis
- acute pancreatiits
* **- hungry bone syndrome post parathyroidectomy- assoc with hypophosphataemia and hypoMg, exacerbated by supressed PTH levels following parathyroidectomy
- osteomalacia
- tumour lysis syndrome
165
Presentation and signs of hypocalcaemia
- paraesthesia
- tetany/fasciulations
- myoclonic jerks
- seizures/convulsions
- chronic- dementia/confusion
- Chvostek's VII CN sign
- Trousseau sign- BP cuff to 20mmHg for 5 mins
166
tx hypocalcaemia
Acute/severe/sx
- 10ml 10% Ca gluconate IV in 10min, slow infusion after
Chronic
- Vit D 1.25-2.5mg per day
- Ca 600mg per day
ie Adcal 1500mg (Ca 600mg), sandocal (Ca 1g)
167
ix hypocalcaemia
- ECG- long QT
- PTH
- Vit D
- amylase
168
what level is hypercalcaemia
>2.6mmol/L
169
causes of hypercalcaemia
- hyperparathyroidism
- malignancy- bone mets, myeloma, lymphoma
- ****sarcoidosis
- paget's
- meds- thiazide like diuretics, ***lithium*****, Ca
- *****thyrotoxicosis
- *****addisons, phaeochromocytoma
- false- sample kept too long/too hot
170
ix hypercalacemia
ECG- short QTc
- vit D
- PTH
- XR- cancer
- Ig - serum (monoclonal bands) , urine (bence jones)
171
sx hypercalcaemia
- Stones
- Moans (psych)
- Groans (abdo pain, N+V)
Thrones- constipation, polyuria
- polydipsia
172
tx hypercalcaemia
- cause
- bisphosponates IV - zolendonate
- Saline
- Ph, Mg
173
level of hypernatraemia
>140mmol/L
174
causes of hypernatraemia
Extra-renal
- dehydration- water intake, D+V, sweating/burn
- excess salt intake
- too much IV saline
Renal
- diabetes insipidus (concentrated)
* ***- Conn's- hyperaldosteronism (reabs)
* ***- Cushings- cortisol exhibits minerlocorticoid activity in high conc
* **- osmotic diuretics, loop, thiazide diuretics, lithium, mannitol
- pseudo- if taken from site near fluid input
175
sx hypernatraemia
- tired, weak, confusion, irritable
Nausea
- thirst, reduced turgor, dry mouth, oliguria, tachycardia, orthostatic hypo
- muscle twitching, seizure, coma
176
ix hypernraemia
- Ca, glucose, UE
| - paired urine and serum osmolarity
177
tx hypernatraemia
- oral rehydration
- IV hypotonic fluids- 5% dextrose, 0.45% saline slowly
- Na reduction <10 mmol/L/day, reduce cerebral oedema
- if in shock, resus with isotonic fluids first
- dialysis if loss of renal function or Na >170mmolL
178
causes of hyponatraemia
```
ABCDEFGH
ACEI/antids (SSRIs), antipsychotics
*Brivaracetam (anticonvulsion)
Carbamazepine
*Desmopressin/Diuretics
*Ethosuximide
Furosemide
Gliclazide
Heparin
*NSAIDs
```
- polydipsia (psychogenic)
- adrenal insufficiency (addisons, hypopituitarism)- low aldosterone, low reabs
- SIADH- dilutional
- chronic, severe D+V, chronic dehydration
- ecstasy
- HF, cirrhosis
- CKD, AKI, nephrotic syndrome
179
sx of hyponatraemia
- confusion
- N+V
- muscle cramps
- drowsiness
- seizures
180
ix of hyponatraemia
- UE
- serum and urine osmolality
- monitoring ACTH/cortisol (adrenal insufficiency)
181
tx hyponatraemia
- SIADH- fluid restrict
- hypertonic saline (3%)
- DEMECLOCYCLINE (ADH agonist)
- hyervolaemic- loop diuretics
182
serum levels of hypkalaemia
>5.4mmol/L
183
causes of hyperkalaemia
**THANKS C
Trimethoprim, Heparin, ACEI/ARBs, NSAIDs, K sparing diuretics, Suxamethonium, Cicocporin
- AKI/CKD (decreased excretion)
- addison's
* *- increased intake- spinach, TPN, fruits, seweed, nuts
* *- metabolic acidosis- dehydration, sepsis
* *- insulin deficiency- moves K into cells (DKA)
- rhabdomyolysis/tumour lysis syndrome- cell breakdown
- iatrogenic- blood transfusions
* *- rewarming after hypothermia
- pseudo- haemolysis of sample- suspect if in isolation (no kidney strain, no acidosis) and pt is clinically stable
184
sx of hyperkalaemia
- ECG changes (asx)
- fatigue
- arrhythmia- palpitations, light-headedness, chest pain
- paraesthesia
- flaccid muscle--> paralysis
- reduced reflexes
- GI sx- diarrhoea N+V, abdo pain
185
ix hyperkalaemia
- UE- cr, urea, eGFR
- Ca and CK- rhabdomyolysis
- blood gas for acidosis
- ECG
- med review
186
ECG changes in hyperkalaemia
- tall tented T waves
- prolonged PR interval, p wave flattening
- Wide QRS/bizzare qrs morphology
- bradycardias, bradyarhythmias
- VT
187
management of hyperkalaemia
- stop K sparring drugs
1. IV 10% Ca gluconate or Cl if ECG changes present
2. Insulin up to 10 units with glucose 10%
3. K binders- Ca resonium, Veltassa
- salbutamol nebs
- loop diuretic- increase excretion
- sodium bicarb infusion- if acidotic
- dialysis
188
level of hypokalaemia
<3.5mmol/L
189
causes of hypokalaemia
Urinary loss
- autoimmune renal issues- SLE, Sjogrens
* *- renal tubular necrosis
- diuretics- thiazide, loop
* *- hypomagnesia- Mg inhibis K excretion, low levels results in increase K excretion
RAAS
- hyperaldosteronism/Conn's- K excretion
* *- renal artery stenosis- RAAS activation
* *- Cushings- cortisol acts as mineralocorticoid in hgih levels- K excretion
* *- D+V, laxative abuse
* *- excess sweating, burns
- decreased intake
* *- insulin and glucose tx (into cells)
- alkalosis
- other dx- adrenaline, dopamine, salbutamol, CCBs, chloroquine and digoxin intoxication
* *- hypothermia
* *- CF
190
sx hypokalaemia
- weakness/paralysis, hypotonia, areflexia, cramps, rhabdomyolysis, myalgia
- tetany, fasciulation
- paraesthesia hands/feet
- fatigue
- constipation--> paralytic ileus (N+V, abdo distension)
-
191
ix hypokalaemia
- UE< Mg, Ca, Ph, gluc
- ABG
- urine K, urine osmolality
- ECG
- serum digoxin
- low dose dexamethasone supression (Cushing's)
- pituitary imaging (cushing's)
- CT adrenals (conns)
- renal angiogram- renal artery stenosis, RAAS)
192
Management of hypokalaemia
- cause
- oral K (sando-K)
- IV K+ slowly <10mmol/hour
- replace Mg2+ if needed
193
What may cause a high serum glucose
PANC
- diabetes mellitus
- acute or chronic pancreatitis
* *- infiltration of pancreas- haemochromatosis , amyloidosis
* *- CF
- pancreatic neoplasia
OTHER ENDO COND.
* *- Acromegaly (insulin res)
- Cushing's- Insulin res
- Pheochromocytoma- catelcholamine excess, gluconeogenesis, decreased gluc uptake
* *- hypothyroidism
DRUGS
- glucocorticoids
- antipsychotics
* *- thiazide like diuretics
* *- protease inhibitors (HIV meds)
STRESSORS- MI, sepsis
194
Cause of diabetes mellitus 1
destruction of the beta cells in the iselts of Langerhans
195
diagnostic criteria for diabetes 1
sx plus random glucose >11mmol/l, fasting >7mmol/L
no sx + GTT (75g glucose) fasting >7mmol/l or 2hr value >11mol/L
196
sx of diabetes type 1
- polydipsia
- plyuria
- blurred vision
- wt loss and fatigue
- immunosupression- pruritis vulvulae, balanitis (candidiasis), chest infection
197
genetic link with diabetes mellitus
90% have HLA DR3/4
198
management of diabetes type 1
education- CHO intake, glucose lowering effect of exercise, LT risks
- test QDS, aiming for fasting level of 5-7mmol/L
Insulin
- quick acting- (novorapid, humalog), give immediately before (up to 15mins before) meal
- short acting- actarapid, humulin S- injected 20min before meal
- Medium actin- humulin I and insulatard- OD/BD
- Longacting- lantus, levemir- OD usually at bedtime
Regime:
- Basal bolus regime- short acting before meal, with BD long acting
- insulin pump- contains short acting insulin only, rate altered depending on glucose levels- if gets disconnected can get hypo and DKA quickly
- Dose adjustment for normal eating course for pts- reduces DKA and severe hypos
199
insluin to CHO ratio, correction of blood glucose for every insulin unit
1 unit for every 15g
1unit brings blood glucose down by 8
200
ix for ?diabetes I
bloods- fasting gluc, HbA1c
urinanalysis- glycosuria, ketones
antibodies- anti-GAD, pancreatic islet cell antibody, islet antigen-2 antibody, ZNT8
201
pathophysio of diabetes II
- insulin tolerance and resistance
| - some decreased secretion
202
sx diabetes II
- asx
- gradual fatigue
- polyuria, polydipsia
- complications- eg neuropathy, retinopathy
203
Management of diabetes II
- lifestyle
1. Metformin
2. Sulphonylureas- gliclazide
- Thiazoldinediones- pioglitazine
- DPP-4 inhibitors '-liptin'
- SGLT2 inhibitors '-flozin'
- glucagon-like peptide - 1 analogs- '-tide'
- insulin therapy
204
SE of metformin
GI upset
weakness
metallic taste in mouth
dont give if kidney function is poor (lactic acidosis risk)
205
example and SEs of sulphonylureas
Gliclazide
- hypoglycaemia!!!!!- sweaty, hot , confused
- weight GAIN
- dont give to older people
206
exmaple and SE of thiazolindinediones
pioglitazone
HF!, bladder cancer, wt GAIN, increases sensitivity to insulin
207
example and SE of DPP-4 inhibitors
algoliptin
GI, hypos
weight neutral
208
example and SEs and SGLT2 inhibitor
- flozin
canagliflozin, dapagliflozin, empagliflozin
SE
- wt loss
- DKA
- UTI (glycosuria)
- necrotising fascitis- advise any pain/erythema in genital or perianal area, fever, malaise
- fournier's gangrene
209
GLP-1 example and SE
exenatide
GI, wt loss
usually administered SC
210
glucagona like peptide-1 analogs- exmaple
exenatide
211
montiroing needed to type 2 diabetics
every 3 months- HbA1c-- keep below 48 mmol/L
annualy
- foot check- sensation, ulcers, infections
- fundoscopy
- BP
- cholesterol
- kidneys- check ACR for renal dunction
212
what is maturity onset diabetes for the young (MODY), tx
monogenic diabetes- autosomal dominant
often diagnosed in <25s, behaves like T2
tx- insulin, sulfonylurea
213
causes of hypoglyaemic epidose
EXPLAIN
- EXogenous drugs (insulin, alcohol, Sulphonylureas)
- Pituitary insufficiency (low ACTH and cortisol)
- Liver failure
- Addison's disease (low cortisol)
- Iset cell tumours (insulinoma)
- non-pancreatic neoplasms
214
sx hypoglycaemic episode
- syncope, dizziness
- shaking, tremor
- anxiety, irritability
- hunger
- impaired vision
- headache
- sweating, tachy/palpitations due to glucagon/arenaline release
- LoC, coma, confusion
215
tx hypoglycaemia
<4mmol/L
- glucose liquid/tablets/ 40% gels/ fruit juice, sugar
- avoid chocolates and biscuits
- once >4mmol/L- give long acting CHO- biscuits, bread, milk
- no response -- IM glucagon or glucose 10% IV infusion
- if unconsious/seizuring/aggressive- glucagon, glucose 10%/20% IV
- omit IV/short acting insulin
- do not omit long acting insulin
216
sx DKA
- N+V
- Abdo pain
^ could be it!
____________
- deep signing breaths- Kaussmals
- pear drop sweat smelling breaths
- bed wetting in prev dry chil
- increased urinary frequency- polyuria
- polydipsia
- wt loss
- pale and thin
- drowsy, LoC
217
DKA Ix
- FBC UE CRP-- hyponatraemia, hypokalaemia and low bicarb (acidosis) in severe cases, increased anion gap
- ABG/UE- metabolic acidosis
- weight pt
- urinanaysis/serum ketones
218
dka diagnostic criteria
- acidaemia <7.3 or low bicarb <15
- ketosis cap sample >3, or >2+ in urine
- hyperglycaemia >11mol/L random
219
expected ABG results during DKA
```
pH <7.3
pO2- high >7
pCO2- low <5
BE- low -2.5
bicarb is <15, 15-18 if mild dka
Glucose high >11
```
220
management of DKA (adult dosages and vols)
Fluid
- shock- NaCl 500ml over 15min, give another is <100mmhg systolic
- not shocked- give 500ml-1L NaCl over an hour, then 250ml/hr until euvolaemic
Insulin
- 50u actarapid in 50ml of NaCl (1u/ml) stat
- continuous IV infusion 0.1u/kg/hour
- fall in glucose should not exceed 5mm/hr
Potassium
- start once K is normal
- KCl 20mmol/hour
- do no give if anuric
- IV glucose 10% 125ml/hour when glucocse <14
- 5000u daily of daltaparin
- when out of DKA< switch to sliding scale insulin
221
Paeds- management in DKA
```
FLUIDS
If shocked:- bolus
- 20ml/kg over 15min
- if still shocked give 10ml/kg
- if still shocked, give inotropes
```
Deficit: -- 48 hour volume
% dehydration x Kg x 10
Maintenance:-- per day
- 100ml/kg for first 10kg
- 50ml/kg for next 20kg
- 20ml/kg for remaining weight
- - up to 80kg
- over 48 hours to reduce risk of cerebral oedema
Potassium
- every 500ml bag contains 20mmol of K (40mmol/L)
- monitor UEs and ECG
Insulin
- 50u actarapid in 50ml of 0.9% NaCl (1u/ml)
- infusion 0.05 or 0.1u/kg/hour
- give normal long acting insulin at normal dose during DKA
- stop usual short acting insulin whilst on infusion
- turn off insulin pump
222
what is hyperosmolar hyperglycaemic state
- high serum osmolality (>320mmol/kg) due to profound hyperglycaemia (often >40mmol/L0 in the absence of an acidosis or ketosis
223
presentation of hyperosmolar hyperglycaemic state
- polyuria, polydipsia
- weakness, nausea
- wt loss
- dehydration - dry mucous membrane, poor turgor
- disorientation
- drowsiness, LoC
- tachy
- hypotension
- shock
224
management of hyperosmolar hyperglycaemic state
- fluids
- correction of electrlytes (K)
- IV insulin
- dalteparin- VTE risk high
225
what LT complications of diabetes are there
- neuropathy (TCA/SSRIs, gabapentin, opioids, capsaicin, TENS,)
- diabetic foot, charcot
- motor nerve damage- clawing, callus
- peripheral vascular disease
- retinopathy- blurred, darkened/distortion, floaters, flashed of light, visual field loss
- nephropathy- proteinuria, nephrotic syndrome, malaise, pruritis, oedema
226
what is an adrenal crisis
- occurs due to acute adrenal insufficiency (addion's (primary), secondary (pituitary/hypothal damage))
227
sx and signs of adrenal crisis
- Abdo, flank pain
- confusion
- dizziness
- LoC, coma
- fatigue, weakness
- fever
- hypotension (low aldosterone)
- Cardiovasc collapse
- hypoglycaemia (low cortisol)
- hyponatraemia (low Aldosterone)
- hyperkalaemia ( low aldosterone)
228
what is carcinoid syndrome
- when neuropeptides like serotonin, histamine and postaglandins are released into circulation by neuroendocrine tumours
- eg phaeochromocytoma, other tumours in appendix, ileum, rectum and elsewhere capable of producing these things
229
sx carcinoid tumours
- flushing
- wheezing
- diarrhoea
- abdo pain
230
management of carcinoid syndrome
- octreotide (somatostatin analogue)
| - tumour resection
231
causes of hypertirchosis
hair everywhere on body
- ciclosporin, drugs
- congenital
- porphyria cutanea tarda
- anorexia nervosa
232
what different serum/urine ix are used for phaeochromocytoma, conns, addisons, cushings
Phaeochromocytoma-
- plasma and urinary metanephrines (breakdown product of catecholamines)
- 24hour catecholamine urine- also an option but is less reliable than the above
Conn's
**- aldosterone:renin serum -- high (aldosterone is high, renin is low)
Adrenal insuff/Addison's
- 9am cortisol levels
* *- ACTH levels (low in secondary insuff, high in Addison's)
* *- ACTH stimulation test (cosyntropin)- stimulates cortisol if central, both low if adrenal, both high if paraneo
* *- Plasma renin and aldosterone levels- renin high and aldo low in Addison's, may be normal in secondary
- Autoantibody- 21-hydroxylase Ab, adrenal cortex Ab
Cushing's-
- 24hour urinary free cortisol
- dexamethasone suppression test,
- midnight cortisol levels
- plasma ACTH
233
which antidiabetics are assoc with wt loss and which with wt gain
LOSS
- GLP-1 - SC (tide)
- SGLT2- PO (flozin)
GAIN
- Insulin- SC
- Sulfonylreas- PO eg gliclazide, tolbutamide, glimepiride
- Thiazolidinediones- PO
NEUTRAL
- DPP-4 (liptin)
234
What type of cancer that causes hyperthyroidism, is inherited
medullary carcinoma
- associated with MEN II
- tx resistant HTN
- one nodule!
235
what does a hot thyroid nodule on scintigraphy suggest ? what would the TSH be?
toxic adenoma, could also be thyroiditis
- low TSH due to thyrotoxicosis
- NB- thyroid cancer rarely cause thyrotoxicosis or hot nodules!
236
an 18 year old female presents with 3 nodules in the right lobe of her thyroid plus cervical lymphadenopathy. Her TFTs are normal. likely diagnosis?
thyroid nodules+ lymphadenopathy= papillary carcinoma
- likely to spread to lymph nodes
- most common type of thyroid cancer
237
causes of cold nodules on thyroid sctintigraphy
- cancers
- cysts
- fibroids
- non functioning adenoma
- thyroiditis
238
causes of hot nodules on sctintigraphy of thyroid
- toxic adenoma
- thyroiditis
- NOT cancer
239
cause of diffuse uptake of radioisotopic iodone on sctintigraphy (diffuse hot)
graves
240
what is MEN 1 assoc with
3ps
- parathyroid (primary hyperparathyroid)
- Pancreatic
- Pituitary (prolactinoma, adenoma)
241
what is MEN 2 assoc with
```
2A
- medullary thyroid cancer
- phaeochrmocytoma
- Primary hyperparathyroid (hyperplasia)
2B
- medullary thyroid cancer
- phaeochrmocytoma
- Marfan or Neuromas
```
242
what is sick euthyroid
- caused by systemic illness- stem will often be person in ITU or recovering from illness in hosp
- low thyroid hormones (mild), normal or low TSH
243
what does an elevated TSH with normal T4 indicate
subclinical hypothyroidism
244
what does a low TSH with normal thyroid hormones mean
subclinical hyperthryoidism
245
most common cause of primary hyperaldosteronism
BL adrenal hyperplasia
246
what type of cancer is hashimoto's thyroidisis associated with
MALT lypmhoma
247
most common cause of addisons in the UK, and worldwide
- uk- autoimmunity (>idiopathic)
| - worldwide- infection (mostly TB)
248
secretion of what hormones is reduced as part of stress reposnse
- insulin
- testosterone
- oestrogen
249
what is latent autoimmune diabetes of adulthood
LADA
- like T1 in older (may present with DKA
- 30-50y
- lack of insulin due to beta islet cell destruction
- No family history
- other autoimmune diseases
- no increase in body habitus
MODY
- like t2 but in younger
- tend to be under 25s
- normal insulin production, decreased sensitivity
- less likely to present with DKA etc
250
what causes hydatid cysts
- tape worm (low B12 sx, pruritis, GI sx)
Dog Tapeworm:
- Cystic echinoccosis (CE)/ hydatid disease
- infection with the larval stage of Echinococcus granulosus
- farming areas- raw meat fed to dogs who then spread it to us
- on aspiration of the liver cyst, people may experience an anaphylactic like reaction, so this is not done on cysts that have a ****detached membrane on CT***
251
what do meduallry cancer of the thyroid produce
calcitonin-
- hormone made by your thyroid to control how the body uses calcium.
- increases bone calcium content and decreases serum calcium level
- levels are used to screen for recurrence after resection of one
252
what type of diabetes does Lithium cause
nephrogenic diabetes insupidus
