Endocrine Flashcards
(81 cards)
1
Q
Thyroid storm is an emergency, (can be fatal) how can it present?
NB: have high index of suspicion in pts with underlying overactive thyroid + precipitating event
A
-delirium
-severe tachycardia
-GI: D&V, dehydration
-v. high fever
(often after a precipitating event)
2
Q
Name possible precipitating events that could lead to a thyroid storm?
A
- systemic insults (surgery, trauma, MI, PE, DKA..)
- discontinuing anti-thyroid meds
- excessive iodine
- radioiodine therapy
- pseudoephedrine and salicylate use
3
Q
Name some differences between hyperthyroidism and thyroid storm. (NB: clinical fts are v similar)
A
- fever differentiates thyroid storm
- high output cardiac failure and new onset AF can also be present
4
Q
What are the core features of thyroid storm?
A
thyrotoxicosis + altered mental status + fever
- tachycardia out of proportion to fever
- (cardio or GI signs can be present too)
5
Q
How is thyroid storm diagnosed?
A
-a scoring system
if >45pts highly suggestive
-if <25 can be excluded
-between suggests impending poss
6
Q
How is thyroid storm managed? Name some principles only
A
- stop synthesis of new TH
- halt release of stored TH
- prevent conversion of T4 -> T3
- control adrenergic symptoms
- control systemic decompensation w supportive therapy
7
Q
Name how beta blockers are used to treat thyroid storm and their routes:
A
- IV propanolol (1mg, repeated in 5mins until desired effect)
- or oral propanolol 20-120mg 6hrly until heart rate under control
8
Q
Other than propranolol what medications are used to treat thyroid storm?
A
- carbimazole 10-30mg/daily or propylthiouracil 75-100mg/three times/day
- iodide
- steroids (dexamethasone 2mg 6hrly)
9
Q
How is iodide used to treat thyroid storm? What route?
A
- Lugol’s iodide solution: 4drops every 12hrs
- reduces the vascularity
- but effect only lasts 7-12days
10
Q
Where in the hospital should a thyroid storm pt be looked after? Other than direct rx, what supportive care is important to monitor/attend to?
A
- High Dependency/ICU
- hydration
- temperature (cool pt down)
- anti-pyretics e.g paracetamol
- AVOID ASPIRIN
- multivitamins esp. THIAMINE
11
Q
What is the logic behind the following in the management of pts with thyroid storm?
- -AVOID ASPIRIN
- multivitamins esp. THIAMINE
A
- AVOID ASPIRIN (causing release of TH from binding globulin)
- multivitamins esp. THIAMINE - important to correct the altered mental state
12
Q
What it used pre-operatively in pts with thyroid storm to get their T4 down into the normal range before thyroidectomy.
A
-anti-thyroid medications: thionamide therapy, if not tolerated iodine may be used.
13
Q
What is likely diagnosis in a 40yo Asian, with muscle weakness and hyperthyroidism, unwell after a vigorous workout
A
Thyrotoxic periodic paralysis
14
Q
When can Thyrotoxic periodic paralysis occur? What is the type/pattern of weakness?
A
- follow a vigorous exercise or a v high carb meal
- you get flaccid ascending paralysis (proximal->distal)
- spares facial and respiratory muscles
- depressed/absent Deep Tendon Reflexes due to weakness
14
Q
What is the biochemical cause of Thyrotoxic periodic paralysis?
A
low serum K+ (aka thyrotoxic hypokalaemic periodic paralysis)
-thyrotoxicosis +
more adrenergic activity, high carb meal/high insulin, increase Na+/K+ ATPase activity, decreases K+ leading to paralysis
15
Q
What is the management of Thyrotoxic periodic paralysis and why?
A
-B blocker e.g. propranolol 60mg inhibits Na/K ATPase
-replace potassium
-treat hyperthyroidism
AVOID IV glucose - as it pushes K+ from serum back into cells so can aggravate hypokalemia.
16
Q
70yo F, decline in function over last few days, c/o: malaise, fatigue, weakness and confusion, O/E: puffy face, depressed reflexes and bradycardic
anaemic, high ESR, low Na+, CK is elevated, hypothermic (35.4), decreasing RR-increased C02 retention on ABG
-T4 and T3 are low and TSH are high
What is the diagnosis
A
Myxoedema coma
17
Q
Name poss precipitating events to myxoedema coma?
A
- infection
- trauma
- CVA
- congestive HF
- exposure to cold
- Drugs: lithium, amiodarone, sedatives..
18
Q
Along with the classic hypothyroidism features, what are the clinical features of myxoedema coma?
A
- hypothermia
- altered mental status e.g. coma, delusions, psychosis
- hyponatraemia: 2dry to decreased free-water clearance
- hypoglycaemia: 2dry to impaired gluconeogenesis
- hypotension
- bradycardia
- respiratory failure
19
Q
Diagnosis of Myxoedema?
A
-clinical scenario and v. high TSH
(Have high index of suspicion
-pts w hypothroidism history
-decline in function onset is often insidious)
20
Q
Name the 3 major causes of myxedma.
A
- undiagnosed hypothyrodism e.g. automimmune thyroiditis
- discontinuation of therapy/run out of meds over months
- iatrogenic (stopping rx for pts having I-131 scan)
21
Q
What is the recommended principles In the treatment of myxoedema, how should pts be re-warmed, to avoid what? What should be monitored?
A
- gradually re-warm hypothermic pts w gentle passive external re-warming
- avoid hypotension from reversal of hypothermic vasoconstriction
- CVS status regularly monitored, and stabilise airway, give adequate O2 and ventilation
22
Q
What are the main targets in treatment of myxoedema?
A
- thyroid hormone replacement (levothyroxine 300micrograms slow IV, then 100 micrograms/day)
- correct metabolic abnormalities
- identify and correct precipitating factors
- give hydrocortisone 100mg IV 8hrly
23
Q
How can you correct the following abnormalities of myxoedema?
- hypoventilation:
- hyponatraemia:
- hypoglycaemia:
A
- hypoventilation: intubate and ventilate
- hyponatraemia: (SIADH so restrict water intake)
- hypoglycaemia: dextrose and IV fluid
24
Why should you avoid/be careful about giving IV thyroxine and pressors together?
Can precipitate VF/VT
| so stop adrenaline/dopamine when giving IV thyroxine
25
```
Synacthen 250mcg test to diagnose hypocortisolaemia:
-Omin: 130nmol/l (low)
-30min: 260nmol/l (expect: 420+ rise)
ACTH: high at 100ng/l
dx? likely cause?
```
Adrenal insufficiency
26
Addison's: adrenal gland doesn't make cortisol (+/-aldosterone, HPA axis intact), what are some symptoms?
- orthostatic hypotension
- hyponatraemia
- hyperkalaemia
- mild metabolic acidosis
- hyperpigmentation of skin
27
Where adrenal insufficiency arise from? If adrenal gland is normal, and K+ and H+ levels normal
-dysfunction of hypothalamus/pituitary/both
28
Name some causes of hypoadrenalism:
- abrupt cessation of exogenous glucocorticoids (99%)
- addison's
- secondary to pituatary disease
- tertiary from damage to hypothalamus e.g. suprasellar tumours
29
Name some causes of Addison's/primary adrenal insufficiency:
- autoimmunity
- infection e.g. TB, fungal..
- haemorrhage
- metastasis
- drugs: etomidate, ketoconazole
30
How may adrenal failure present?Name 5 features
- weakness/fatigue
- anaorexia/weight loss
- N&V
- diziness/orthostatic syx
- hyponatramia
- hypotension, shock and death
- hyperkalaemia and hyperpigmentation in primary Addison's
31
What may precipitate acute adrenal insufficiency?
- post stress (of trauma, surgery, infection, fasting) in pt w latent insufficiency
- post sudden withdrawal of adrenocortical hormone in pt w chronic insufficiency
- post bilat adrenalectomy or injury to both adrenals
- post sudden destruction of the pituitary
32
In hypopituitarism, why is hydrocortisone replaced before thyroxine?
Thyroxine causes a state of stress and can precipitate an adrenal crisis
so replace hydrocortisone for 48hrs+ before starting thyroxine
33
What test is used to diagnose adrenal failure? What is the levels at which suggests/excludes diagnosis?
- short synacthen test: baseline level, inject 250mg, measure plasma cortisol level at 60mins.
- exclude diagnosis of adrenal failure if basal or test level is >525nmol/l
- if <83nmol/L cortisol level at 8-9am this is likely to be primary adrenal crisis
34
Adrenal insufficiency treatment?
- initially give 2mg dexamethasone (doesnt affect ACTH/synacthen test, so once test done can switch to 50mg IV Hydrocortisone 6hrly until results come back)
- taper to 20mg IV 6hrly then oral equivalent as stress resolves
35
What shedule of hydrocortisone doses are pts who presented with adrenal failure, usually discharged on ?
10 : 5 : 5
| ie. 10mg in morning, then 5mg midday, 5mg in afternoon
36
What do you suspect here:
-unexplained low Na+, high K+, with hypotension unresponsive to catecholamine and fluids
?
-Adrenal crisis
37
In an insulin stress test (hypoglycamia) what does a cortisol <420 suggest
ACTH deficiency
38
In an insulin stress test (hypoglycamia) what does a GH <0.3 suggest?
GH deficiency
39
Pituitary apoplexy results from what?
acute haemorrhage/infarction of the gland
40
What is the clinical syndrome Pituitary apoplexy characterised by? Name 5 symptoms
- headache
- vomiting
- visual disturbances, ophthalmoplegia (esp CN III)
- meningismus
- fever
- decreased consciousness/death
41
What are some precipitating factors for the clinical syndrome Pituitary apoplexy? Name 5
- Diabetes
- acromegaly
- cushing's
- cardiac surgery
- radiotherapy
- use of oestrogens
- hypertension
- sudden head trauma, raised ICP
42
What is the treatment for the clinical syndrome Pituitary apoplexy characterised by?
- monitor fluid/electrolyte balance
- replace deficient hormone esp. Corticosteroids
- long term monitor for hypopiuitarism and recurrence of pituatary adenomas
- pituitary surgery (if LOC/vision loss)
43
Symptoms of phaeochromocytoma:
- treatment resistant HTN (can be labile)
- headache
- sweating
- palpitations
- chest pain
- anxiety
- glucose intolerance
44
Treatment of of phaeochromocytoma (after dx via plasma metanephrines):
(fact: sometimes -Magnesium, nitroprusside, CCB, ACEi also used)
- surgery but first prepare pt with...alpha blockers: phentolamine 5mg IV or phenoxybenzamine 10mg PO
- beta blockers: AFTER ABOVE ACHIEVED, propranolol 10mg PO
45
50yo F admitted with abdo pain,
- corrected calcium: 3.23mmol/L,
- vit D 89 (low),
- PTH 16.1 ng/L (high)..likely dx?
Primary hyperparathroidismm
46
Normal calcium is (2.0-2.5)
| Hypercalcaemic crisis when Ca2+ is over __can present with:
>3.5mmol/L
| -vomiting, bone pain, delirium, confusion...
47
Name 5 ddx of hypercalcaemia:
- hyperparathyroidism (ca and PTH both high)
- malignancy (high ca, supressed PTH)
- non-parathyroid endocrine disorder e.g. -granulomatous disease, -vitamin D intoxication, drugs like: lithium, thiazide diuretics, vitamin A
48
Hypercalcaemic crisis treatment:
- hydration: 2-4L IV daily to increase excretion
- loop diuretics e.g. furosemide
- bisphosphonates prevent bone resorption e.g pamidronate
- calcitonin: inhibits bone resorption and increases renal excretion
- glucocorticoids inhibit vit D activation
- haemodialysis if over 3.0mmol/L
49
Overweight is BMI>__
| Obesity is BMI>__
25-30 overweight
| 30kg/m2 obesity
50
Obese patients are at increased risk of premature ___ mainly from __, ___ heart disease and _____ disease.
Other associated conditions include:
- death: diabetes, ischaemic heart disease and cerebrovascular disease
- associated: HT, hyperlipidaemia, OSA, OA, fatty liver disease, gallstones and increased cancer risk
51
What drug treatment can be used for 3months in severely obese
Its MOA is an inhibitor of _____ ___ and hence fat digestion
- olistat
| - pancreatic lipase
52
Bariatric surgery indications:
- morbid obesity >40kg/m2
- obesity >35kg/m2 and obesity-related complications
- after conventional medical rx has failed
53
What are the 2 poss ,types of bariatric surgery:
- restrictive (gastric banding: which restricts ability the ability)
- intestinal bypass (which reduces the ability to absorb nutrients
- or combo Roux-en-Y
54
GnRH pulsatile release from the ____ around puberty stimulates the secretion of which 2 hormones from where? What effects do these 2 hormones have on subsequent hormone production from where in male sexual development?
- hypothalamus
- LH and FSH from anterior pituitary
- LH -> stimulates testosterone production from Leydig cells
- FSH -> stimulates testes to produce mature sperm and the inhibins A and B (B feeds back to pituitary to inhibit FSH)
55
After GnRH pulsatile release from hypothalamus in puberty, -LH and FSH are released from anterior pituitary
-LH -> stimulates testosterone production from Leydig cells
-how does testosterone circulate? Which receptor does it bind to?
what effect does testosterone have on male sexual development? name 4 things
- circulates bound to sex-hormone binding globulin
- acts via nuclear androgen receptor
- effects: pubic, axillary and facial hair growth, enlargement of external genitalia, deepening of voice, muscle growth and frontal balding and maintenance of libido
56
male hypogonadism can result from problems where? (3) how may it present?
- testes disease (primary hypogonadism)
- pituitary or hypothalamus disease (secondary hypogonadism)
- defect in ability to respond to testosterone
- androgen deficiency -> subfertility and delayed puberty and eunuchoid body proportions (long legs and arms relative to upper body and height as long bones continue to grow with delayed epiphyses fusion)
57
Kleinfelter's causes what? What is the genetic cause? What are 3 features?
- primary hypogonadism
- extra X chromosome --> 47 XXY
- accelerated atrophy of testicular germ cells -> sterility and small firm testes
- variable presentation, can be complete failure of sexual maturation, eunuchoid body proportions, gynaecomastia and learning difficulties
58
male hypogonadism can be caused by abnormalities such as:
-testes disease (primary hypogonadism) - congenital or acquired
-pituitary or hypothalamus disease (secondary hypogonadism)
-defect in ability to respond to testosterone
Give 6 examples of conditions that fit with these causes:
- hypopituitarism, Kallman's S. (selective gonadotrophic deficiency), severe systemic illness, severe underweight
- hyperprolactinemia (interferes with pulsatile LH/FSH release)
- congenital gonadal disease: cryptorchidism, kleinfelter's, 5a-reductase deficiency
- acquired gonadal disease: testicular torsion, sickle cell, orchidectomy, chemo/radio toxicity, orchitis (e.g. mumps), CKD, cirrhosis/alcohol
- androgen receptor (FSH/LH) deficiency/abnormality
59
What are the features of Kallman's syndrome and what causes it?
- congenital deficiency of GnRH
- anosmia
- colour blindness
- cleft palate
- renal abnormalities
60
What are 2 most common causes of gynaecomastia?
- liver disease
- drug SEs e.g. digoxin (oestrogenic), spironolactone (anti-androgen), cimetidine, diamorphine, cannabis
- (bronchial carcinoma, testicular tumours, hyperthyroidism rarer)
- any cause of hypogonadism (leading to low testosterone) or of high oestrogen/HCG e.g. secreting tumours
61
In the adult female, GnRH pulses stimulate LH and FSH release.
-what effect do these hormones have?
- LH: stimulates ovarian androgen production
| - FSH: stimulates follicular development and aromatase activity
62
Oestrogen replacement is most effective rx for relief of menopausal sx and reduces risk of ___ cancer and _____ however it increases the risk of: ___ cancer, _____ ___ disease, s____ and v___. Therefore name 3 CIs?
- reduces: colorectal cancer and osteoporosis
- increases: breast cancer, coronary heart disease, stroke and VTE
- CI: HX OF BREAST CANCER, CORONARY HD, STROKE OR VTE
NB: unopposed oestrogen increase endometrial cancer risk too
63
Oestrogen deficiency can present with a/oligo-mennorhoea, what other sx may be present?
- atrophy of breast and vagina
- loss of pubic hair
- osteoporosis
64
Hirsutism indicates increased _____ production by the ovaries or ____ glands, most common cause is ____, 3 rarer causes include:
- oestrogen production by ovaries or adrenal glands
- PCOS
- also: CAH, ovarian or adrenal androgen-secreting tumour, prolactinoma, Cushing's disease
65
Substantial androgen excess can be caused my multiple things, usually not PCOS, and presents with signs of virilisation such as:
- hirsutism
- clitoromegaly
- frontal balding
- deepening of voice
- loss of female body shape
66
PCOS fts:
- multiple small cysts in ovary (due to arrested follicular development)
- excess androgen production from ovaries (+adrenals)
- hyperinsulinemia and T2DM, HT, hyperlipidaemia, increased CVD risk
- may present w: hirsutism, acne, amenorrhoea +/- obesity
67
The Rotterdam criteria for diagnosis of PCOS needs 2 of the following 3 criteria to be present and other ddx are excluded (e.g. androgen-secreting tumour, Cushing's, CAH)
-
-
-
- menstrual irregularity due to oligo/an-ovulation
- clinical: hirsutism, acne, frontal balding/biochemical evidence of hyperandrogenism
- polycystic ovaries (multiple cysts) on US exam
68
Ix and ddx for hirsutism
- sex hormones: androgen index calculated by: serum total testosterone conc / sex hormone binding globulin, indicates bioavailable testosterone >1.5/2x upper limit normal suggests androgen secreting tumour
- serum prolactin: slightly high in PCOS, values >1.5/2x upper limit normal suggests pituitary/hypothalamic disease
- serum 17-hydroxyprogesterone: high in pts with non-classic CAH
- TV US - to visualise ovaries
69
3 fts of DKA are:
3 sx:
3 clinical signs:
- hyperketonaemia,-hyperglycaemia, -metabolic acidosis
- sx: polyuria and dypsia, weight loss, malaise, abdo pain, N&V, SOB, blurred vision, confusion, drowsiness, coma
- signs: flushed, dry mucous membranes, ketotic breath, postural hypo, tachyC, depressed consciousness
70
3 principles of DKA rx is..
- replace fluid (e.g. 500ml saline over 15mins if shock, then 1L saline over 1hr)
- give insulin
- correct electrolyte imbalances
71
1st principle of DKA rx is fluid replacement, suggest what you'd give if pt is shocked/BP<100 or if not shocked?
-monitor glucose how often, at what BM do you switch fluid to what?
- shock: 500ml saline over 15mins, then 1L saline over 1hr
- not shocked: 1L saline over 1hr
- monitor BM hourly
- when BM <15mmol/L switch to dextrose 5% (and insulin) treats acidosis and ketosis
72
In treating DKA, how do you give insulin (after fluid replacement)
- via what
- reduce by how much /hr, for how long
- what 2 things are monitored 4 hrly?
- via pump
- aim reduce 3mmol/hr
- continue insulin and dextrose until acidosis clears
- ABG and K+ checked 4 hourly
73
Per L fluid resus in treating DKA what amount of K+ roughly should be given?
-20-40mmol K+ per L fluid given
74
How does Hyperosmolar Hyperglycemic state present? In what pt groups does it occur?
- develops over weeks, BG v. v. high, presents w dehydration, impaired consciousness, v. .v high Na+
- in older pts, w relative insulin deficiency, T2DM or undiagnosed
75
What is the plasma osmolality like in HSS (hyperosmolar hyperglycaemic state) what is the consequence? so give what?
- v high osmolality so viscosity is very increased, so blood is like treacle so risk of clot formation etc
- anticoagulate to reduce VTE risk
76
what 2 medications can precipitate HSS?
- steroids
| - diuretics
77
Hypoglycaemia can occur in pts on insulin or what other medication class? name a couple of drugs in this class?
-Sulfonylureas e.g. gliclazide (diamicron), glipizide (minidiab), glipenclamide (daonil), chlorpropamide (hypomide)
78
Name 2 autonomic sx of hypoglycaemia
| and 3 neuroglycopenic sx:
- autonomic: hunger, confusion, tachyC (from adrenaline/glucagon fight/flight)
- neuroglycopenic: drowsy, slurred speech, irritable, LOC, convulsions, coma
79
In mild hypoglycaemia can treat with oral glucose e.g. how many g?
-if unable to swallow give IV ___ AND __(orange box, T1DM partners can give) ?
- 15-20g oral
| - or IV 50% dextrose (30-50mls) and IM GLUCAGON (1mg) as they wake up get them to take oral glucose
80
- if unable to swallow- treat hypoglycaemia with
- IV 50% dextrose (30-50mls) and IM GLUCAGON (1mg)
- NB pt should recover immediately, if they don't what may it be due to?
- cerebral oedema
- post ictal state
- other cause of coma e.g. CVA
