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Endocrine Flashcards

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)

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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
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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

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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)
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5
Q

How is thyroid storm diagnosed?

A

-a scoring system
if >45pts highly suggestive
-if <25 can be excluded
-between suggests impending poss

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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
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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
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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)
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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
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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
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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
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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.

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13
Q

What is likely diagnosis in a 40yo Asian, with muscle weakness and hyperthyroidism, unwell after a vigorous workout

A

Thyrotoxic periodic paralysis

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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
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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

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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.

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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

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17
Q

Name poss precipitating events to myxoedema coma?

A
  • infection
  • trauma
  • CVA
  • congestive HF
  • exposure to cold
  • Drugs: lithium, amiodarone, sedatives..
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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
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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)

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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)
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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
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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
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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
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24
Q

Why should you avoid/be careful about giving IV thyroxine and pressors together?

A

Can precipitate VF/VT

so stop adrenaline/dopamine when giving IV thyroxine

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25
Q 
Synacthen 250mcg test to diagnose hypocortisolaemia:
-Omin: 130nmol/l (low)
-30min: 260nmol/l (expect: 420+ rise)
ACTH: high at 100ng/l
dx? likely cause?
A

Adrenal insufficiency

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26
Q

Addison’s: adrenal gland doesn’t make cortisol (+/-aldosterone, HPA axis intact), what are some symptoms?

A
  • orthostatic hypotension
  • hyponatraemia
  • hyperkalaemia
  • mild metabolic acidosis
  • hyperpigmentation of skin
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27
Q

Where adrenal insufficiency arise from? If adrenal gland is normal, and K+ and H+ levels normal

A

-dysfunction of hypothalamus/pituitary/both

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28
Q

Name some causes of hypoadrenalism:

A
  • abrupt cessation of exogenous glucocorticoids (99%)
  • addison’s
  • secondary to pituatary disease
  • tertiary from damage to hypothalamus e.g. suprasellar tumours
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29
Q

Name some causes of Addison’s/primary adrenal insufficiency:

A
  • autoimmunity
  • infection e.g. TB, fungal..
  • haemorrhage
  • metastasis
  • drugs: etomidate, ketoconazole
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30
Q

How may adrenal failure present?Name 5 features

A
  • weakness/fatigue
  • anaorexia/weight loss
  • N&V
  • diziness/orthostatic syx
  • hyponatramia
  • hypotension, shock and death
  • hyperkalaemia and hyperpigmentation in primary Addison’s
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31
Q

What may precipitate acute adrenal insufficiency?

A
  • 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
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32
Q

In hypopituitarism, why is hydrocortisone replaced before thyroxine?

A

Thyroxine causes a state of stress and can precipitate an adrenal crisis
so replace hydrocortisone for 48hrs+ before starting thyroxine

33
Q

What test is used to diagnose adrenal failure? What is the levels at which suggests/excludes diagnosis?

A
  • 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
Q

Adrenal insufficiency treatment?

A
  • 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
Q

What shedule of hydrocortisone doses are pts who presented with adrenal failure, usually discharged on ?

A

10 : 5 : 5

ie. 10mg in morning, then 5mg midday, 5mg in afternoon

36
Q

What do you suspect here:
-unexplained low Na+, high K+, with hypotension unresponsive to catecholamine and fluids
?

A

-Adrenal crisis

37
Q

In an insulin stress test (hypoglycamia) what does a cortisol <420 suggest

A

ACTH deficiency

38
Q

In an insulin stress test (hypoglycamia) what does a GH <0.3 suggest?

A

GH deficiency

39
Q

Pituitary apoplexy results from what?

A

acute haemorrhage/infarction of the gland

40
Q

What is the clinical syndrome Pituitary apoplexy characterised by? Name 5 symptoms

A
  • headache
  • vomiting
  • visual disturbances, ophthalmoplegia (esp CN III)
  • meningismus
  • fever
  • decreased consciousness/death
41
Q

What are some precipitating factors for the clinical syndrome Pituitary apoplexy? Name 5

A
  • Diabetes
  • acromegaly
  • cushing’s
  • cardiac surgery
  • radiotherapy
  • use of oestrogens
  • hypertension
  • sudden head trauma, raised ICP
42
Q

What is the treatment for the clinical syndrome Pituitary apoplexy characterised by?

A
  • 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
Q

Symptoms of phaeochromocytoma:

A
  • treatment resistant HTN (can be labile)
  • headache
  • sweating
  • palpitations
  • chest pain
  • anxiety
  • glucose intolerance
44
Q

Treatment of of phaeochromocytoma (after dx via plasma metanephrines):
(fact: sometimes -Magnesium, nitroprusside, CCB, ACEi also used)

A
  • surgery but first prepare pt with…alpha blockers: phentolamine 5mg IV or phenoxybenzamine 10mg PO
  • beta blockers: AFTER ABOVE ACHIEVED, propranolol 10mg PO
45
Q

50yo F admitted with abdo pain,

  • corrected calcium: 3.23mmol/L,
  • vit D 89 (low),
  • PTH 16.1 ng/L (high)..likely dx?
A

Primary hyperparathroidismm

46
Q

Normal calcium is (2.0-2.5)

Hypercalcaemic crisis when Ca2+ is over __can present with:

A

> 3.5mmol/L

-vomiting, bone pain, delirium, confusion…

47
Q

Name 5 ddx of hypercalcaemia:

A
  • 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
Q

Hypercalcaemic crisis treatment:

A
  • 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
Q

Overweight is BMI>__

Obesity is BMI>__

A

25-30 overweight

30kg/m2 obesity

50
Q

Obese patients are at increased risk of premature ___ mainly from __, ___ heart disease and _____ disease.
Other associated conditions include:

A
  • death: diabetes, ischaemic heart disease and cerebrovascular disease
  • associated: HT, hyperlipidaemia, OSA, OA, fatty liver disease, gallstones and increased cancer risk
51
Q

What drug treatment can be used for 3months in severely obese
Its MOA is an inhibitor of _____ ___ and hence fat digestion

A
  • olistat

- pancreatic lipase

52
Q

Bariatric surgery indications:

A
  • morbid obesity >40kg/m2
  • obesity >35kg/m2 and obesity-related complications
  • after conventional medical rx has failed
53
Q

What are the 2 poss ,types of bariatric surgery:

A
  • restrictive (gastric banding: which restricts ability the ability)
  • intestinal bypass (which reduces the ability to absorb nutrients
  • or combo Roux-en-Y
54
Q

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?

A
  • 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
Q

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

A
  • 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
Q

male hypogonadism can result from problems where? (3) how may it present?

A
  • 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
Q

Kleinfelter’s causes what? What is the genetic cause? What are 3 features?

A
  • 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
Q

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:

A
  • 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
Q

What are the features of Kallman’s syndrome and what causes it?

A
  • congenital deficiency of GnRH
  • anosmia
  • colour blindness
  • cleft palate
  • renal abnormalities
60
Q

What are 2 most common causes of gynaecomastia?

A
  • 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
Q

In the adult female, GnRH pulses stimulate LH and FSH release.
-what effect do these hormones have?

A
  • LH: stimulates ovarian androgen production

- FSH: stimulates follicular development and aromatase activity

62
Q

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?

A
  • 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
Q

Oestrogen deficiency can present with a/oligo-mennorhoea, what other sx may be present?

A
  • atrophy of breast and vagina
  • loss of pubic hair
  • osteoporosis
64
Q

Hirsutism indicates increased _____ production by the ovaries or ____ glands, most common cause is ____, 3 rarer causes include:

A
  • oestrogen production by ovaries or adrenal glands
  • PCOS
  • also: CAH, ovarian or adrenal androgen-secreting tumour, prolactinoma, Cushing’s disease
65
Q

Substantial androgen excess can be caused my multiple things, usually not PCOS, and presents with signs of virilisation such as:

A
  • hirsutism
  • clitoromegaly
  • frontal balding
  • deepening of voice
  • loss of female body shape
66
Q

PCOS fts:

A
  • 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
Q

-
-

A
  • menstrual irregularity due to oligo/an-ovulation
  • clinical: hirsutism, acne, frontal balding/biochemical evidence of hyperandrogenism
  • polycystic ovaries (multiple cysts) on US exam
68
Q

Ix and ddx for hirsutism

A
  • 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
Q

3 fts of DKA are:
3 sx:
3 clinical signs:

A
  • 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
Q

3 principles of DKA rx is..

A
  • replace fluid (e.g. 500ml saline over 15mins if shock, then 1L saline over 1hr)
  • give insulin
  • correct electrolyte imbalances
71
Q

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?

A
  • 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
Q

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?
A
  • via pump
  • aim reduce 3mmol/hr
  • continue insulin and dextrose until acidosis clears
  • ABG and K+ checked 4 hourly
73
Q

Per L fluid resus in treating DKA what amount of K+ roughly should be given?

A

-20-40mmol K+ per L fluid given

74
Q

How does Hyperosmolar Hyperglycemic state present? In what pt groups does it occur?

A
  • 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
Q

What is the plasma osmolality like in HSS (hyperosmolar hyperglycaemic state) what is the consequence? so give what?

A
  • 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
Q

what 2 medications can precipitate HSS?

A
  • steroids

- diuretics

77
Q

Hypoglycaemia can occur in pts on insulin or what other medication class? name a couple of drugs in this class?

A

-Sulfonylureas e.g. gliclazide (diamicron), glipizide (minidiab), glipenclamide (daonil), chlorpropamide (hypomide)

78
Q

Name 2 autonomic sx of hypoglycaemia

and 3 neuroglycopenic sx:

A
  • autonomic: hunger, confusion, tachyC (from adrenaline/glucagon fight/flight)
  • neuroglycopenic: drowsy, slurred speech, irritable, LOC, convulsions, coma
79
Q

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) ?

A
  • 15-20g oral

- or IV 50% dextrose (30-50mls) and IM GLUCAGON (1mg) as they wake up get them to take oral glucose

80
Q
  • 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?
A
  • cerebral oedema
  • post ictal state
  • other cause of coma e.g. CVA

medicine (10 decks)

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