Endocrinology Flashcards

1
Q

thyrotoxicosis

A

the clinical state associated with excess thyroid hormone activity, usually due to inappropriately high-circulating thyroid hormones. The clinical presentation varies, ranging from asymptomatic to life-threatening thyroid storm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

thyrotoxicosis presentation

A

hyper active
resting tremor
NO tenderness to thyroid (goiter is smooth but no actual inflammation- otherwise itd be sub acute thyroiditis)

heat intolerance, palpitations, anxiety, fatigue, weight loss, muscle weakness, and, in women, irregular menses.
tremor, tachycardia, lid lag, and warm moist skin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Graves’ disease

A

autoimmune disease attack on thyroid
antibodies produced against thyroid and eyes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

proptosis

A

symptom of graves’ disease
eyes pushed forwards
lid retracted
can lead to loss of vision
pressure on optic nerves

paralysis of eye muscle
double vision

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

CRP result

A

marker for inflammation
normal for Graves’
high for thyroiditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

T3 , T4 and TSH in Graves’

A

higher production of T3 in circulation
high T4
LOWER TSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

hyperthyroidism and symptom

A

overactive thyroid
aka thyrotoxicosis
increased activity of the sympathetic nervous system
increased activity of muscle that controls the upper lid
upper lids retracted
lid lag

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

thyroid physiology

A

hypothalamus releases TRH

anterior pituitary releases TSH

T3 and T4 released in thyroid in negative feedback loop
inhibits TSH or TRH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

thyrotoxicosis due to Graves’ disease

A

immune system producing autoimmune antibodies directed against TSH receptor

mimics TSH but constant stimulation

increases synthesis of thyroid hormones
leads to goiter formation

runs in families
female side

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

symptoms of hyperthyroidism

A

hyperactivity
heat intolerance
fatigue
weight loss
(despite always hungry)
diarrhoea
tachycardia
tremor
goiter
warm, moist skin
lid lag

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

causes of thyrotoxicosis

A

graves’ (TSH receptor stimulating antibody)
toxic nodule
toxic multinodular goitre
factitious thyrotoxicosis (external supplementation)

thyrotoxicosis associated with subacute thyroiditis is diff

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

detection of thyrotoxicosis

A

TSH receptor antibody

positive for graves
negative use other scans/goiter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

treatment of Graves’

A

1) peripheral adrenergic blockade:
propranolol (BB)
blocks tachycardia and tremor

diltiazem (calcium antagonist) if asthma

2) inhibit hormone synthesis of TPO thyroid peroxidase:

CBZ or PTU
risk of liver problems

3) removal of thyroid:
thyroxine for life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

myxoedema

A

swelling of skin
excess deposition of glycans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

hypothyroidism
things to look for in blood test

A

cortisol level too high = cushings
too low = addisons

TSH raised
low T4 T3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

hypothyroidism causes

A

subclinical disease -> myxoedema coma

primary disease most common:
autoimmune
latrogenic (caused by medicine)

elderly obese females

radiotherapy damaging thyroid for throat cancer

17
Q

hypothyroidism symptoms

A

myxoedema

nervous system:
forgetfulness, slow
carpal tunnel

cardiovascular:
bradycardia
decreased cardiac output
dependent oedema

Gastrointestinal:
constipation
ascitic fluid

renal:
hyponatremia
decreased glomerular filtration
reduced excretion of water

pulmonary:
respiratory compromise with hyperventilation
airway obstruction

musculoskeletal:
muscle cramps
myopathy

anaemia:

skin and hair:
loss of lateral eyebrows
dry cool skin
puffy face

metabolism:
hypothermia
intolerance to cold
weight gain

reproductive system:
heavy periods

18
Q

diagnosis of hypothyroidism

A

high TSH and low T4 = primary hypothyroidism

low/normal TSH and low T4 = secondary
pituitary disease
critically ill

19
Q

myxoedema treatment

A

levothyroxine
check cortisol level first
lower dose if old
hypothyroidism may be protecting them from heart failure due to slowed metabolic rate

20
Q

hyperpigmentation

A

caused by ACTH
Addison’s disease
primary adrenal insufficiency

21
Q

lab results suggesting adrenal insufficiency

A

low na high K = aldosterone deficiency
less reabsorption of Na, more excretion of K

low cortisol
high ACTH to compensate

22
Q

adrenal insufficiency

A

an absolute or relative deficiency of adrenal hormones
cortisol
aldosterone
androgen

23
Q

cortisol

A

glucocorticoid
Cortisol is a steroid hormone that is produced by your 2 adrenal glands, which sit on top of each kidney. When you are stressed, increased cortisol is released into your bloodstream

immune response
stress factors cause adrenal cortex to release cortisol

24
Q

aldosterone

A

Aldosterone (ALD) is a hormone that helps regulate your blood pressure by managing the levels of sodium (salt) and potassium in your blood and impacting blood volume.

retains Na, loses K

25
Q

Primary adrenal insufficiency (Addison’s disease) and
lab results diagnosis

A

autoimmune usually
whole cortex/adrenals is damaged
pituitary is fine

low cortisol
ACTH high
pigmentation
low aldosterone
Na low
K high
hypovolaemia (Na and water loss)

26
Q

secondary adrenal insufficiency

A

pituitary disease (pituitary releases ACTH)

low cortisol
ACTH low
no pigmentation
normal aldosterone
Na low
K normal
euvolaemia (normal fluid level in body)

27
Q

Addison’s symptoms

A

weakness
pigmentation
weight loss
vomiting/anorexia
hypotension
abdominal pain
salt craving
diarrhoea…

28
Q

causes of Addison’s

A

idiopathic- autoimmune, antibodies against adrenal cortex

infectious- viral, fungal

latrogenic- adrenals removed
haemorrhage

29
Q

causes of secondary adrenal insufficiency

A

exogenous glucocorticoids (medicine induced) (suppression of adrenal axis by negative feedback on ACTH)

pituitary insufficiency- ACTH deficiency, tumour, haemorrhage

hypothalamic insufficiency

head trauma

autoimmune disease

pituitary tumors or infection

bleeding in the pituitary

genetic diseases that affect the way the pituitary gland develops or functions

surgical removal of the pituitary to treat other conditions

30
Q

signs of excess glucocorticoids cushing’s syndrome

A

obesity
muscle weakness
skin ulcers
osteoporosis
hypertension

31
Q

adrenal crisis

A

Acute adrenal crisis is a medical emergency caused by a lack of cortisol. Patients may experience lightheadedness or dizziness, weakness, sweating, abdominal pain, nausea and vomiting, or even loss of consciousness.

long term steroid usage
infections
stress of surgery

32
Q

adrenal crisis pathophysiology

A

inadequate response to stress
causes
hypotension:
decreased myocardial contractility
hypovolemia (low extracellular fluid)

hypoNa, hypoK, hyperCa

hypoglycemia

33
Q

adrenal crisis treatment

A

give steroids

hypotension: fluid resuscitation, saline for Na loss

glucose infusion for hypoglycaemia

correct hyperkalaemia

correct hormone deficiency:
hydrocortisone

34
Q

prevention of adrenal crisis

A

acute illness: double dose of oral hydrocortisone (normal steroids)

severe:
IV hydrocortisone

emergency kit injection when waiting for ambulance