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ECOS2 Exam 1 > Approach to Endocrine Complaints2: Thyroid, Parathyroid, Adrenal Disorders > Flashcards

Approach to Endocrine Complaints2: Thyroid, Parathyroid, Adrenal Disorders Flashcards

1
Q

What H is made in the pituitary and what is found in the periphery

A

T4

T3 - in periphery

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2
Q

Thyroid H released by Hypothalamus and AP

A

TRH

TSH

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3
Q

Hypothyroidism causes

A 
I deficiency 
Hashimoto’s Thyroiditis (autoimmune)
Iatrogentic cause (from hyperthyroidism Tx)
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4
Q

Hashimoto’s Thyroiditis

A

Most common in US
Hypothyroidism
If goiter then it will be : irregular and firm

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5
Q

Hypothyroidism Sx:

A 
Fatigue,
Dry skin 
COLD
Constipation 
Hair loss
Weight gain 
HYPOrefelx, Edema
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6
Q

labs show what in hypothyroidism

A

High TSH,
LOW T4, = * primary hypothyroidism
* if thyroid peroxidase present : autoimmune

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7
Q

3 causes of hyperthyroidism

A
  1. Graves Disease
  2. Toxic Multinodular goiter
  3. Toxic Adenomas : benign hot nodules
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8
Q

Graves Disease what is it

A

Most common in US
Hyperthyroidism
Autoimmune

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9
Q

Graves Disease Sx

A 
Hyperactive, irritability
HOT
Palpitations
Weigh loss
Decrease menses
Tremor 
GOITER (large, firm)
HYOERreflex 
Eyelid retraction + opthalmopathy
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10
Q

Labs show what in hyperthyroidism

A

Low TSH
HIGH T4 or T3 - *primary hyperthyroidism
TX: block with anti-thyroid drug or remove thyroid

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11
Q

Parathyroid Glands

A

Maintain Ca+2 in Blood Stream
Increase bone resorption
Increase intestinal Ca+2 secretion by VIT D
Decrease. Ca+2 excretion in kidney

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12
Q

PTH function

A

Increase CA

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13
Q

Primary Hyperparathyroidism

Cause

A

Autonomously functioning adenomas

Hyperplasia

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14
Q

Primary Hyperparathyroidism Sx:

A

most are asymptomatic
Just elevated CA
Renal Stones, Abnormal bones, ABD pains, psychic groans
Neuromuscular Sx, proximal muscle, weakness, easy fatigability, atrophy

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15
Q

Hypercalcemia or malignancy

A

Can cause Primary hyperparathyroidism only it is symptomatic and has extreme high CA

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16
Q

What do labs show for HPT

A

High PTH= *Primary HPT, due to high CA excreted in urine

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17
Q

Sx of Hypoparathyroidism

A 
Painful face spasms 
Pins and needles
HypOtention
Heart failure
CHVOSTEK’S SIGN
TROUSSEAU SIGN
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18
Q

Chvosteks sign

A

Same side contraction of facial muscles when tapping on facial nerve (ant to ear)

19
Q

Trousseau’s Sign

A

Carpal spasm when sphygmomanometer is inflated to above systolic BP for 3mins

20
Q

What do labs show when you have hypoparathyroidism

A

LOW PTH, low excretion of CA in urine

21
Q

Mineralcortricoids

A

Aldosterone

Corticosterone

22
Q

Glucocorticoids

A

Cortisol

Cortisone

23
Q

Catecholamines

A

EPIN + NEPIN

24
Q

How is Cortisol excreted
Low cortisol
Excess cortisol

A

By ACTH signal
Adrenal insufficiency (primary and secondary)
Crushing syndrome

25
Q

How is Aldosterone released and controlled

A

Low Blood volume or BP ——> low renal P ——> Juxtaglomerulous cells secrete RENIN

  1. Angiotensinogen ->Angiotensin 1(by renin)
  2. Angiotensin 1-> Angiotensin 2 (by ACE)
  3. AT2 receptor activated on adrenal gland = ALDOSTERONE
  4. VASOCONTRICTION = increase renal P and release Angiotensiongen
26
Q

Low aldosterone

Excess aldosterone

A 
Adrenal insufficiency (primary= CONN’S and secondary)
Aldosteronism
27
Q

Hypoadrenalism 2 major causes

A

ADDISON’S DISEASE : Autoimmune destruction of adrenal gland

EXOGENOUS GLUCOCORTICOIDS: suppress HPA axis, hypothalamic failure

28
Q

Adrenal insufficiency Sx: for glucocorticoids

A 
Fatigue
Weight loss
Hypoglycemia
Low BP
Postural hypotension
29
Q

Adrenal insufficiency Sx: for mineralocorticoids

A

Salt craving
Low BP
Hyponatremia
Hyperkalemia

30
Q

Hyperpigmentation when does this happen

A

For PRIMARY ADRENAL INSUFFICIENCY

31
Q

Addison’s disease hallmark

A

You will see hyperpigmentation

32
Q

Adrenal insufficiency what will you see in labs

A

ACTH stimulation test : measuring cortisol after

If LOW CORTISOL, test levels of ACTH, RENIN, ALDOSTERONE to know secondary vs primary

33
Q

Primary adrenal insufficiency

A

No cortisol

No aldosterone

34
Q

Secondary adrenal insufficiency

A

No cortisol

35
Q

Hypercortisolism 3 major types

A
  1. CRUSHING SYNDROME : ACTH dependent, AP adenoma makes excess acth, or adenoma other place causes high acth secreted ion
  2. Adrenocortical adenoma or carcinoma : ACTH independent
  3. Iatrogenic : Drugs to treat inflammation cause upregulation of cortisol
36
Q

Crushing Syndrome Sx

A 
Weight gain around abd
Easy bruising, acne 
weakness
Abnormal menses
Depression
Hirsutism
37
Q

What do you see in labs for crushing syndrome

A

Dexamethasone Suppression Test : suppress cortisol and then measure amount of cortisol
Measure midnight or 24hr urine excretion

38
Q

Primary aldosteronism

A

CONN’S syndrome
Adrenal adenoma or hyperplasia
5%-12% with HTN

39
Q

Aldosteronism hallmark

A

HTN + LOW K
Hypokalemic
NA is normal

40
Q

What do you see in labs for aldosteronism

A

Measure renin (low) and aldosterone (high) levels

41
Q

Adrenal Mass
benign
When to diagnose it
EX

A

Most are inactive for endocrine function
If >1cm
Phenochromocytoma

42
Q

Phenochromocytoma

A

Tumor making Catecholamines

  1. Palpitations
  2. Headache
  3. Profuse sweating
    * episodic HTN
43
Q

Pituitary Tumor

A

Usually discovered if an imaging is done

  1. Headache
  2. Vision loss
    * if non-functional adenoma just monitor no surgery needed

ECOS2 Exam 1 (15 decks)

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