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Chemistry year 2 > Week 8 Endocrine > Flashcards

Week 8 Endocrine Flashcards

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1
Q

why do disorders of the endocrine system occur

A

too much or too little

Hyposecretion - depressed hormone
-tumor, cell death, autoimmunity , target cell insensitivity

Hypersecretion -elevated hormone
tumour, autoimmunity, failure of feedback

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2
Q

Normal system of Hypothalamus, tsh and tsh

A

Hypothalamus
➢ secretes Thyrotropin-Releasing Hormone (TRH)

TRH
➢ stimulates Anterior Pituitary to synthesize & secrete Thyroid-Stimulating Hormone (TSH or Thyrotropin)

TSH
➢ regulates synthesis & secretion of iodinated thyroid hormones Thyroxine (T4) & Triiodothyronine (T3)

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3
Q

How are T3 and T4 found in the body

A

-after secretion they circulate in plasma bound to 3 thyroid binding proteins
-0.04 of plasma T4 is unbound = FT4 biologically active
-0.4 of T3 is unbound
-most of t4 is converted into t3 in liver and kidney
-t3 is more active then t4

When t3/t4 get too high, theyll turn off TSH and TRH = negative feedback

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4
Q

Calcitonin

A

secreted by parafollicular C cells
-part of Ca homeostasis

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5
Q

Metabolism of Thyroxine (T4)

A

-derived from glycoprotein: thyroglobulin
-dietary iodine is critical
-t4 has 4 iodine and t3 has 3
-most of t4 is converted into t3 active and if inactive it is rT3
-iodine deficiency can cause hypothyroidism

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6
Q

Physiological effect of T4 & T3

A

tissue growth
brain maturation
increased heat production
increased oxygen consumption
increased metabolism

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7
Q

What is done in a lab investigation of thyroid disease

A

-use an immunoassay - chemiluminescent - Access
-TSH - best for monitoring thyroid function
-Total t4 and t3: alterations in the binding proteins can lead to levels out of RI - not thyroid related

-FT3/FT4- replaced Total T4T3

-Thyroglobulin- tumor marker for thyroid cancer- produced by follicular cells

Thyroid Autoimmunity
-Anti thyroid antibodies

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8
Q

Non lab investigations

A

Cytology - microscopic examination from FNA to look for Hurthle Cells - large

Nuclear Medicine
Radioactive Iodine Update RAIU
-decreased uptake = gland not active follow up with cold scan
-increased uptake = gland is active = hot scan

Ultrasound = look for tumor

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9
Q

Hypothyroidism

A

Low free T4 levels with a normal or high TSH

Primary-defect in thyroid gland > cant produce thyroxine (T4)
Hashimoto’s Disease

Secondary -defect in pituitary gland > cannot produce TSH (which stimulates T4 production)
pituitary adenoma, pituitary radiation

Tertiary-defect in hypothalamus (cannot produce TRH): rare

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10
Q

Hashimoto’s Disease

A
  • Chronic Lymphocytic Thyroiditis
    inflammation of thyroid gland
  • cause of primary hypothyroidism
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11
Q

Etiology of Hashimoto’s

A

Autoimmune destruction of thyroid in 2 ways:

  1. Massive infiltration of lymphocytes-gland enlarges (goitre produced):
  2. Thyroid auto-antibodies detected/measured in serum/plasma:
    anti-thyroglobulin antibody (anti-Tg)and anti-thyroidal peroxidase antibody (anti-TPO)

Causing:
cell death
thyroid unable to oxidize inorganic iodine & synthesize T3 & T4
Leads to underactive thyroid gland
increasing fibrosis

Low T4 and T3 levels > Pituitary will secrete more TSH > Thyroid doesn’t respond to TSH so it’ll just become bigger (constantly being stimulated but unable to respond

most common in women over 50

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12
Q

How does Hashimotos present

A

painless goiter
-round face = edema , slow speech
-dry skin hair
-decrease metabolic resistance -lack of t4 = EVERYTHING SLOWS DOWN

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13
Q

Hashimotos’s Disease: Laboratory Investigation

A

TSH increased
-measured by immunoassay - Access best for early detection
-confirms its disease of thyroid and not pituitary
-in 2ndary TSH in decreased

Confirm with
FT4= LOW
ANTI-TPO - present
FT4/FT3 =LOW

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14
Q

Treatment
of primary thyroid diseases

A

Oral thyroxine replacement therapy: Levothyroxine (Synthroid)

first you have high tsh but with T4 therapy it should even out

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15
Q

Hyperthyroidism

A

thyrotoxicosis
caused by Graves
Autoimmune - ABs are produced that activated the TSH receptor
-produces excessive thyroid hormone causing thyroid gland to grow

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16
Q

Etiology of graves

A

-Auto-antibodies called Thyrotropin-Receptor Antibodies
-may occur after a viral infection
-may be a genetic component
- auto-antibodies Mimic TSH & stimulate release of excess T

Results in:
-thyroid growth (hyperplasia)
non-suppressible, overproduction of excess thyroid hormones due to IgG antibody binding to TSH receptors

-Excess thyroid hormones turn off TSH (negative feedback) component

20-50 mostly women , familial

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17
Q

Clinical Presentation
of graves

A

Increased metabolic rate:
weight loss
bulging eyes
diarrhea increased GI motility
thin skin

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18
Q

Graves’ Disease: Laboratory Investigation

A

TSH: decreased (or undetectable)

Confirmatory Tests:
FT4: increased
T4, T3: increased
anti-TPO, anti-Tg antibodies: increased
Thyrotropin-Receptor Antibodies (TRAb): positive

Anti-TPO and Anti-Tg – These are produced in Hashimoto’s but is also increased in Grave’s because it’s created due to immune response (inflammation of thyroid

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19
Q

Non-Laboratory Investigation
of graves

A

Nuclear Medicine: RAIU
‘Hot’ scan (= increased radioactive uptake)

Cytology exam
FNA

Imaging: CT, MRI
detects developing exophthalmos
rules out thyroid or pituitary tumour

20
Q

Treatment of Graves

A

Anti-thyroid drugs
interfere with iodine uptake

  • Radioactive iodine
    damages some of thyroid cells
    monitor patient for hypothyroidism
  • Beta-blockers
    block action of thyroid hormones
  • Surgery
    to correct eyes (exophthalmos)
    Thyroidectomy – removal of thyroid gland
21
Q

What is the adrenal gland

A

-found above the kidney
-produces Adrenaline, steroids , aldosterone, and Cortisol
-has outer and inner medulla
-the outer cortex has 3 zones

22
Q

Hypothalamic-Pituitary-Adrenal Axis

A

Hypothalamus
secretes Corticotropin-releasing hormone (CRH) in response to stress, circadian signals, low serum cortisol levels

CRH
stimulates Anterior Pituitary to secrete Adrenocorticotropic hormone (ACTH)

ACTH
also called Corticotropin
-release is episodic or circadian
stimulates transport of free cholesterol into adrenal cortex mitochondria, initiating steroid production
e.g. stimulates cortex to synthesize & secrete hormones cortisol release also episodic or circadian: main feedback regulator
Recall: cholesterol is pre-cursor for all cortex steroids

23
Q

Adrenal Cortex Hormones

A

Mineralocorticoids (SALT)
regulates Renin- angiotensin system
secreted from Zona glomerulosa (G-zone)
Aldosterone: Na retention, K excretion & acid-base balance & regulation of blood pressure (blood volume)

Glucocorticoids (SUGAR)
regulates Cortisol
secreted from Zona fasciculata (F-zone)
Cortisol: regulates blood glucose & blood pressure (BP), secrete DHEA (dehydroepiandrosterone)
precursor for androgen hormones

Sex Hormones (SEX)
secreted from Zona reticularis (R-zone)
DHEA sulphated to DHEAS (dehydroepiandrosterone sulfate)
Produces precursor for sex hormones like testosterone & estradiol

24
Q

Cortisol

A

controlled by negatie feedback system
-excess Cortisol turns off ACTH and CRH
-ACTH is circadian or diurnal, producing the most Cort in the am and least in the pm
-90% of cort is bound to CBG corticosteroid-binding protein (CBG)
-while the other 10 is free and filter through the kidneys and liver , this is measured in urine and saliva

-increases glucose levels
-increases protein breakdown and lipolysis
-maintains BP preventing hypotension
-anti inflammatory
-increases stress response for glucose production for flight or fight
-treatment for autoimmune disease

25
Q

Cushings Disease /syndrome etiology

A

Hypercortisolism: excessive production/secretion of cortisol

  • Endogenous cortisol:
    3 types:
    1. If pituitary, it’s called secondary Cushing’s
    2. If adrenal, it’s called primary Cushing’s
    3. If ectopic: it’s related to presence of tumour ( not located in pituitary or adrenal)

Cushing’s can be classified as:
ACTH-dependent or ACTH-independent disease

  • Exogenous cortisol: prolonged steroid therapy
26
Q

ACTH-Dependent Cushing’s Disease

A

Disease of anterior pituitary (Secondary)
-benign pituitary tumour (adenoma) secretes excess ACTH

-excess ACTH from pituitary causes
-overproduction of cortisol in adrenal
-serum cortisol and ACTH both increased
-imaging (CT or MRI) of pituitary needed to confirm

27
Q

ACTH-Dependent Cushing’s Syndrome

A

-Ectopic ACTH-secreting tumour
-non-endocrine malignant tumour
-Lung-tumour or gut-tumour or ovarian-tumour secretes excess ACTH
-excess ACTH from ectopic tumour causes overproduction of cortisol in adrenal
-serum cortisol and ACTH both increased
imaging (CT or MRI) needed to confirm location of tumour

28
Q

. ACTH-Independent

A

This type of Cushing’s is not due to excess ACTH

Disease of adrenal (Primary Cushing’s)
-adenoma or carcinoma of adrenal cortex
-causes increased secretion of cortisol
-increased cortisol suppresses (turns off) ACTH
-atrophy of non-tumorous part of adrenal gland

  1. long-term treatment with injected, oral or inhaled corticosteroids (prednisone) for non-related condition

serum cortisol is increased
ACTH is decreased
-imaging (CT or MRI) of adrenal glands needed to confirm

29
Q

Clinical Features of Hypercortisolism

A

weight gain
moonface
hirsutism
easy bruising
hyperpigmentation :if pituitary or ectopic due to excess ACTH (high levels of ACTH stimulate melanocytes)

30
Q

Lab Investigation

A

screening tests:
Urine free cort collected over 24 hours
Dexamethasone suppression testing
midnight salivary cortisol (Patients with excess endogenous production of cortisol will lose diurnal variability in cortisol production (both morn and evening cortisol levels will be increased)

then a differential diagnostic test

31
Q

24 hour Urinary Free Cortisol (UFC)

A

-measures cortisol not bound to plasma protein aka free which is filtered and excreted in urine
-most sensitive test when you are looking at excess Cortisol production
-collect 24 hour urine - measure volume ACCURATELY
-measure free cortisol and calc the amount that is excreted per day

if<100 ug a day then NOT cushings
if >120 ug then Cushings in likely but you have to do more testing

not good for differentiating if the cause is pituitary, adrenal or ectopic tumor

32
Q

Dexamethasone Suppression

A

after a pt is given dexamethasone the AM cort should be LOW but for a person with Cushings the morning Cort will stay high

-used for overactive glands so pt is given this to turn off hormone
-Dexa suppresses Pituitary ACTH decreasing production of Cortisol in adrenal

Testing
administer btwn 11pm-12 am , measure at 8 am and if AM cort is low then it was suppressed

33
Q

Serum Cortisol

A

after you see there is hypercortisolism

-measure by immunoassay like Access
-helps with seeing if diurnal vairation is lost take one at 8 and other at 2000
-healthy people evening levels that are lower than days but if evening stays high then you have lost diurnal variation aka excess cortisol from adrenal aka Cushings

does not differentiate what the cause is

34
Q

plasma ACTH level

A

if ACTH decreased:
Cushing’s related to adrenal
-excess cortisol from adrenal turns off pituitary ACTH (negative feedback)
adrenal tumors or hyperplasia
-confirm location of tumour in adrenal with imaging (CT, MRI)

if ACTH increased:
-Cushing’s related to pituitary or an ectopic tumour
-imaging needed to determine the location of tumour

35
Q

measuring ACTH in plasma

A

-breaks down quickyl in plasma after collection, spin cold and freeze
-measure with immunoradiometeric assay

RI <26 pmol

Adrenal tumor <2 pmol
high = pituitary tumour
very high >50 pmol - Ectopic tumor

36
Q

other lab tests for Cushings

A

Aldosterone can be increased
-hypokalemia - decreased potassium (increased urine excretion)
-hypernatremia -increased Na retention (urine retention
-metabolic alkalosis with high pH increased urine output

increased sex hormones

37
Q

non-Laboratory Investigation
for cushings

A

MRI / CT imaging: clarifies tumour location:

Scan pituitary gland-shows adenoma

Scan adrenal gland
-shows hyperplasia / enlargement
s-hows adenoma or carcinoma

Scan chest/abdominal
-used to locate ectopic tumour in lung

38
Q

Cushing’s: Treatment

A

surgery
removal of tumour (from pituitary)
adrenalectomy (lifetime replacement of hormones)
radiation
chemotherapy

39
Q

What is addison’s Disease

A

Primary adrenal insufficiency
-destruction of adrenal cortex
-leads to hypofunction
-disease of adrenal, rarely pituitary

Causes Decreased production of all 3 classes of steroids:
-mineralocorticoids: aldosterone
-glucocorticoids: cortisol
-androgens (sex hormones)

Leads to Increased production of pituitary ACTH in effort to stimulate underactive adrenals

40
Q

Addison’s: Etiology

A

most from autoimmune process with circulating anti-adrenal antibodies (auto antibodies)
-chronic form due to atrophy of adrenal

-tb
-metastatic tumor
-AIDS associated
-fungal infections

41
Q

Pathophysiology of Addison’s

A

Deficiency of all 3 classes of steroids
-No symptoms until 90% of cortex destroyed
-Progressive loss of Aldosterone & Cortisol
-Increasing ACTH levels: in effort to correct hormone deficiencies

Aldosterone acts on kidney to increase blood pressure through volume expansion
Aldoesterone secretion is regulated by Angiotensinogen

Low sodium and high potassium will turn on renin angiotensin system to stimulate production of aldosterone

42
Q

Addison’s: Clinical Presentation

A

weight loss, fatigue
-GI issues
-dehydration volume depletion
-hypotension
-hypoglycemia
-hyperpigmentation

Addisonian or Adrenal crisis: acute adrenal insufficiency
-low BP
-insufficient levels of cortisol hormone

43
Q

Lab Investigation: Addison’s

A

metabolic acidosis: pH low
Urine sodium: increased
hyperkalemia
low sugar and salt
-decreased aldosterone no reabsorption of sodium
ACTH increased but only in primary adrenal insufficiency
-cortisol may be decreased

44
Q

CTH Stimulation Test

A

tests for underactive glands
-CRT0 before dose
-inject with synthetic ACTH (cosyntropin) , collected CRT30, CRT 60
-measure all 3 for serum CORT

-must see doubling
-pts with decreased Cortisol response means there was no response to the ACTH given

diagnostic of Addisons

45
Q

Treatment for Addisons

A

replacement therapy
oral synthetic G/F

normal saline for hypovolemia and hyponatremia

Chemistry year 2 (12 decks)

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