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Endocrine II > Thyroid Disorders > Flashcards

Thyroid Disorders Flashcards

1
Q

What is the etiology of Hypothyroidism

A

Decrease in thyroid function
Primary:Peripheral(thyroid) disorder
T3/T4 decreased
TSH increased
CausesL Autoimmune: Hashimoto thyroiditis
surgery, irradiation, radiotherapy
Drugs: lithium, iodide, p-aminosalicyclic acid
Iodine deficiency
Congenital hypothyroidism

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2
Q

What is the etiology of secondary hypothyroidism

A

central hypothyroidism
*Pituitary disorders-dec TSH, T3/T4 {Pituitary tumor, postpartum pituitary necrosis, trauma & non-pituitary tumors}
*Hypothalamic disorders
dec TRH levels, TSH, T3/T4
{tumors, trauma, radiation therapy, or infiltrative diseases

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3
Q

What is the alter physiology hypothyroidism

A

slowing of thyroid
accumulation of glycoaminoglycan —>myxoedema

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4
Q

What is the alter physiology hyperthyroidism

A

catabolism
SNS
impaired reproductive sys
goitre—> hyperplasia & hypertrophy

Compression by goitre
trachea—.dyspnoea, oesophagus, dysphagia
Recurrent laryngeal N—> Hoarseness of voice
SVC syndrome: facial & arm swelling
Cervical sympathetic plexus—> Horner

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5
Q

Clinical presentation of hypothyroidism

A

Cool and pale skin
yellowish discoloration
dry skin
dry, brittle, coarse hair & brittle nails
less sweating
nonpitting edema(myxedema)

MSK:
muscle weakness, cramps, and myalgias; carpal tunnel syndrome, hyporeflexia, dyspnoea
GI: constipation, weight gain
Neuro: depression, cognitive dysfunction
Metabolic:hyponatremia
Eye: Periorbital edema
Hyperprolactinemia
amenorrhea; menorrhagia

CVS: reduced cardiac output:reductions in heart rate(bradycardia)
HTN, hypercholesterolemia
hematogical: Macrocytic (megaloblastic)

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6
Q

Subclinical hypothyroidism levels

A

mildly inc TSH, normal T3/T4

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7
Q

Primary hypothyroidism

A

inc TSH
dec T3
dec or normal

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8
Q

secondary and tertiary hypothyroidism

A

dec TSH
dec T4

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9
Q

Thyroid antibody testing

A

TPOAb
TgAB
TRAbs{Hashimoto}

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10
Q

Euthyroid sick syndrome/non thyroidal disease

A

dec T3
T4 & TSH normal

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11
Q

alters thyroid hormone synthesis and release by inhibibitors

A

IL-1, Il-6, TNF-alpha, and IFN beta

Disrupts target tissue response of thyroid hormones»> TBG reduction or thyroid receptor down regulation due to protease clevage

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12
Q

Most common mutation in pituitary adenoma involves

A

Activated G protein mutations

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13
Q

Pt presents with white fluid from breast not associated with pregnancy causes

A

Pituitary adenoma Dopamine antagonist injury to stalk

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14
Q

H/A Bitemporal visual loss, Past History of adrenal gland surgery ACTH very high

A

Nelson syndrome

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15
Q

Fatigue, dizziness, weight loss, reduced muscle mass/muscle weakness, low blood sugar and low blood pressure

A

Low ACTH

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16
Q

Irregular menses, loss of libido

A

Low FSH/LH

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17
Q

Cold intolerance, weight gain, brittle nails & hair irregular menses, decreased growth in children

A

TRH

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18
Q

Stunted growth, increased body fat decreased muscle mass

A

GHRH

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19
Q

Obese hypertensive lady with hypopituitarism, enlarged sella pituitary gland height loss

A

Empty sella syndrome

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20
Q

H?A, blurring of peripheral vision, sudden hypopituitarism

A

Pituitary apoplexy
Pituitary hemorrhage

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21
Q

Failure of migration of neurons olfactory to hypothalamus»> Delayed puberty, Testis is <1-2 mL volume & ANOSMIA GnRH def

A

Kallman syndrome
KAL 1 gene mutation

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22
Q

Abnormalities in growth hormone receptors (GHR) due to mutations Low GH & IGF-1 low

A

Larron syndrome

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23
Q

Bitemporal hemianopsia

A

Optic chiasm

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24
Q

Increases prolactin

A

Dopamine block and high TRH, Prolactinoma

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25
Q

Any blood disorder that can cause pituitary infarction

A

SCD

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26
Q

Galactorrhea loss of lateral vision headache

A

Prolactinoma

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27
Q

Grossly machine oil like secretions seen

A

Craniopharynigioma

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28
Q

Child, brain tumour squamous cells seen on histopathology

A

Craniopharyngioma

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29
Q

Pituitary tumour tumous shows GNAS mutation IGF 1 RAISED

A

Somatroph adenoma GH

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30
Q

Tumour is a derivative of Rathkes pouch child calcified tumour

A

Craniopharyngioma

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31
Q

Most common mutation in pituitary adenoma involves

A

Activated G protein mutations

32
Q

Pr presents with white fluid from breast not associated with pregnancy causes

A

Pituitary adenoma Dopamine antagonist injury to stalk

33
Q

Pt on Haloperidol what clinical symptom expected, Why??

A

Increase prolactin dopamine antagonist

34
Q

Headaches, Bitemporal visual loss, Past History of adrenal glands surgery ACTH very high

A

Nelson syndrome

35
Q

Desmopressin

A

V2 agonist; Central diabetes insipidus; Enuresis; Hemophilia A; Von Willebrand disease
A/E: GI, hyponatremia

36
Q

Oxytocin

A

Activates Gq-IP-DAP-Ca2+
Uterine tone, induction labor, PPH
A/E: fetal distress, uterine rupture

37
Q

Bromocriptine
Cabergoline

A

Activates dopamine
D2 receptions,
Suppresses the prolactin & GH
Hyperprolactinemia, acromegaly, parkinson disease
A/E: GI, orthostatic hypotension, psychosis, vasospasm

38
Q

Follitropin alpha

A

Activates FSH receptors
Controlled ovarian stimulation, infertility due to hypogonadotropic, hypogondadism in men(MHH)
A/E: multiple pregnancies,gynecomastia in men

39
Q

hCG

A

Agonist at LH receptors
Initiation of final oocyte maturation and ovulation during controlled ovarian stimulation, MHH
A/E: depression

40
Q

Leuprolide

A

GnRH agonist. Increase LKH & FSH secretions with intermittent administration. Reduced LH and FSH secretion with continuous admin.
Ovarian suppression, controlled ovarian stimulation, central precocious puberty, prostate cancer, endometriosis, breast cancer
A/E: H/A, nausea

41
Q

Ganirelix

A

Blocks GnRH receptors, reduces endogenous LH, FSH
Prevention of premature LH surge during controlled ovarian stimulation
A/E: H/A, nausea
Contraindications: pregnancy

42
Q

Mecasermin

A

R IGF-1
IGF-1 deficiency that is not responsive to exogenous GH
Hypoglycemia, intracranial hypertension, hepatotoxicity

43
Q

Somatropin: Recombinant Human GH (rhGH)

A

• Mechanism of action: Activates JAK tyrosine kinase and STAT → IGF-1 →
longitudinal bone growth → GH → reduces insulin sensitivity → IGF-1 →
glucose uptake → In patients with GH receptor mutation → rIGF-1 →
hypoglycemia
• Peak levels occur in 2–4 hours, and active blood levels persist for
approximately 36 hours.

44
Q

Somatropin: Recombinant Human GH (rhGH)
Clinical use:

A

Growth: Growth failure in paediatric patients associated with:
• Growth hormone deficiency
• Prader-Willi syndrome
• Turner syndrome
• Chronic renal insufficiency pre-transplant
• Small-for-gestational-age with failure to catch up by age 2 years
• Noonan syndrome
• Short stature homeobox-containing gene (SHOX) deficiency
• Idiopathic short stature, pituitary dwarfism
• Improved metabolic state, increased lean body mass, sense of wellbeing
• Growth hormone deficiency in adults
• Increased lean body mass, weight, and physical endurance
• Wasting in patients with HIV infection
• Improved gastrointestinal function
• Short bowel syndrome in patients who are also receiving specialized nutritional support

45
Q

Adverse Effects and Contraindications: GH

A

Pseudotumor cerebri, slipped capital femoral epiphysis, scoliosis, edema,
hyperglycaemia, asphyxiation in severely obese patients with Prader-Willi
syndrome
• Patients with turner syndrome → risk of otitis media
• Pancreatitis, gynecomastia, and nevus growth
• Peripheral edema, myalgia, and arthralgia
• Contraindications:
• Malignanc

46
Q

Mecasermin
Uses:
A/E:

A

▪ Recombinant human IGF-1
▪ Uses:
▪ Treatment of severe IGF-1 deficiency that is
not responsive to GH
▪ Laron syndrome is the most common cause
of growth hormone insensitivity and
caused by mutations in the GH receptor
gene
▪ Adverse effects:
▪ Hypoglycemia
▪ Intracranial hypertension, lipohyp

47
Q

Pharmacotherapy of Growth Hormone Excess

A

▪ Gigantism or acromegaly
▪ Transsphenoidal surgery, radiation, and drugs
▪ Somatostatin analogs: Octreotide, Lanreotide
▪ Growth hormone receptor antagonist: Pegvisomant
▪ Dopamine agonist: Cabergoline

48
Q

Octreotide, Lanreotide

A

▪ It is not identical to SS, only 8 amino acids,
▪ Mechanism of action: Somatostatin analog → Inhibiting GH,
IGF-1, TSH, glucagon, insulin, serotonin, VIP, secretin, motilin,
pancreatic polypeptide, LH, and gastrin release

49
Q

Uses & A/E Octreotide, Lanreotide

A

Uses:
• Acromegaly, gigantism
• Carcinoid tumor, gastrinoma, glucagonoma
• Insulinoma, VIPoma, ACTH secreting tumor
• Secretory diarrhea, portal hypertension
• Somatostatin receptor scintigraphy
• Control of bleeding from esophageal varices
Adverse effects:
Nausea, vomiting, abdominal cramps, flatulence, steatorrhea,
biliary sludge, gall stones, hypertension, peripheral edema,
alopecia, bradycardia, vitamin B12 deficiency

50
Q

Pegvisomant

A

Pegvisomant is a GH receptor antagonist
MOA: Pegvisomant binds to the GH receptor
→ blocking the binding of endogenous GH
→ prevents activation of JAK-STAT signaling
or stimulate IGF-1 secretion→ normalizes
serum IGF-1
Uses:
• Acromegaly
• Alternative for use in patients not
respond to SST
Adverse effects:
• Diarrhea, antibody formation,
elevation of liver transaminase,
infection
• Lipohypertrophy

51
Q

Hypothalamic-Pituitary-Gonadal Axis

A

GnRH → Gq-IP3-PLC-DAG-Ca→
LH & FSH → Ovaries & Testis →
androgens, estrogens, &
progesterone
Preovulatory surge of estrogen
→ ↑ GnRH

52
Q

Drugs having Agonist or Antagonist
Effects of Gonadotropins

A

• Hypothalamus
• GnRH
• Agonist
• Gonadorelin
• GnRH receptor agonist
• Leuprolide
• GnRH receptor antagonist
• Ganirelix
• Anterior pituitary
• Gonadotropins
• FSH
• Follitropin
• LH
• hCG
• FSH & LH
• Menotropin

53
Q

Gonadotropins [FSH & LH] & Human
Chorionic Gonadotropin

A

FSH, LH, and hCG– Alpha subunit, LH & hCG share beta subunit.
Signaling pathway: Camp
Menotropins [human menopausal gonadotropin-hMG]
• Both FSH & LH, follicle development in women
• Follitropin alfa and beta
• Recombinant FSH
hCG, Choriogonadotropin alfa, Lutropin alfa [withdrawn in 2012]
Identical to LH

54
Q

Uses of Gonadotropins

A

Infertility in women
• Anovulation that is secondary to hypogonadotropic
hypogonadism, polycystic ovary syndrome, and other causes
• FSH & LH → induction of ovulation
• Assisted reproductive technology
• Invitro fertilization
• FSH [menotropins or follitropin] each day, for 9 to 12 days →
to stimulate maturation of the ovarian follicle → On the day
after the last dose is given, a single dose of an LH
preparation such as chorionic gonadotropin is administered
to induce ovulation followed by insemination or oocyte
retrieval for in vitro fertilization procedures.

55
Q

Uses of Gonadotropins

A

Infertility in men
Menotropins → spermatogenesis
hCG [LH] → testosterone production
Cryptorchidism - hCG
Adverse effects:
Multiple pregnancies and the ovarian hyperstimulation
syndrome [OHSS

56
Q

Gonadotropin Releasing Hormone Agonists

A

GnRH: Gonadorelin, leuprolide, nafarelin, histrelin, etc.
Pharmacokinetics: SC, IV, nasal spray, depot preparations, pellets
Mechanism of action:
GPCR – IP3 → pulsatile administration → ↑ FSH, LH
→ continuous administration → down regulation of GnRH
receptors → ↓ FSH, LH → ↓ estrogen, testosterone
Uses:
• Advanced prostate cancer, breast cancer, endometriosis,
and uterine fibroids, central precocious puberty, suppress
premature LH surge in the treatment of infertility.
Adverse effects:
• Hot flashes, depression, diminished libido, generalized pain,
vaginal dryness, and breast atrophy

57
Q

Gonadotropin Releasing Hormone Antagonists

A

GnRH antagonists: Ganirelix, Cetrorelix, & degarelix
Mechanism of action:
• Competitive antagonist at GnRH receptors → ↓ IP3 → ↓ FSH
& LH
Uses:
• Infertility, inhibits premature LH surge in women ovarian
hyperstimulation
• Prostate cancer: ↓ Testosterone
Adverse effects:
• Hypersensitivity, allergy and anaphylaxis
Contraindications:
• Pregnancy

58
Q

Gonadotropin Releasing Hormone Antagonists

A

Pregnancy testing.
• The placenta produces significant amount of hCG
• Detected in maternal urine few days after first missed
menstrual period
• Estimate plasma hCG
Timing ovulation
• Urine LH levels on day 10-12
Localization of endocrine disease
• Measurements of plasma LH and FSH → low levels in
hypogonadotropic hypogonadism and hypothalamic or
pituitary disease.
• → high levels → Primary gonadal disease
Male primary hypogonadism
• hCG → stimulates Leydig cell → Testosterone

59
Q

Prolactin & Related Drugs

A

Prolactin:
• 198 amino acids, anterior pituitary, structurally like growth hormone
• Mammary gland → tissue growth & milk production in the presence of estrogen,
progestin, and other hormones
• Prolactin secreting adenoma & TRH → Hyperprolactinemia → infertility &
galactorrhea → inhibits GnRH → inhibits ovulation in females & spermatogenesis
in males → hypogonadism → osteoporosis
• Dopamine antagonists → hyperprolactinemia
Cabergoline or bromocriptine:
• Activates dopamine D2 receptors → ↓ Prolactin
Uses:
• Hyperprolactinemia, mixed growth hormone and prolactin secreting pituitary
adenoma
Adverse effects:
• Nausea, headache, dizziness, vasospasm, psychosis, etc.

60
Q

Sheehan Syndrome

A

Pituitary infarction
A history of postpartum hemorrhage
Inability to lactate
Los of all anterior pituitary hormones

61
Q

Drugs Affecting Prolactin Levels

A

Drugs that block dopamine D2 receptors cause
hyperprolactinemia by blocking the inhibitory effects of
endogenous dopamine on the pituitary cells that release
prolactin.
• The older antipsychotic drugs (e.g., phenothiazines,
haloperidol), with their strong dopamine D2 receptor-blocking
activity, are most likely to be the pharmacologic cause of
hyperprolactinemia.
• This adverse effect is less likely with atypical antipsychotic drugs
(e.g., olanzapine).
• Drugs or drug groups that cause hyperprolactinemia through
mechanisms that are not well characterized include methyldopa
(an antihypertensive), amphetamines, tricyclic and other types
of antidepressants, and opioids.

62
Q

Oxytocin

A

Posterior pituitary hormone, nonapeptide
Clinical uses:
• To induce & augment labor
• Milk letdown reflex
• To control of uterine hemorrhage after vaginal
or cesarean delivery
Adverse effects:
• Excessive stimulation of uterine contractions
before deliver can cause fetal distress,
placental abruption, or uterine rupture, fluid
retention, hyponatremia, heart failure, seizures,
and death
Contraindications:
• Fetal distress, Prematurity, cephalopelvic
disproportion
Atosiban:
• Antagonist of oxytocin receptor used to
suppress preterm labor [Not FDA approved]

63
Q

Vasopressin (Antidiuretic Hormone; ADH)

A

ADH: Posterior pituitary hormone
• Release → plasma tonicity or ↓ BP
• Deficiency: central diabetes insipidus
Desmopressin:
• Long acting, intravenously, subcutaneously, intranasally, or orally
MOA:
• V1 of vascular smooth muscle → Gq +PLC +IP3 → vasoconstriction
• V2 of renal tubular cells → Gs + AC → ↑ water permeability &
reabsorption; extra-renally release of factor VIII and von Willebrand
Uses:
• Pituitary diabetes insipidus, nocturnal enuresis, esophageal variceal
bleeding, hemophilia A and von Willebrand disease
Adverse effects:
• Headache, nausea, abdominal cramps, agitation, and allergic
reactions

64
Q

Vasopressin (Antidiuretic Hormone; ADH)

A

• V1a – vasoconstriction
• V1b – ACTH release
• V2- ADH response
• ↑ vasopressin & hyponatremia → heart failure
• Conivaptan antagonist of V1a and V2 receptors
• Uses: Hypervolemic, euvolemic hyponatremia, SIADH, & heart failure
• Tolvaptan more selective for V2 → ↑ free water clearance → ↓ urine
osmolality → ↑ serum sodium concentrations.
• Use. Autosomal dominant polycystic kidney disease, SIADH,
cirrhosis.
• Demeclocycline & Lithium:
• Demeclocycline and lithium act on the collecting tubule cell to diminish
its responsiveness to ADH, thereby increasing water excretion.
• Both drugs causes nephrotoxicity

65
Q

̄decT3,dec T4,­ incTSH.
- The thyroid gland itself is under-producing thyroid hormone. TSH goes ­ due to ̄ negative-feedback at hypothalamus + anterior pituitary.
- HY examples are Hashimoto thyroiditis (autoimmune destruction of thyroid gland) and iodine deficiency (insufficient thyroid hormone precursor).

A

Primary hypothyroidism

66
Q

Secondary hypothyroidism

A

The thyroid gland is under-producing thyroid hormone due to inadequate stimulation (i.e., the anterior pituitary isn’t producing sufficient TSH).
- HY causes are Sheehan syndrome (ischemic infarction of anterior pituitary postpartum) and pituitary tumors (e.g., prolactinoma, which impinge on and necrose the thyrotropes in the anterior pituitary that produce TSH).
- ̄ TRH from the hypothalamus causing ̄ TSH could be another theoretical cause, but I’ve never seen this assessed. Dec T3, dec T4, dec TSH.

67
Q

TSH- or TRH-secreting tumor causing over-stimulation of thyroid gland.
- Despite the ­ thyroid hormone, TSH can’t be suppressed because there is autonomous secretion from a tumor.
- In theory, hypothalamic / anterior pituitary glandular hyperplasia, or inflammation (autoimmune hypophysitis) could also cause ­ TSH leading to secondary hyperthyroidism. Inc T3/4/TSH

A

Secondary hyperthyroidism

68
Q

Primary hyperthyroidism

A

-increased T3,­increase T4,decrease TSH.
- The thyroid gland itself is over-producing, causing suppression of TSH.
- HY example is Graves disease (activating-antibody against TSH receptor), toxic adenoma (autonomously secreting nodule), and toxic multinodular goiter (multiple autonomously secreting nodules).
- TSH is suppressed due to ­ negative-feedback at the hypothalamus / anterior pituitary.

69
Q

Aka subacute granulomatous thyroiditis, or just simply subacute thyroiditis.
- Mechanism is viral infection followed by a painful/tender thyroid. There is inflammation of the thyroid gland, which causes the spacing between the cells to increase slightly, allowing for the release of pre-formed thyroid hormone into the blood. Therefore we have ̄ TSH, ­ T3, ­ T4, ̄ 131I uptake.
- The gland is not over-producing thyroid hormone. This is why uptake is not increased.
- Subacute granulomatous thyroiditis can be either hypo- or hyperthyroid. The key detail you need to know is that uptake is always decreased even if the patient is hyper-.

A

deQuervain thyroiditis

70
Q

Subclinical hypothyroidism

A

Inc TSH,<—>T3,<—->T4.
- In subclinical hypothyroidism, the patient will be asymptomatic (hence subclinical) and will have normal T3 and T4, despite an elevated TSH.
- Most patients with subclinical do not need to be treated.
- Don’t treat unless TSH >10, patient is pregger, or anti-Hashimoto Abs are +.

71
Q

Drug-induced thyroiditis

A

Caused by lithium or amiodarone on USMLE.
- Can in theory be hypo-, eu-, or hyperthyroid.
- Will usually present on USMLE as painless hypothyroidism in patient being treated for bipolar disorder (lithium) or started on new anti-arrhythmic (amiodarone).
- Will present with ̄ 131I uptake, where inflammation of the gland can sometimes cause leakage of thyroid hormone into the blood, but the gland itself is not demonstrating increased production of hormone.

72
Q
What is the drug name?
A

PTU
Methimazole

73
Q
What is the drug name?
A

Lugol’s solution
Potassium iodide

74
Q

What is propranolol MOA, Uses, Kinetics and A/E

A
75
Q

What drug do you give your pregnant patients with hyperthyroidism?

A
76
Q

The most common cause of hyperpituitarism is

A

Anterior lobe pituitary adenoma

Endocrine II (16 decks)

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