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Endocrine Flashcards

1
Q

Describe the development of the thyroid. What is the most common ectopic thyroid tissue site? What is a thyroglossal duct cyst? How does it present?

A

Thyroid divertic arises from floor of primitive pharynx and descends into neck.

Connected to tongue by thyroglossal duct, which may persist

Foramen cecum is normal remnant of thyroglossal duct

Tongue

Anterior midline neck mass that moves with swallowing or protrusion of tongue

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2
Q

What is the the adrenal cortex derived from? Medulla? Describe the layers of the adrenal gland what what their secretory products are as well as their primary reg control. What is a pheochromocytoma? Epid? Results? What is a neuroblastoma? results?

A

Cortex=mesoderm
medulla=neural crest

Zona glomerulosa=renin angiotensin, aldosterone
zona fasciculata=ACTH, CRH; cortisol, sex hormones
Zona reticularis=ACTH, CRH; sex hormones

Medulla (chromaffin cells)=preganglionic symp fibers; catecholamines (NE and E)

Pheo=most common tumor of adrenal medulla in adults; presents as episodic hypertension
Neuro=most common tumor of adrenal medulla in children; rarely causes hypertension

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3
Q

What do the acidophils in the anterior pituitary secrete? The basophils? What is the anterior pituitary derived from? From is secreted from the intermediate lobe? What is the alpha subunit? Which hormones possess it? What is the beta subunit?

A

Acido=GH, Prolactin
Baso=FSH, LH, ACTH, TSH

B=FLAT
FLAT PIG=FSH, LH, ACTH, TSH, ProlactIn, GH

Intermediate=melanotropin (MSH)

Oral ectoderm (rathke pouch)

Alpha subunit-common to TSH, LH, FSH, hCG
beta subunit-gives them specificity

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4
Q

What does the post pit secrete? Where these hormones made specifically? path? Derivation of post pit?

A

Secretes vasopressin (SON) and Oxytocin (PVN)

Transported from hypothalamus to post pit by neurophysins (carrier proteins)

Neuroectoderm

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5
Q

What are the islets of langerhans made up of? organization? What do they arise from? What is the function of the cells?

A

Alpha cells on periph=glucagon
beta cells on the inside=insulin
delta cells interspersed=somatostatin

pancreatics buds

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6
Q

Describe the formation of functional insulin? How can endogenous insulin be differentiated from exogenous?

A

Preporinsulin (synth in RER) has its presignal cleaved off and become proinsulin which is stored in secretory granules.
Preinsulin is cleaved and insulin and C peptide are equally exocytosed

Endogenous=insulin and c peptide incr.
exo=just insulin incr.

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7
Q

What receptors does insulin bind? What kind of receptor is it? What are its basic functions? What are its specific functions (7)? Can it cross placenta? What is the cellular pathway of these functions?

A

Insulin receptor (tyrosine kinase)

results in inducing glucose uptake and gene transcription

Incr. glucose transport in skel muscle and adipose tissue
Incr. glycogen synth and storage
Incr. TG synth
Incr. Na retention (kidneys)
Incr. protein synth (muscles)
Incr. cellular uptake of K+ and amino acids
Decr. glucagon release

Does not cross placenta

Tyrosine kinase activates phosphoinositide 3 kinase pathway which results in glycogen, lipid, and protein synth, as well as the transport of GLUT-4 channels to PM.
The kinase also activates the RAS/MAP kinase pathway which results in cell growth and DNA synth

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8
Q

Which is the insulin dependent glucose transporter? Where is it found? Which are the insulin independent glucose transporters? Where are they found?

A

GLUT 4=adipose tissue, striated muscle (exercise can also incr. GLUT 4

GLUT1=RBCs, cornea, braine
GLUT2 (bidirectional)=beta islet cells, liver, kidney, brain, small intestine
GLUT 3=brain
GLUT 5 (fructose)=spermatocytes, GI tract
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9
Q

What is the major regulator of insulin release? What does GH do? Beta 2 agonists? Describe the steps in the cellular pathway of insulin rlease regulation.

A

Glucose

GH—>insulin resistance leading to incr. insulin rlease

Beta 2 agonists lead to incr. insulin secretion
G

Glucose enters beta cell through GLUT 2.
Glycolysis leads to incr. ATP/ADP ratio
ATP closes K+ channels (K+ can’t leave cell)
This leads to depolarization
Voltage gated Ca channels open
Incr. intracellular Ca leads to exocytosis of insulin granules

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10
Q

What are the effects of glucagon? How is it regulated?

A

Glycogenolysis
gluconeogenesis
lipolysis
ketone production

Secreted in response to Hypoglycemia
Inhibited by insulin, hyperglycemia, and somatostatin

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11
Q

What is the function of CRH release from hypothalamus to pituitary? What can cause it to be decr? Dopamine? What can dopamine antagonists lead to? GHRH? GnRH? How is it regulated? What does tonic GnRH do? What does pulsatile GnRH do? Prolactin? What does a pituitary prolactinoma lead to? Somatostatin? What are its analogs used to treat? TRH?

A

CRH=incr. ACTH, MSH, beta endorphin
Decr. in chronic exogenous steroid use

DA=decr. prolactin
Antipsychotics can cause galactorrhea due to hyperprolactinemia

GHRH=incr. GH

GnRH=incr. FSH, LH
Regulated by prolactin
Tonic=HPA axis suppression (no FSH/LH)
Pulsatile=puberty, fertility

Prolactin=Decr. GnRH
Pituitary prolactinoma–>amenorrhea, osteoporosis, hypogonadism, galactorrhea

Somatostain=Decr. GH, TSH
Acromegaly

TRH=incr. TSH, prolactin

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12
Q

Where is prolactin secreted from? Functions? Regulation?

A

Ant. Pit

Stimulates milk production in breast
Inhibits GnRH synth and release

Tonically inhibited by CA from hypo
TRH results in incr. prolactin secretion
Dopamine agonist can be used from prolactinoma
DA antag and estrogens (pregnancy, OCPs) stimulate prolactin secretion

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13
Q

Where is GH secreted from? What is its function? How? What is its release/regulation like? What will excess secretion of GH result in?

A

Ant Pit

Linear growth and muscle mass through IGF-1 secretion
Incr. insulin resistance

Released in pulses in response to GHRH
Secretion incr. during exercise and sleep
Inhibited by glucose and somatostatin release via negative feedback by IGF-1

excess=acromegaly or gigantism

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14
Q

What is the function of ghrelin? Where is it produced? When is it increased?

A

Stimulates hunger and GH release

Produced by stomach

Incr. with sleep loss and prader-willi syndrome

Ghrelin=Gain weight
Ghrelin=hunghre

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15
Q

What is the function of leptin? Produced by? When is it decr. What will a mutation result it?

A

Satiety hormone

Adipose tissue

Decreased in starvation
Sleep deprivation decreases it

Mutation leads to cong obesity

Leptin=lose weight=thIN

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16
Q

What is the effect of endocannabinoids on appetite? pathway?

A

Stimulate cortical reward centers which increases the desire for high fat foods

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17
Q

Where is ADH synth/released? Functions? What can cause nephrogenic DI? What is the ADH level like in CDI and NDI? What is a treatment for CDI? Regulation?

A

SON of hypothal, released by post pit

Primarily Regulates serum osmolarity (V2 receptors) through aquaporin channels in collecting duct

also regulates blood pressure (v1) by vasocontriction

V2 receptor mutation can lead to NDI (normal or incr. ADH)
In CDI (decr. ADH)

Desmopressin (ADH analog) used for CDI

Primary regulation=Osmoreceptors in hypothal
SEcondary=hypovolemia

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18
Q

What enzyme is activated by ACTH/inhibited by ketoconazole in the adrenal cortex? What is its function? What is the function of 17 alpha hydroxylase? 21 hydroxylase? 11 beta hydroxylase? What enzyme is activated by ATII? What does it do? Describe the steps in the formation of testosterone? Describe the formation of estrone, estradiol, and dihydrotestosterone.

A

Cholesterol desmolase=cholesterol to pregnenolone

Pregnenlone is converted to progesterone

Pregnenolone and progesterone are converted into their 17 hydroxy counterparts in the cortisol pathway by 17 alpha hydroxylase.

They 17 hydroxypregnenolone and 17 hydroxyprogesterone are converted to their androgen counterparts, DHEA and androstenedione respectively.

21 hydroxylase converts the progesterone to 11 deoxycorticosterone and 11 deoxycortisol

11 beta hydroxylase converts those into corticosterone and cortisol.

ATII activates aldosterone synthase which converts corticosterone to aldosterone

DHEA is convr. to androstenedione which is converted to testosterone.

These are then converted to estrone and estradiol by aromatase.

Testosterone is converted to Dihydrotestosterone by 5 alpha reductase.

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19
Q

Compare and contrast 17 alpha hydroxylase defic, 21 hydroxylase defic, and 11 beta hydroxylase defic concerning mineralocorticoid, cortisol, and sex hormone levels? BP, K+, and relevant lab findings? Presentation in males and females? How are they all characterized? Why?

A

17 ALPHA HYDROXYLASE

mineral: Incr.
cortisol: decr.
sex hormones: decr.
BP: incr.
K+: decr.
Labs: decr. androstenedione
XY: pseudohermaphroditis\m (ambiguous genitalia, undescended testes
XX: lack secondary sexual development

21 HYDROXYLASE DEFIC

mineral: decr.
cortisol: decr.
sex hormones: incr.
BP: decr.
K+: incr.
Labs: incr. renin activity, incr. 17 hydroxyprogest
XY: Infancy (salt wasting) or child hood (precocioius puberty)
XX: virilization

11 BETA HYDROXYLASE DEFIC

mineral: Decr. aldo, incr. 11 deoxycorticosterone (incr. BP)
cortisol: decr.
sex hormones: incr.
BP: incr.
K+: decr.
Labs: decr. renin activity
XY: normal
XX: virilization

All are characterized by enlargment of both adrenal glands due to incr. ACTH stimulation (due to decr. cortisol)

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20
Q

What is cortisol bound to? What are the effects of cortisol on blood pressure? Mechanisms? What are the effects of cortisol on inflammation and immune response? Mechanism? How does it affect bone formation? Mechanism? What are the other effects of cortisol? What can exogenous corticosteroids cause (immune response)? How? What is the regulation of cortisol? What induces prolonged secretion?

A

Corticosteroid binding globulin

BIG FIB

Blood pressure increase (upregulates alpha 1 receptors on arterioles and at high conc acts like aldosterone)
Insulin resistance incr.
Gluconeogenesis, lipolysis, proteolysis incr.
Fibroblast activity decr. (striae)
Inflammatory and immune response decr.
(inhibits production of leukotrienes and prostaglandins
inhibits WBC adhesion–>neutrophilia
blocks histamine release from mast cells
reduces eosinophils
blocks IL-2 production (activates T cells))
Bone formation decr. (decr. osteoblast activity)

Reactivation of TB and candidiasis (blocks IL-2)

CRH (hypothalamus) stimulates ACTH release (pit) leading to cortisol production in adrenal zona fasciculata. Excess corisol decr. CRH, ACTH, and cortisol secretion

Chronic stress

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21
Q

What are the 3 forms of plasma Ca? Percentage of each? What is the effect of pH on plasma calcium levels? Mechanism? Symptoms?

A

Ionized (45%)
Bound to albumin (40%)
Bound to anions (15%)

Incr. in pH leads to incr. affinity of albumin to Ca which leads to hypocalcemia

Cramps, muscle spasms, pain, paresthesias.

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22
Q

What are the different forms of Vitamin D? What are their sources? What is the function of active vitamin D? How is it regulated? What does deficiency lead to? What causes it?

A 
D3 from sun exposure in skin
D2 is ingested from plants
Both converted to 25-OH form in liver
25-Oh converted to 1,25-(OH) form in kidney
24,25-(OH)2 is an inactivated form

Incr. absorption of dietary Ca and PO4
Iincr. bone resorption leading to Incr. Ca and PO4

Incr. PTH, decr. calcium, decr. PO4 lead to incr. active vit D production
1,25-OH form feedback inhibition

Rickets in kids
Osteomalacia in adults

Malabsorption, decr. sunlight, poor diet, chronic kidney failure

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23
Q

What secretes PTH? What are its functions? Mechanism? How is it regulated?

A

chief cells of parathyroid

Incr. bone resorption of Ca and PO4 (Works directly on blasts, indirectly on clasts: incr. production of macrophage colony stimulating factor—>more osteoclasts. Incr. production of RANK-L (released from clasts and blasts) leads to stimulation of osteoclasts))
Intermittent PTH release can stimulate bone formation
Incr. kidney reab of Ca in DCT
Decr. kidney reab of PO4 in PCT
Incr. 1,25-(OH)2 D3 (calcitriol) production by stimulating kidney 1 alpha hydroxylase in PCT

Decr. serum calcium, incr. serum PO4, decr. serum Mg all result in incr. PTH secretion
Severely decr. Mg leads to decr. PTH secretion

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24
Q

What releases calcitonin? What is its function? Regulation? When is it important?

A

Parafollicular cells (C cells) of thyroid

Decr. bone resorption of Ca

Incr. serum Ca—>calcitonin secretion

Opposes actions of PTH. Not important in normal Ca homeostasis

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25
Q

What endocrine hormones use a cAMP pathway?

A

FSH, LH, ACTH, TSH, CRH, hCG, ADH (V2), MSH, PTH, calcitonin, GHRH, glucagon

FLAT ChAMP

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26
Q

What endocrine hormones use a cGMP pathway?

A

ANP, BNP, NO (EDRF)

vasodilators

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27
Q

What endocrine hormones use an intracellular pathway?

A

Vit D, Estrogen, Testosterone, T3/T4, Cortisol, Aldo, Progesterone

VETTT CAP

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28
Q

What endocrine hormones use an intrinsic tyrosine kinase pathway?

A

Insulin, IGF-1, FGF, PDGF, EGF

MAP Kinase pathway
Think growth factors

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29
Q

What endocrine hormones use a receptor associated tyrosine kinase pathway?

A 
Prolactin
Immunomodulators (cytokines)
GH
G-CSF
EPO
Thrombopoetin

JAK/STAT
Think acidophils and cytokines

PIGGlET

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30
Q

What endocrine hormones use an IP3 pathway?

A

GnRH, Oxytocin, ADH (V1), TRH, Histamine (H1), Angiotensin II, Gastrin

GOAT HAG

31
Q

What is the signaling pathway of steroid hormones? How do they circulate? What can go wrong in circulation in men and in women? What effects do OCPs and pregnancy have on this circulation?

A

Steroids hormones are lipophilic and therefore must circulate bound to specific binding globulins, which incr. their solubility

In men, incr. sex binding globulin lowers free testosterone leading to gynecomastia
In women, decr. SHBG raises free testosterone leading to hirsutism

Hormone diffuses across PM and binds to receptor located in nucleus or cytoplasm
The receptor exposes DNA binding domain (enhancer) leading to incr. mRNA—->proteins—>response

32
Q

What are T3/T4? Sources? What are their functions? How does it circulate? What affects this circulation? How is T4 converted to T3? Which has greater affinity for nuclear receptor? What is the function of peroxidase? What are the actions of Propylthiouracil and methimazole? Describe the regulation of T3/T4 release? Describe the Wolff-Chaikoff effect. Describe the cellular pathway for production of T3/T4. What is the effect of anions such as perchlorate, pertechnetate, and thiocyanate? What are the functions of t3/T4?

A

Iodine containing hormones that control body’s metabolic rate.

Follicles of thyroid, though T3 is mainly formed in target tissue
T4 is major thyroid product, converted to T3 by 5’ deiodinase in periph tissues.
T3 has the most affinity for receptor

Thyroxine binding globulin binds most T3/T4 in blood; only free hormone is active.
Decr. TBG in hepatic failure, steroid use leads to incr. thyroid activity
Incr. TBG in pregnancy or OCP use

Peroxidase oxidates and couples I2 with thyroglobulin to form MIT/DIT

PTU inhibits perioxidase and 5’ deiodinase
Methimazole inhibits peroxidase

TRH stimulates TSH which stimulates follicular cells to transport iodine into cell as well as form and transport thyroglobulin into the lumen. Thyroglobulin then combines with Iodide to form MIT and DIT which are used to form T3/T4 which are transported back into cell and back into circulation
T3,T4 make anterior pituitary less sensitive to TRH

Wolff-Chaikoff=excess iodine temporarily inhibits thyroid peroxidase which decr. iodine organification leading to decr. T3/T4 production

Perchlorate, pertechnetate, and thiocyanate all prevent the transport of iron in follicular cells

Bone growth (synergism with GH)
CNS maturation
Incr. B1 receptors in heart=incr. CO, HR, SV, contractility
Incr. BMR via Incr. Na/K-ATPase activity leads to incr. O2 consumption, RR, body temperature
Incr. glycogenolysis, gluconeogenesis, lipolysis

T3 leads to 4B’s

Brain maturation
Bone growth
Beta adrenergic effects
Basal metabolic rate incr.

33
Q

What are the etiologies/pathophysiologies of cushing syndrome? What are the findings? Describe an algorithm to make the diagnosis/find etiology.

A

Incr. cortisol due to a variety of causes

Exogenous corticosteroids: Decr. ACTH, bilateral adrenal atrophy. Most common cause

Primary adrenal adenoma, hyperplasia, or CA-result in decr. ACTH, atrophy of uninvolved adrenal gland. Can also present with pseudohyperaldosteronism

ACTH-secreting pituitary adenoma (Cushing’s disease)
Paraneoplastic ACTH secretion (small cell lung cancer, bronchial carcinoids)
Incr. ACTH, bilateral adrenal hyperplasia.
Cushing disease is responsible for majority of endogenous cases of Cushing syndrome

Hypertension, weight gain, moon facies, truncal obesity, buffalo hump, skin changes (thinning striae), osteoporosis, hyperglycemia (insulin resistance), amenorrhea, immunosuppression

Screening tests: Incr. free cortisol on 24 hr. urine test, incr. midnight salivary cortisol, and no suppression with overnight low dose dexamethasone test (rule out exogenous). If there are abnormalities, move on.

Measure serum ACTH.

If elevated (>20pg/mL), cause is not exogenous or primary (ACTH dependent).
Do a high dose dexamethasone test.
If it is adequately suppressed, it is cushing disease (ant. pit). If it is not suppressed, ectopic (small cell lung cancer)
OR
Do a CRH stimulation test.
If it results in more ACTH and cortisol, Cushing disease
If it has no effect, ectopic

If ACTH is suppressed (<5pg/mL), it is ACTH indepedent cushing syndrome or a primary adrenal tumor

34
Q

What is adrenal insufficiency? What are the symptoms? What are two ways in which teh diagnosis can be made?

A

Inability of adrenal glands to generaate enough glucocorticoids and/or mineralocorticoids for the body’s needs.

Weakness, fatigue, orthostatic hypo, muscle aches, weight loss, GI disturbances, sugar and/or salt cravings

Measurement of serum electrolytes, morning/random serum cortisol and ACTH, and response to ACTH stimulation test.

Metyrapone stimulation (blocks production of cortisol which should incr. ACTH. If it doesn’t incr. it, it means cortisol wasn’t being produced in the first place.

35
Q

What is the pathophys and symptoms of primary adrenal insufficiency? Cause and presentation of acute primary? Chronic? Another name? What is waterhouse friderichsen syndrome?

A

Deficiency of aldo and cortisol due to loss of gland function

Hypotension, hyperkalemia, metabolic acidosis
Skin and mucosal hyperpigmentation (MSH formed in production of ACTH)

Acute: Sudden onset (massive hemorrhage). Shock in acute adrenal crisis
Chronic: Addison disease. Adrenal atrophy or destruction by disease.

Acute primary adrenal insufficiency due to adrenal hemorrhage associated with septicemia (N. menin), DIC, endotoxic shock

36
Q

What is the pathophys of secondary adrenal insuff? How do the symptoms differ from primary?

A

Decr. pit ACTH production
No skin/mucosal hyperpigmentation
no hyperkalemia

37
Q

What is the pathophyss of tertiary adrenal insuff? Symptoms?

A

Withdrawal of chronic exogenous steroid use.

Aldo synth is unaffected

38
Q

What is a neuroblastoma? Epid? Origin? Histo? Where does it occur? Most common Presentation? What should this be differentiated from? Another presentation? Lab findings? Staining? Mutation?

A

Most common tumor of adrenal medulla in children, usually < 4 years old

Neural crest cells

Homer-Wright Rosettes

Anywhere along symp chain

Abdominal distention and a firm, irregular mass that can cross midline (Wilms=smooth and unilateral)
Opsoclonus-myoclonus syndrome (dancing eyes-dancing feet)

Homovanillic acid (from DA) and Vanillylmandelic acid (NE) are incr. in urine

Bombesin and neuron specific enolase +

N-myc oncogene

39
Q

What is the epid of a pheochromocytoma? Origin? What ist the rule of 10’s? What is the pathophys? What are the symptoms? What are the symptoms like? 5 Ps? What are its associations? What are the lab findings? Treatment?

A

Most common tumor of adrenal medulla in adults

Chromaffin cells (from neural crest)

10% malignant, bilateral, extra-adrenal, calcify, and kids

Most tumors secrete E, NE, DA leading to episodic hypertension
Symptoms occur in spells; relapse and remit

pressure (incr. BP)
Pain (headache)
Perspiration
Palpitations
Pallor

NF-1, VHL, MEN 2A/2B

Incr. catecholamines and metanephrines in urine and plasma

Irreversible alpha antagonists (phenoxybenzamine) then beta blockers then resection

40
Q

Compare and contrast hyperthyroidism and hypothyroidism concerning signs/symptoms, and lab findings?

A

HYPO

Cold intolerance (decr. heat production)
Weight gain, decr. appetite
Hypoactivity, lethargy, fatigue, weakness
Constipation
Decr. reflexes
Myxedema (facial, periorbital)
Dry, cool skin; course, brittle hair
Bradycardia, dyspnea on exertion

Incr. TSH (if primary)
Decr. free T3 and T4
Hypercholesterolemia (due to decr. LDL receptor expression)

HYPER

Heat intolerance (incr. heat production)
Weight loss, incr. appetite
Hyperactivity
Diarrhea
Incr. reflexes
Pretibial myxedema (Graves disease), periorbital edema
Warm, moist skin; fine hair
Chest pain, palpitations, arrhythmias (incr number and sensitivity of beta receptors in heart)

Decr. TSH (if primary)
Incr. free or total T3/T4
Hypocholesterolemia (incr. LDL receptor expression)

41
Q

What is epid of hashimoto thyroiditis? Pathophys? HLA type? Risk? Progression? HIsto? Findings?

A

Most common cause of hypothyroidism in places where iodine isn’t insufficient.

Autoimmune (DR5) disorder=Abs against thyroid peroxidase, microsomes, and thyroglobulin

Incr. risk of Non hodgkin lymphoma

Hyperthyroid early in course due to rupture

Hurthle cells, lymphoid aggregates in germinal centesr

Moderately enlarged, non tender thyroid

42
Q

What is congenital hypothyroidism? Another name? Etiologies? Findings?

A

Cretinism

Severe fetal hypothyroidism due to maternal hypothyroidism, thyroid agenesis, thyroid dysgenesis, iodine deficiency, dyshormonogenetic goiter

Pot bellied
Pale
Puffy faced child with
Protruding umbilicus
Protuberant tongue
Poor brain developemtn
43
Q

What is the pathophys/progression of subacute thyroiditis? Another name? Histo? Findings?

A

de Quervain

Self limited disease following a flu like illness

May be hyperthyroid early on, then hypothyroid

Granulomatous inflammation

Incr. ESR, jaw pain, early inflammation, very tender thyroid

44
Q

What is reidel thyroiditis? Pathophys? What can it be confused with? Findings?

A

Thyroid replaced by fibrous tissue. May extend to local structures

Anaplastic CA

IgG4 related systemic disease

Fixed, hard (rock like), painless goiter

45
Q

What are some other causes of hypothyroidism?

A

Iodine defic, goitrogens, wolff chaikoff effect

46
Q

What is epid of graves disease? Pathophys? Symptoms? Time of presentation?

A

Most common cuase of hyperthyroidism.

IgG stimulation of TSH receptors on thyroid

Hyperthyroidism
Diffuse goiter
Retro orbita fibroblasts (exopthalmos, proptosis, extraocular muscle swelling)
Dermal fibroblasts (pretibial myxedema)

During stress such as childbirth

47
Q

What is a toxic multinodular goiter? pathophys? Lab findings?

A

Focal patches of hyperfunctioning follicular cells working independently of TSH due to TSH receptor mutation

Incr. release of T3/T4

Hot nodules rarely malignant

48
Q

What is a thyroid storm? Pathophys? How does it present? Lab findings? How is it treated?

A

Stress induced catecholamine surge seen as a serious complication of thyrotoxicosis due to diseaes and other hyperthyroid disorders.

Agitation, delirium, fevers, diarrhea, coma, and tachyarrhythmia (death)

Increased ALP due to bone turnover

Beta blockers
PTU
Corticosteroids

49
Q

What is Jod-Basedow phenomenon?

A

Thyrotoxicosis when iodine deficient pt is given iodine.

50
Q

When is thyroidectomy an option? What are some complications? How do they happen ?

A

Thyroid cancers and hyperthyroidism

Hoarseness (recurrent laryngeal nerve damage)

Hypocalcemia (removal of PT glands)

Transection of recurrent and superior laryngeal nerves (ligation of inferior thyroid artery and superior laryngeal artery)

51
Q

What is epid of papillary CA of thyroid? Prognosis? Histo? Spread? Mutations? Risk factors?

A

Most common

Excellent prognosis

Empty appearing nuclei with central clearing (orphan annie eyes), psammoma bodies, nuclear grooves.

Lymphatic invasion common

Incr. risk with RET and BRAF mutations, childhood irradiation

Orphan annies (with swirling hair=psammoma) mom had previous died during the yellow (lymph) invasion (asian invasion). Her dad BRETT (RET and BRAF), then died due to the radiation that was left behind after the invasion. Her heart was empty (empty nucleus) b/c she did not have a papi (papillary) and or psa “momma”. However, no one can defeat annie (good prognosis)

52
Q

What is the prognosis of a follicular CA? Spread? Histo?

A

Good prognosis. Invades thyroid capsule (unlike adenoma)

Uniform follicules

53
Q

What is the origin of medullary CA? Histo? Spread? Associations?

A

Parafollicular C Cells

Produces calcitonin, sheets of cells in an amyloid stroma

Hematogenous spread.

MEN 2A and 2B (RET mutations)

There were two men jews: Men jew Larry (2a) and Men Jew RET (2b)
During the red invasion (nazi’s), the nazis destroyed their bones releasing their medulla (medulla de los huesos) and thus a lot of calcium into their bodies. As a result, calcitonin was also released.

54
Q

What is the epid of undifferentiated/anaplastic CA? Spread? Prognosis?

A

Older patients; invades local structures, very poor prognosis

55
Q

What is lymphoma of the thyroid associated with?

A

Hashimoto thyroiditis.

56
Q

What are some causes of hypoparathyroidism? What are some findings? What are some signs? What is pseudohypoparathyroidism? Another name? Symptoms? Inheritance? What are some causes of 2ndary hyperparathyroidism? Lab findings? Hypoparathyroidism? PTH independent hypercalcemia? Primary hyperparathyroidism?

A

Acccidental surgical excision of parathyroid glands, autoimmune destruction, or DiGeorge syndrome

Hypocalcemia, tetany

Chvostek sign-tapping of facial nerve (tap the cheek) leads to contraction of facial muscles
Trousseau sign-occlusion of brachial artery with BP cuff leads to carpal spasm

Pseudohypoparathyroidism (Albright Hereditary Osteodystrophy): Unresponsiveness of kidney to PTH. Auto Dom. Hypocalcemia, shortened 4th/5th digits, short stature

57
Q

What is pathophys of familial hypocalciuric hypercalcemia?

A

Defective Ca sensing receptor on parathyroid cells

PTH cannot b y supressed by an increased level of Ca leading to mild hyperalcermia with normal to incr. PTH levels.

58
Q

What is the usual cause of primary hyperparathyroidism? What are the lab findings? Usual presentation? Other presentations?

A

usually due to parathyroid adenoma or hyperplasia

Hypercalcemia, hypercalciuria (renal stones), hypophosphatemia, Incr. PTH, Incr. ALP, Incr. cAMP in urine.

Most often symptomatic

Stones (renal stones)
Bones (osteitis fibrosa cystica=cystic bone spaces filled with brown fibrous tissue (hemosiderin) causing bone pain)
Groans (constipation and weakness, abdominal/flank pain=kidney stones/acute pancreatitis)
Psychiatric overtones (depression)
59
Q

What is pathophys of secondary hyperthyroidism? Causes? Symptoms? Lab findings? What is tertiary hyperpara? Lab findings?

A

secondary hyperplasia due to decr. Ca absorption and/or incr. PO4

Chronic renal disease (low vit. D)

Hypocalcemia
Hyperphosphatemia
Incr. ALP
Incr. PTH
Renal osteodystrophy (bone lesions due to secondary or tertiatry hyperparathyroidism due in turn to renal disease)

Refractory (autonomous) hyperparathyroidism resulting from chronic renal disease.
Incr. Incr. PTH
Incr. Ca

60
Q

What does a pituitary adenoma usually consist of? Presentations? Pathophys of presentation? What is the treatment for a prolactinoma?

A

Most commonlly prolactinoma (benign)

Functional=hormone producing
Presentation depends on hormone
Prolactinoma: amenorrhea, galactorrhea, low libida, infertitlity
Somatotropic: acromegaly

Dopamine agonists (bromocriptine or cabergoline); transphenoidal resection

Non functional=no hormone, mass effect
bitemporal hemianopsia, hypopituitarism, headache

61
Q

What is the pathophys of acromegaly? Findings? Risks? How is diagnosis made? Treatments?

A

Excess GH in adults. Pituitary adenoma.

Large tongue with deep furrows
Deep voice
Large hands and feet
coarse facial features
Impaired glucose tolerance (insulin resist)

Incr. risk of colorectal polyps and cancer

Incr. serum IGF-1
Failure to suppress GH following glucose tolerance test
Pituitary mass seen on brain MRI

Pituitary adenoma resection.
Octreotide (somatostatin analog)
Pegvisomant (GH receptor antag)

62
Q

What is gigantism? pathophys? Symptoms? Risks?

A

Incr. GH in children

Gigantism (incr. linear bone growth)

HF most ommon cause of death

63
Q

What are the symptoms of DI? What is pathophys of CDI? NDI? Compare and contrast CDI and NDI concerning etiology, lab findings, water deprivation test results, and treatment?

A

Intense thirst and polyuria with ainability to concentrate urine due to lack of ADH (CDI) or failure of response to circulating ADH (NDI)

CDI

Etiology: Pituitary tumor, autoimmune, trauma, surgery, ischemic encephalopathy, idiopathic

Findings: decr. ADH; urine specific gravity < 1.006; serum osmolality > 290; hyperosmotic volume contraction

WDT: >50% incr. in urine osmolality only after admin of ADH analog

Treatment: Intranasal desmopressin acetate, hydration

NDI

Etiology: Hereditary (ADH receptor mutation), secondary to hypercalcemia, lithium, demeclocycline (ADH antag)

Findings: Normal ADH levels; urine specific gravity < 1.006; serum osmol >290; hyperosmotic volumne contraction

WDT: minimal change in osmol even after ADH analog

Treatment: HCTZ, indomethacin, amiloride, hydration

64
Q

What is the pathophys/results of SIADH? Symptoms? Treatment? Causes?

A

Syndrome of inappropriate ADH secretion

Excessive free water retention
euvolemic hyponatremia with continued urinary Na excretion
Urine osmolality > serum osmol

Body responds to water retention with decr. aldosterone which maintains volume but leads to hyponatremia.

Low sodium leads to:
Cerebral edema and seizures

Fluid restriction
IV hypertonic Saline (must correct slowly to prevent osmotic demyelination syndrome)
Conivaptan
Tolvaptan
Demeclocycline
65
Q

What are some causes of hypopituitarism? Explain them? Treatment?

A

Nonsecreting pit adenoma, craniopharyngioma

Sheehan syndrome-ischemic infarct following post partum bleeding=failure to lactate, absent menstruation, cold intolerance

Empty sella syndrome-atrophy or compression of pit ggland, often idiopathic, common in obese women

Pit apoplexy-sudden hemorrhage of pit gland, often in presence of an existing pit adenoma

Brain injury

Radiation

HRT

66
Q

What are the presenting symptoms of diabetes mellitus? Pathophys? What are some rare causes? How is the diagnosis made?

A

Polydipsia, polyuria, polyphagia, weight loss, DKA (type I), hyperosmolar coma (type 2)

Rarely, can be cause by unopposed secretion of GH and epi. Also seen in patients on glucocorticoid therapy.

Insulin deficiency or insensitivity (and glucagon excess) leads to decr. serum glucose uptake, incr. protein catab, incr. lipolysis (only in insulin defic).
Decr. serum glucose uptake leads to hyperglycemia, glycosuria, osmotic diuresis, and electrolyte depletion which leads to dehydration +/- acidosis
Incr. protein catab leads to incr. plasma amino acids, nitrogen loss in urine leading to osmotic diuresis
Incr. lipolysis leads to incr. plasma FFAs, ketogenesis, ketonuria, and ketonemia, which leads to dehydration and acidosis
Dehydration and acidosis leads to coma and death

Fasting serum glucose, oral glucose tolerance test, HbA1c

67
Q

What are some chronic complications of DM and what are their mechanisms?

A

Nonenzymatic glycation:
Small vessel disease (diffuse thickening of basement membrane): Retinopathy (hemorrhage, exudates, microaneurysms, vessel prolif), glaucoma, neuropathy, nephropathy (nodular glomerulosclerosis, Kimmelstein Wilson nodules—>progressive proteinuria and arteriolosclerosis leading to hypertension and chronic renal failure)
Large vessel atherosclerosis, CAD, peripheral vasc occlusive disease, gangrene (limb loss and cerebrovascular disease). MI most common cause of death.

Osmotic damage (sorbitol accumulation in organs with aldose reductase and decr. or absent sorbitol dehydrogenase):
Neuropathy (motor, sensory, and autonomic degeneration)
Cataracts
68
Q

Compare and contrast type 1 and type 2 DM concerning:

primary defect:
Insulin necessary:
Age of onset:
Assocation with obesity:
Genetic predispo:
HLA type:
Glucose intolerance:
Insulin sensitivity:
Ketoacidosis:
Beta cell numbers:
Serum insulin level:
Classic symptoms
Histo:
A

TYPE I

primary defect: autoimmune destruciton of beta cells
Insulin necessary: always
Age of onset: 40
Assocation with obesity: yes
Genetic predispo: relatively strong
HLA type: no
Glucose intolerance: mild to moderate
Insulin sensitivity: low
Ketoacidosis: rare
Beta cell numbers: variable
Serum insulin level: variable
Classic symptoms: sometimes
Histo: islet amyloid polypeptide (IAPP) deposits
69
Q

Waht is a glucagonoma? Presentation?

A

Tumor of pancreatic alpha cells leading to incr. glucagon secretion

Dermatitis (necrolytic migratory erythema)
diabetes (hyperglycemia)
DVT
Depression

70
Q

What is an insulinoma? Symptoms? Treatment?

A

Tumor of pancreatic Beta cells leading to overproduction of insulin leading to hypoglycemia.

Whipple triad: Low blood glucose, symptoms of hypoglycemia (lethargy, syncope, diplopia), and resolution of symptoms after normalization of glucose levels.

Surgical resection

71
Q

What is pathophys of carcinoid syndrome? Symptoms? Lab findings? Rules of 1/3s? Treatment?

A

Carcinoid tumors, especially small bowel tumors, which secrete high levels of 5-HT.
Not seen if tumor is limited to GI tract (first pass)

Recurrent diarrhea, cutaneous flushing, asthmatic wheezing, and right sided valvular disease

Incr. 5-HIAA in urine
Niacin deficiency (pellagra) due to 5-HT production using up all the tryptophan

1/3 metastasize
1/3 present with second malig
1/3 are multiple

Surgical resection
Somatostatin analog

72
Q

What is ZE syndrome? Symptoms? Presentation? Diagnosis? Association?

A

Gastrin secreting tumor of pancreas of duodenum.

Acid hypersecretion leads to recurrent ulcers in duodenm and jejunum

Abdominal pain (ulcers) and diarrhea (malabsorption).

Positive secretin stim test: gastrin levels remain elevated after admin of secretin which would normall inhibit it.

MEN 1

73
Q

What is the inheritance of MEN syndromes? Compare and contrast MEN 1, MEN 2A, and MEN 2B concerning which tumors they involve, mutations, and assocations.

A

MEN1

Parathyroid tumors
Pituitary tumors (prolactin or GH)
Pancreatic endocrine tumors (ZE, insulinomas, VIPomas, glucagonomas)

Mutation of MEN1 gene

3P’s: draw a diamond (2 parathyroids on side (bilateral organ), a pituitary above, and pancreas below)

MEN 2A

Parathyroid hyperplasia
Pheochromocytoma
Medullary thyroid CA

Marfanoid habitus
Mutation in RET gene (receptor tyrosine kinase)

2P’s: draw a square (2 parathyroids above (bilateral), 2 pheos below (adrenal is bilateral), medullary thyroid right in the middle (second overlying square))

MEN 2B

Pheochromocytoma
Medullary thyroid CA
Oral/intestinal ganglioneuromatosis (mucosal neuromas)

Marfanoid habitus
Mutation in RET gene

1 P: draw a triangle (neuromas on top, pheo on bottom (bilateral) and medullary thyroid in the middle).

Step One (49 decks)

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