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Physiology Flashcards

1
Q

What is the thyroid derived from?

A

floor of primitive pharynx, descends into neck

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2
Q

what are the remnants of the thyroglossal duct

A

pyramidal lobe of thyroid and foramen cecum

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3
Q

What is the most common site of ectopic thyroid tissue?

A

base of the tongue-> lingual thyroid

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4
Q

What are the symptoms of a thyroglossal duct cyst?

A

cystic dilation of thyroglossal duct remnant; presents as anterior midline neck mass that moves with swallowing

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5
Q

What are the thyroid follicular cells derived from?

A

outpouched pharyngeal epithelium

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6
Q

What are the thyroid parafollicular cells (C-cells) derived from?

A

4th pharyngeal pouch

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7
Q

What do the thyroid follicular cells produce? What do the thyroid parafollicular cells (C cells) produce?

A

follicular cells - T3 and T4

parafollicular cells - calcitonin

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8
Q

What are the adrenal cortex and medulla derived from?

A

adrenal cortex- mesoderm

medulla - neural crest

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9
Q

What are the layers of the adrenal cortex?

A 
Zona glomerulosa (most peripheral)
Zona fasciculata
Zona reticularis (most internal)
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10
Q

What are the secretory products from the zona glomerulosa and what is the primary regulatory control?

A

produces Aldosterone in response to increased Renin-angiotensin (low BP/low osmolarity)

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11
Q

What are the secretory products from the zona fasciulata and what is the primary regulatory control?

A

Produces cortisol and sex hormones in response to increased ACTH, CRH

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12
Q

What are the secretory products from the zona reticularis and what is the primary regulatory control?

A

Produces sex hormones in response to increased ACTH, CRH

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13
Q

What are the cells of the adrenal medulla and what are their secretory products and primary regulatory control?

A

Chromaffin cells

Secretory product: catecholamines (E 80%, NE 20%)
Primary regulatory control: Preganglionic sympathetic fibers releasing ACh

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14
Q

What is the most common tumor of the adrenal medulla in adults? in children?

A

Adults - pheochromocytoma (episodic HTN)

Children - neuroblastoma (rarely causes HTN)

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15
Q

What is the anterior pituitary (adenohypophysis) derived from?

A

Derived from oral ectoderm; out-pouching of pharyngeal roof: Rathke’s pouch

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16
Q

What are the hormones secreted by the anterior pituitary and which are acidophils and which are basophils?

A

Acidophils - GH, prolactin

Basophils - FSH, LH, ACTH, TSH

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17
Q

Which hormones have a common alpha subunit? How are they differentiated?

A

TSH, LH, FSH and hCG have common alpha subunit

Beta subunit determines specificity

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18
Q

What is the posterior pituitary (neurohypophysis) derived from?

A

derived from neuroectoderm; extension of hypothalamic neurons

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19
Q

Where are ADH and oxytocin made?

A

Both made in the hypothalamus: ADH - supraoptic nuclei, oxytocin - paraventricular nuclei

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20
Q

How are ADH and oxytocin transported to the posterior pituitary?

A

From the hypothalamus via neurophysins (carrier protiens)

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21
Q

What are the endocrine pancreas cell types and what do they produce?

A

alpha cells: glucagon (peripheral) ~30%
beta cells: insulin (central) ~70%
delta cells: somatostatin (interspersed)

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22
Q

How is insulin synthesized?

A

preproinsulin (synth in RER) cleaved into “presignal” and proinsulin (stored in secretory granules) -> cleavage of proinsulin into insulin and C-peptide (exocytosis)

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23
Q

What type of receptor does insulin use? What is the mechanism of action?

A

Tyrosine kinase -> phosphorylates PIP3 kinase which increases intracellular Ca2+ to promote vesicles containing GLUT4 (glucose uptake) as well as stimulate glycogen, lipid and protein synthesis

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24
Q

What are the insulin-dependent glucose transporters and where are they found?

A

GLUT4 on adipose and striated muscle tissue

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25
Q

What are the effects of insulin

A 
Increases:
glucose transport in muscle and adipose
glycogen synthesis and storage
triglyceride synthesis
Na+ retention (kidneys)
protein synthesis (muscles)
cellular reuptake of K+ and amino acids (can cause hypokalemia)

Decreases: glucagon release

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26
Q

Which tissues have insulin-independent glucose uptake? What are their GLUT transporters?

A

GLUT1- RBCs, brain, cornea
GLUT2 (bidirectional)- beta islet cells liver, kidney, small intestine
GLUT3 - brain
GLUT5 (fructose)- spermatocytes, GI tract

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27
Q

What are the major regulators of insulin?

A

Stimulated by glucose, GH, beta2 receptor action

Inhibited by glucagon, somatostatin, catecholamines, cortisol, alpha2 receptor

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28
Q

What is the mechanism of insulin secretion by pancreatic beta cells?

A
  1. glucose enters beta cells via GLUT2
  2. increased ATP is generated from glycolysis
  3. increased ATP closes ATP-sensitive K+ channel -> Depolarization
  4. Voltage-gated Ca2+ channels open -> increase intracellular Ca2+
  5. Exocytosis of insulin granules
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29
Q

What are the effects of glucagon?

A

Glycogenolysis, gluconeogensis in liver

lipolysis and ketone production

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30
Q

What is the mechanism of the glucagon receptor activation?

A

glucagon receptor is coupled to Gs which activates AC and converts ATP-> cAMP. Increased cAMP activates PKA which phosphorylates:

  • Hormone sensitive lipase -> lipolysis
  • Glycogen phosphorylase -> glycogen breakdown
  • Acetyl CoA carboxylase (becomes inactivated) -> decreased fatty acid synthesis
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31
Q

How is glucagon regulated?

A

stimulated in response to hypoglycemia

inhibited by insulin, hyperglycemia, somatostatin

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32
Q

What is the function of CRH?

A

Stimulates production of POMC –> ACTH, MSH and production of beta-endorphin

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33
Q

What is the function of dopamine?

A

decreases prolactin *dopamine antagonists can cause galactorrhea from hyperprolactinemia

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34
Q

What is the function of GHRH?

A

increases GH, GnRH

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35
Q

What is the function of GnRH?

A

Increases FSH and LH

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36
Q

What is the function of prolactin?

A

Decreases GnRH

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37
Q

What is the function of somatostatin?

A

decreases GH, TSH

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38
Q

What is the function of TRH?

A

increases TSH, prolactin

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39
Q

What are the anterior pituitary cell types?

A 
lactotrophs- prolactin
corticotrophs- ACTH
somatotrophs - GH
thyrotrophs - TSH
gonadotrophs - LH, FSH
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40
Q

What is the function of prolactin?

A

stimulates milk production in breast

inhibits ovulation in females and spermatogenesis in males by inhibiting GnRH synthesis and release

Note; excessive prolactin associated with decreased libido

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41
Q

How is prolactin regulated?

A

TRH increases prolactin

prolactin tonically inhibited by dopamine from hypothalamus

prolactin inhibits own secretion via stimulation of dopamine synthesis from hypothalamus

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42
Q

What drugs stimulate prolactin secretion?

A

dopamine antagonists( most antipsychotics), estrogens, opiates, serotonin, ACh

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43
Q

What is the function of Growth hormone?

A

Stimulates secretion of IGF-1 from liver -> stimulates linear growth and muscle mass, increases insulin resistance

  • decreases glucose uptake in fat, muscle -> increased blood glucose
  • increases hormone sensitive lipase -> mobilize fat stores
  • increases amino acid uptake -> muscle building
  • chondrocytes -> linear bone growth
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44
Q

How is GH regulated?

A

GHRH stimulates pulsatile release of GH; secretion increases during exercise and sleep

Secretion inhibited by glucose and somatostatin via negative feedback by somatomedin

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45
Q

What are the functions of ghrelin?

A

produced by stomach

stimulates hunger and GH release

Ghrelin increases with sleep loss and Prader-Willi syndrome

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46
Q

What are the functions of leptin?

A

Satiety hormone produced by adipose, decreases during starvation

Sleep deprivation-> decreased leptin -> increased appetite

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47
Q

What are the receptors for ADH? Where are they located and what is their function?

A

V1 receptors on smooth muscle, myocytes, adrenals, platelets -> increase blood pressure

V2 receptors in collecting ducts -> decreases serum osmolarity and increases urine osmolarity

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48
Q

What is the mechanism of V1 receptors?

A

V1 receptors - are on smooth muscle myocytes, adrenals and platelets

Gq -> activate phospholipase C -> IP3 -> increase calcium

  • vasoconstriction
  • increased ACTH
  • increases glycogenolysis in liver
  • increases platelet aggregation
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49
Q

What is the mechanism of V2 receptors?

A

Gs -> AC -> increased cAMP -> increased aquaporin-2 inserted in principal cells -> increases urine osmolarity

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50
Q

How is ADH regulated?

A

primarily by osmoreceptors in hypothalamus -> increased ADH released when high blood osomolarity

secondarily by hypovolemia (low BP) -> increased ADH released -> increases BP

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51
Q

A mutation in the V2 receptor can cause what?

A

Nephrogenic DI

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52
Q

What is the function of ACTH on the adrenals?

A

stimulates cholesterol breakdown in zona glomerulosa via cholesterol desmolase to pregnenolone; increases synthesis of mineralocorticoids, glucocorticoids and androgens

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53
Q

How is ACTH regulated?

A

stimulated by CRH from hypothalamus and inhibited by cortisol (neg feedback)

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54
Q

How does 17alpha-hydroxylase deficiency affect mineralocorticoids, cortisol and sex hormone levels? How does it present?

A

minearalocorticoids- Increase
coritsol- Decrease
sex hormones- Decrease

Presentation

boys: pseudo-hermaphroditism (ambiguous genitalia, undescended testes)
girls: lack secondary sex characteristics

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55
Q

How does 21-hydroxylase deficiency affect mineralocorticoids, cortisol and sex hormone levels?

A

minearalocorticoids- Decrease
coritsol- Decrease
sex hormones- Increase

Presentation:

  • Salt wasting in infancy (if presenting before childhood)
    boys: precocious puberty
    girls: virilization, ambiguous gneitalia
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56
Q

How does 11beta-hydroxylase deficiency affect mineralocorticoids, cortisol and sex hormone levels?

A

minearalocorticoids- Increase (via 11-deoxycorticosterone; low aldosterone)
coritsol- Decrease
sex hormones- Increase

Presentation:
boys:
girls: virilization

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57
Q

What are the clinical findings (BP, Na+, K+, labs) for 17alpha-hydroxylase deficiency?

A

BP: high (increased mineralocorticoids)
Na+: high (increased mineralocorticoids)
K+: low (increased mineralocorticoids)
labs: low androstenedione (decreased sex hormones)

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58
Q

What are the clinical findings (BP, Na+, K+, labs) for 21-hydroxylase deficiency?

A

BP: low (decreased mineralocorticoids)
Na+: low (decreased mineralocorticoids)
K+: high (decreased mineralocorticoids)
labs: high renin activity, high 17-hydroxyprogesterone

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59
Q

What are the clinical findings (BP, Na+, K+, labs) for 11beta-hydroxylase deficiency?

A

BP: high (increased mineralocorticoids 11-DOC)
Na+: high (increased mineralocorticoids)
K+: low (increased mineralocorticoids)
labs: low renin activity

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60
Q

What is cortisol bound to?

A

Corticosteroid-binding globulin aka transcortin; made in liver

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61
Q

What are the functions of cortisol?

A
  • increase BP
  • increase insulin resistance (diabetogenic)
  • increase gluconeogenesis, lipolysis, porteolysis
  • decrease fibroblast activity (causes striae)
  • decreases inflammatory and immune responses
  • decreases bone formation (decreased osteoblast activity)
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62
Q

How does cortisol affect BP?

A
  • upregulates alpha1 receptors on arterioles -> increased sensitivity to E and NE
  • at high concentrations cortisol can bind to mineralocorticoid receptors
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63
Q

How does cortisol affect inflammatory and immune responses?

A

decreases inflammation and immune response by:

  • inhibits phospholipaseA2 -> inhibits production of PGs and LTs
  • inhibits WBC adhesion -> demargination of PMNs -> increased PMNs
  • inhibits PMN apoptosis
  • blocks histamine release from mast cells
  • reduces eosinophils
  • Blocks IL-2 production
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64
Q

How do cortisol levels fluctuate?

A

Highest around noon; disturbed by stress -> prolongs secretion

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65
Q

how is cortisol regulated?

A

CRH (hypothalamus) stimulates ACTH release (ant pit) to increase cortisol production in adrenal zona fasciulata

Cortisol is inhibited by neg feedback -> cortisol decreases CRH, ACTH and cortisol secretion

66
Q

How do calcium levels change with pH?

A

increased pH -> higher affinity of calcium to albumin -> less free Ca2+ -> hypocalcemia (cramps, pain, paresthesias, carpopedal spasm)

67
Q

What are the functions of vitamin D (cholecalciferol)?

A
  • increase absorption of calcium and phosphate in intestines

- increase bone resorption of calcium and phosphate

68
Q

how is vitamin D regulated?

A

increased PTH, decreased Ca2+ and decreased phosphate cause increased 1,25(OH)2 production

Negative feedback with increased 1,25(OH)2 levels

69
Q

Where is PTH produced? What are its functions?

A

produced in parathyroid chief cells

Functions:

  • increases bone resporption of calcium and phosphate
  • increases resorption of calcium in DCT
  • decreases resorption of phosphate in PCT
  • increases 1,25-(OH)2 (calcitriol) by stimulating 1alpha-hydroxylase in PCT of kidney

increases serum calcium, decreases serum phosphate and increases urine phosphate

70
Q

How does PTH stimulate calcium resorption from bone?

A

PTH stimulates osteoblasts to increase macrophage colony-stimulating factor and RANK-L (receptor activator of NF-kB ligand) secretion which binds RANK on osteoclasts and their precursors to stimulate osteoclasts and increase calcium release from bone

71
Q

How is PTH regulated?

A

PTH increases with:

  • decreased serum calcium
  • increased serum phosphate
  • decreased serum Mg2+

PTH decreases with:
-very low serum Mg2+ (diarrhea, aminoglycosides, diuretics, EtOH abuse)

72
Q

What is the source, function and regulation of calcitonin?

A

Source: parafollicular cells (C cells) of thyroid
Function: decrease bone resporption of calcium
Regulation: increased serum calcium stimulates calcitonin

73
Q

What hormones act via cAMP signaling?

A 
'FLAT ChAMP'
FSH
LH
ACTH
TSH
CRH, calcitonin
hCG, Histamine (H2)
ADH (V2)
MSH
PTH
GHRH
glucagon
74
Q

What hormones act via cGMP signaling?

A

ANP, BNP, NO (EDRF) ‘vasodilators’

75
Q

What hormones act via IP3 signaling?

A 
GnRH
Oxytocin
ADH (V1)
TRH
Histamine (H1)
Angiotensin II
Gastrin
76
Q

What hormones act via intracellular receptor?

A

Vitamin D, Estrogen, Testosterone, T3/T4, Cortisol, Aldosterone, Progesterone

77
Q

What hormones act via intrinsic tyrosine kinase receptors (autophosphorylation)?

A

MAP kinase pathway

Insulin, IGF-1, FGF, PDGF, EGF

78
Q

What hormones act via receptor-associated tyrosine kinase (cannot autophosphorylate)?

A

JAK/STAT pathway, ‘acidophils and cytokines’
Prolactin
Immunomodulators (cytokines IL-2, IL-6, IFN)
GH
G-CSF
EPO
TPO

79
Q

What is the effect of corticosteroids on CBC?

A

Increase PMNs

Decrease: lymphocytes, monocytes, basophils, eosinophils

80
Q

Where are the thyroid hormones T3 and T4 produced?

A

Follicles of thyroid, most T3 formed in target tissues

81
Q

What are the functions of T3/T4?

A
  • Bone growth
  • CNS maturation
  • Beta1 adrenergic receptors increased -> more sensitive to E, NE -> increased CO, HR, SV, contractility
  • Increased basal metabolic rate via Na/K-ATPase activity -> increased O2 consumption, RR, body temp
  • increased glycogenolysis, gluoneogenesis, lipolysis -> increased ATP
82
Q

How are thyroid hormones regulated?

A

TRH (hypothal.) -> TSH (ant. pit.) -> thyroid follicular cells -> T3/T4

Negative feedback by free T3,T4 to ant. pit -> decreased sensitivity to TRH

83
Q

What is the Wolff-Chaikoff effect?

A

Excess iodine temporarily inhibits thyroid peroxidase -> decreased T3, T4 production

84
Q

How do changes in thyroxine-binding globulin (TBG) affect free T3/T4 levels?

A

decreased TBG in hepatic failure, steroids -> increased free T3/T4

increased TBG in pregnancy or OCP use -> decreased free T3/T4

85
Q

What is the role of peroxidase?

A

responsible for oxidation and organification of iodide and coupling of MIT and DIT into T3/ T4

86
Q

What is responsible for T4 to T3 conversion in peripheral tissue?

A

5’-deiodinase

87
Q

How does propylthiouracil affect T3 and T4 synthesis?

A

inhibits both peroxidase and 5’-deiodinase

88
Q

Etiology of Cushing syndrome

A

Increased cortisol levels due to:

  • Exogenous corticosteroids (most common cause)
  • Primary adrenal adenoma, hyperplasia or carcinoma
  • ACTH-secreting pituitary adenoma (Cushing disease)
  • Ectopic ACTH secretion (small cell carcinoma or carcinoid)
89
Q

Findings in Cushing syndrome

A 
HTN
weight gain
moon facies
truncal obesity
buffalo hump
skin changes - thinning, striae
osteoporosis
hyperglycemia (insulin resistance)
amenorrhea
immunosupression
90
Q

What are the ACTH levels and size of adrenals with Cushing syndrome from exogenous corticosteroids?

A

decreased ACTH

BILATERAL adrenal ATROPHY

91
Q

What are the ACTH levels and size of adrenals with Cushing syndrome from primary adrenal adenoma, hyperplasia or carcinoma?

A

decreased ACTH

UNILATERAL adrenal ATROPHY of unaffected adrenal gland and HYPERPLASIA of affected adrenal gland

92
Q

What are the ACTH levels and size of adrenals with Cushing syndrome from ACTH-secreting pituitary adenoma?

A

increased ACTH, BILATERAL HYPERPLASIA

93
Q

What are the ACTH levels and size of adrenals with Cushing syndrome from paraneoplastic ACTH-secretion?

A

increased ACTH, BILATERAL HYPERPLASIA

94
Q

What are the screening tests to diagnose Cushing syndrome?

A

increased free cortisol on 24hr UA
increased midnight salivary cortisol
no suppression with low-dose dexamethasone test

measure ACTH ->
if low suspect adrenal tumor, exogenous corticosteroids
if high need to differentiate Cushing disease (ACTH secreting pit. adenoma) from ectopic ACTH secretion

95
Q

How are Cushing disease (ACTH secreting pit. adenoma) and ectopic ACTH secretion differentiated?

A

High-dose dexamethasone test:
suppression –> Cushing disease
no suppression –> ectopic ACTH secretion

CRH stimulation test:
Increased ACTH and cortisol –> Cushing disease
No increase in ACTH or cortisol –> ectopic ACTH secretion

96
Q

Adrenal insufficiency

A

Deficiency of adrenal hormones glucocorticoids +/- mineralocorticoids

symptoms: weakness, fatigue, orthostatic hypotension, myalgias, weight loss, GI distress, sugar/salt cravings

97
Q

What are causes of acute and chronic primary adrenal insufficiency?

A

Primary Acute insufficiency:
1. Waterhouse-Friderichsen syndrome. N. meningitidis infection -> DIC -> endotoxic shock -> hemorrhagic necrosis of adrenal glands

Primary Chronic insufficiency (Addison disease) - progressive destruction of adrenal glands:
1. autoimmune destruction (most common in developed world)

  1. TB (most common in developing world)
  2. metastatic carcinoma (usually from lung)
98
Q

What are causes of Tertiary adrenal insufficiency?

A
  1. Abrupt withdrawal of glucocorticoids (most common). Symptoms: weakness, shock

No hyperkalemia since aldosterone synthesis unaffected

99
Q

What are the symptoms of primary adrenal insufficiency?

A

Deficiency of aldosterone and cortisol -> hyponatremia, hyperchloremia, hypotension, hyperkalemia, non-anion gap metabolic acidosis, skin and mucosal hyperpigmentation (increased ACTH-> increased POMC -> increased MSH)

100
Q

What causes secondary adrenal insufficiency?

A

Decreased pituitary ACTH production, can be caused by chronic exogenous corticosteroids and tumors

No skin/mucosal hyperpigmentation or hyperkalemia

101
Q

Neuroblastoma

A

Most common tumor of adrenal medulla in kids

102
Q

Pheochromocytoma -etiology and rule of 10s

A

Most common tumor of adrenal medulla in adults, derived from chromaffin cells (neural crest)

Rule of 10:
10% malignant
10% bilateral
10% extra-adrenal
10% calcify
10% kids
103
Q

Pheochromocytoma symptoms and findings?

A

Tumors secrete E, NE and Dopamine: episodic hyperadrenergic symptoms

Pressure - increased BP
Pain - HA
Perspiration
Palpitations (increased HR)
Pallor

Findings: increased catecholamines and metanephrines and VMA in urine and plasma

104
Q

What is pheochromocytoma associated with?

A

NF type 1, VHL, MEN 2A and 2B

105
Q

What is the treatment for pheochromocytoma?

A

Phenoxybenzamine (irreversible alpha agonist) to prevent HTN crisis then beta-blockers

106
Q

What are the signs/symptoms of hyperthyroidism?

A

Increased # and sensitivity of beta-receptors

Heat intolerance (increased heat produced)
Weight loss, increased appetite
Hyperactivity, tremor
Diarrhea
Increased DTR
Pretibial myxedema (Graves disease), periorbital edema
Warm, moist skin; fine hair
angina, increased HR, arrhythmias
Widened pulse P, vasodilation (increased systolic P)
hyperglycemia
hypocholesterolemia (increased LDL receptor expression)
bone resporption
decreased muscle mass

107
Q

What are the signs/symptoms of hypothyroidism?

A

decreased # and sensitivity of beta-receptors

Cold intolerance (less heat production)
Weight gain, decreased appetitie
Hypoactivity, lethargy, fatigue
Constipation
Decreased DTR
Myxedema (facial/periorbital)
Dry, cool skin; coarse, brittle hair
Decreased HR, narrowed pulse P (increased diastolic P), vasoconstriction
Hypercholesterolemia (decreased LDL receptor expression)
108
Q

What drug can cause hypothyroidism and how is it treated?

A

Amiodarone (class III anti-arrhythmatic) - cause thyroid dysfunction bc high iodide content which causes hypothyroidism

Treat with levothyroxine

109
Q

Hashimoto thyroiditis - etiology and associations

A

Most common cause of hypothyroidism in developed world (iodine sufficient)

  • Autoimmune disorder -> anti-thyroid peroxidase, antimicrosomal and antithyroglobulin (anti-TGB) antibodies
  • Associated with HLA-DR5, increased risk of non-Hodgkin (B-cell marginal zone) lymphoma
  • hyperthyroid early in course due to released T3/T4 from follicular rupture and then progresses to hypothyroid
110
Q

Hashimoto thyroiditis - histological and clinical findings

A

histo- Hurthle cells (enlarged epithelial cells w pink granular cytosol), lymphoid aggregate with germinal centers

clinical findings: moderately enlarged NON-tender thyroid

TPO antibodies

111
Q

Cretinism

A

Congenital hypothyroidism

-due to maternal hypothyroidism, thyroid agenesis, thyroid dysgenesis (most common cause in US), iodine deficiency, dyshormonogenetic goiter

Findings:
pot-bellied
pale
puffy-faced
protruding umbilicus
protuberant tongue
poor brain development
short stature
112
Q

Subacute granulomatous tyroiditis (de Quervain)

A

granulomatous thyroiditis following a viral infection (multinucleated giant cells on histo)

usually middle aged women

presents as TENDER thyroid with transient hyperthryoidism followed by hypothyroidism

  • Increased ESR
  • jaw pain
113
Q

Riedel thyroiditis

A

Thyroid replaced by fibrous tissue, fibrosis may extend to local structures like airway mimicking anaplastic carcinoma

  • thyroid fixed, NON-tender, “hard as wood”
  • manifestation of IgG related systemic disease (autoimmune pancreatitis, retroperitoneal fibrosis, noninfectious aortitis)
114
Q

Graves Disease

A

most common cause of hyperthyroidism, usually women 20-40yo; often presents during stress (childbirth)

Autoantibodies (IgG) stimulate:

  • ->TSH receptors - diffuse goiter (thyroid hyperplasia and hypertrophy)
  • ->Retro-orbital fibroblasts (exophthalmos: proptosis, extraocular muscle swelling), Dermal fibroblasts (pretibial myxedema) from increased glycosaminoglycan buildup

Histo: Irregular follicles with “scalloped colloid” and chronic inflammation

115
Q

Graves disease - lab findings

A

Increased total and free T4, decreased TSH
Hypochoesterolemia
Hyperglycemia

116
Q

Toxic multinodular goiter

A

Caused by relative iodine deficiency. Focal patches of hyperfunctioning follicular cells

Mutation in TSH receptor, so work independent of TSH -> increase T3 and T4 in ‘hot nodules’; cold nodules don’t produce T3/T4

Irregular radioiodide uptake

Histo: follicles of varying sizes distended with colliod and lined by flattened epithelium with areas of fibrosis and hemorrhage

117
Q

Thyroid storm

A

Stress-induced cathecholamine surge, complication of thyrotoxicosis

Presents: agitation, delirium fever diarrhea, coma, tachyarrhythmia (cause of death)

May see increased ALP (increased bone turnover)

118
Q

How is thyroid storm treated?

A

3Ps
Beta-blocker (Propranolol)

Propylthiouracil (PTU), inhibits peroxidase and 5’-deiodinase

Corticosteroids (Prednisolone)

119
Q

Jod-Basedow phenomenon

A

Thyrotoxicosis if patient with iodine deficiency goiter is made iodine replete

120
Q

Complications of thyroidectomy

A
  • hoarseness (recurrent laryngeal n damage)
  • hypocalcemia (removal of PTH glands)
  • transection of recurrent laryngeal nerve (ligation of inferior thyroid artery)
  • transection of superior laryngeal nerve (ligation of superior laryngeal artery)
121
Q

Follicular adenoma

A

Benign proliferation of follicles surrounded by fibrous capsule

-usually nonfunctional, rarely secretes thyroid hormone

122
Q

Papillary carcinoma of thyroid

A

Most common thyroid cancer, excellent prognosis

Histo: Papillae lined by cells with ‘Orphan Annie’ eyes nuclei - empty appearing with central clearing, psammoma bodies, nuclear grooves

Lymphatic invasion common to cervical LNs

Increased risk with RET and BRAF mutations

123
Q

Follicular carcinoma of thyroid

A

Good prognosis, invades thyroid capsule, uniform follicles

F>M, 50-60s

Metastasizes via blood -> bone, lung, brain, liver

124
Q

Medullary carcinoma of thyroid

A

From parafollicular ‘C cells’ produce calcintonin
Associated w MEN2A and 2B, RET mutations

sheets of cells in amyloid stroma (calcitonin deposits as amyloid)

hematogenous spread

125
Q

Undifferentiated/anaplastic carcinoma of thyroid

A

rarest thyroid cancer, associated with p53 and beta cantenin mutations

Older patients

rapidly enlarging; invades local structures -> dysphagia and respiratory compromise

very poor prognosis

126
Q

What are causes and findings of hypoparathyroidism?

A

causes: accidental surgical excision, autoimmune destruction, DiGeorge syndrome

Causes low PTH, presents with:

  • hypocalcemia
  • tetany: elicitation with BP cuff (Trousseau sign - carpal spasm with occlusion of brachial artery), tapping facial nerve (Chvostek sign)
  • numbness and tingling, especially around mouth
127
Q

Primary hyperparathyroidism - what are the PTH and calcium findings?

A

High PTH and high calcium

128
Q

Secondary hyperparathyroidism - what are the PTH and calcium findings?

A

High PTH and low calcium

129
Q

Pseudohypoparathyroidism

A

Albright hereditary osteodystrophy AD- kidney resistant to PTH

hypocalcemia
shortened 4th and 5th digits
short stature

130
Q

Familial hypocalciuric hypercalcemia

A

defective calcium sensing receptor on parathyroid cells

mild hypercalcemia with normal/high PTH

131
Q

Primary hyperparathyroidism

A

Caused by parathyroid adenoma or hyperplasia

-HYPERCALCEMIA, hypercalciuria (renal stones), hypophosphatemia, increased PTH, increased ALP, increased cAMP in urine

May present with weakness and constipation;
abdominal/flank pain (kidney stones, acute pancreatitis); depression (psych overtones)

can cause osteitis fibrosa cystica - cystic bone spaces filled with brown fibrous tissue

132
Q

Secondary hyperparathyroidism

A

Secondary hyperplasia of parathyroid from decreased calcium or increased phosphate
- renal disease most common cause

HYPOCALCEMIA –> causes increased PTH, hyperphosphatemia in renal failure and hypophosphatemia with other causes, increased ALP

133
Q

Renal osteodystrophy

A

bone lesions due to secondary or tertiary hyperparathyroidism from renal disease

134
Q

Pituitary adenoma

A

Most commonly prolactinoma

May be:
-functional (hormone producing) -> presentation of prolactinoma: amenorrhea, galactorrhea, low libido, infertility

-nonfunctional -> mass effect bitemporal hemianopia, hypopituitarism, HA

somatotropic adenoma: acromegaly

135
Q

What is the treatment for prolactinoma?

A

dopamine agonists (bromocriptine or cabergoline), resection

136
Q

Acromegaly

A

Excess GH in adults, usually from pituitary adenoma

Findings: large tongue with deep furrows, deep voice, large hands and feet, coarse facial features, insulin resistance

Diagnosis:
increase serum IGF-1
failure to suppress serum GH after oral glucose tolerance test
pituitary mass on MRI

Treatment: resection, octreotide (somatostatin analog) or pegvisomant (GH receptor antagonist)
- increase risk of colorectal polyps and cancer

137
Q

Central diabetes insipidus

A

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

Findings: polydipsia, polyuria
Decreased ADH
Urine specific gravity 290
Low urine osmolality

Water deprivation test: >50% increase in urine osmolality after ADH administration

Treatment: Intranasal desmopressin, hydration

138
Q

Nephrogenic diabetes insipidus

A

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

Findings: polyuria, polydipsia
Normal ADH
Urine specific gravity 290
Low urine osmolality

Water deprivation test: minimal change in urine osmolality even after ADH administration

Treatment: HCTZ, indomethacin, amiloride, hydration

139
Q

SIADH pathophysiology and features

A

Syndrome of inappropriate ADH secretion

  • Excessive free water retention
  • EUVOLEMIC hyponatremia with continued Na+ excretion
  • Urine osmolality > serum osmolality
  • Body responds to water retention with decreased aldosterone (hyponatremia) to keep volume normal
  • very low serum Na+ can lead to cerebral edema, seizures –> correct slowly to prevent osmotic demyelination syndrome (formerly central pontine myelinolysis)
140
Q

Causes of SIADH

A

Ectopic ADH (small cell lung cancer)
CNS disorders/head trauma
Pulmonary disease
Drugs (cyclophophamide)

141
Q

Treatment of SIADH

A 
Fluid restriction
IV hypertonic saline
conivaptan
tolvaptan
demeclocycline
142
Q

Hypopituitarism - causes and treatment

A

Undersecretion of pituitary hormones (usually LH/FSH decrease first, followed by GH, TSH and ACTH last) due to:

  • Nonsecreting pituitary adenoma, craniopharyngioma
  • Sheehan syndrome
  • Empty sella syndrome
  • Pituitary apoplexy
  • Brian injury
  • Radiation

Treatment: HRT (corticosteroids, thyroxine, sex steroids, human growth hormone)

143
Q

Sheehan syndrome

A

ischemic infarct of pituitary following postpartum bleeding; usually presents with failure to lactate, absent menstruation, cold intolerance

144
Q

Empty sella syndrome

A

atrophy or compression of pituitary, often idiopathic, common in obese women

145
Q

Pituitary apoplexy

A

sudden hemorrhage of pituitary, often in presence of existing pituitary adenoma

presents with severe HA, bitemporal hemianopsia

146
Q

Diabetes mellitus - general mechanism and symptoms

A

Insulin deficiency or insensitivity (and glucagon excess)

Polydipsia, polyuria, polyphagia, weight loss, DKA (type1), hyperosmolar coma (type2)

Also seen in patients on glucocorticoid therapy (steroid diabetes). Rarely can be caused by unopposed secretion of GH and epinephrine.

147
Q

Chronic complications of diabetes mellitus

A

Nonenzymatic glycation

  • small vessel disease (diffuse thickening of basement membrane)
  • -> retinopathy (hemorrhage, exudates, microaneurysms, vessel proliferation)
  • ->glaucoma
  • ->neuropathy
  • ->nephropathy (Kimmelsteil-Wilson nodules -> progressive proteinuria and arteriolosclerosis ->HTN; chronic renal failure

-Large vessel atherosclerosis, CAD, peripheral vascular occlusive disease, gangrene, cerebrovascular disease. MI most common cause of death

Osomotic damage (sorbital accumulation in organs with aldose reductase and low/absent sorbitol dehydrogenase) :

  • Neuropathy (motor, sensory and autonomic degeneration)
  • Cataracts
148
Q

Diabetes mellitus diagnosis

A

Fasting serum glucose, oral glucose tolerance test, HbA1c

149
Q

Type 1 diabetes mellitus

A

Defect: autoimmune destruction of beta cells, Low beta cell numbers in islets

Insulin necessary in treatment

Age: usually

150
Q

Type 2 diabetes mellitus

A

Defect: increased resistance to insulin, progressive pancreatic beta cell failure

Age of onset usually >40

Associated with obestiy and strong genetic component.

Mild/moderate glucose intolerance

DKA is very rare

Classic symptoms are less common

Histology: islet amyloid polypeptide (IAPP) deposits

151
Q

Diabetic ketoacidosis (DKA) etiology

A

Complication of diabetes (usually type 1 since endogenous insulin in type2 prevents lipolysis),

-usually manifests from increased insulin requirements from stress (ex infection)

Increased free fatty acids -> fat breakdown and increase ketogenesis –> ketone bodies (beta-hydroxybutyrate > acetoacetate)

152
Q

Diabetic ketoacidosis (DKA) - signs/symptoms and labs

A 
Signs/symptoms:
Kussmaul respirations (rapid/deep breathing)
nausea/vomiting
abdominal pain
psychosis/delirium
dehydration
fruity breath odor

Labs:
Hyperglycemia
Increased anion gap metabolic acidosis (high H+, low bicarb)
Increased blood ketones
leukocytosis
Hyperkalemia (but depleted intracellular K+ due to cellular shift from decreased insulin)

153
Q

Diabetic ketoacidosis (DKA) - Complications and treatment

A 
Complications:
Mucormycosis (usually from Rhizopus infection)
cerebral edema
cardiac arrhythmias
heart failure
Treatment:
IV fluids
IV insulin
K+ (replete intracellular stores)
glucose if necessary
154
Q

Glucagonoma

A

Tumor of pancreatic alpha cells causes overproduction of glucagon

Presents with 
Dermatitis (necrolytic migratory erythema)
Diabetes (hyperglycemia)
DVT
Depression
Diarrhea (GI symptoms)
155
Q

Insulinoma

A

Tumor of pancreatic beta cells causes overproduction of insulin –> Hypoglycemia

May see Whipple triad: hypoglycemia, symptoms of hypoglycemia (lethargy, syncope, diplopia) and resolution of symptoms after normalization of glucose levels

156
Q

Carcinoid syndrome

A

Rare syndrome from carcinoid tumors (neuroendocrine cells) especially metastatic small bowel tumors –> secrete high levels 5HT

Symptoms: recurrent diarrhea, cutaneous flushing, asthmatic wheezing, right-sided valve disease, increased 5-HIAA in urine, niacin deficiency

Histology: prominent rosettes

157
Q

Zollinger-Ellison syndrome

A

Gastrin-secreting tumor of pancreas or duodenum

Acid hyper-secretion -> recurrent ulcers in duodenum and jejunum

Presents: abdominal pain (ulcers), diarrhea (malabsorption)

Positive secretin stimulation test: gastrin levels elevated after administration of secretin

May be associated with MEN1

158
Q

Multiple endocrine neoplasias (MEN) inheritance

A

ALL are autosomal dominant!

159
Q

MEN 1

A

‘3 Ps’

  • Parathyroid tumors
  • Pituitary tumors (prolactin or GH)
  • Pancreatic endocrine tumors (Zollinger-Ellison syndrome, insulinomas, VIPomas, gucagonomas [rare])

Associated with mutation of MEN1 gene (menin tumor suppressor)

160
Q

MEN 2A

A

‘2 Ps’

  • Parathyroid hyperplasia
  • Pheochromocytoma
  • Medullary thyroid carcinoma (secretes calcitonin)

Associated with: marfanoid habitus, mutation in RET gene (codes for receptor tyrosine kinase)

161
Q

MEN 2B

A

‘1 P’

  • Pheochromocytoma
  • Medullary thyroid carcinoma (secretes calcitonin)
  • Oral/intestinal ganglioneuromatosis (mucosal neuromas)

Associated with: marfanoid habitus, mutation in RET gene

162
Q

Thyroid cancer risks

A

External radiation therapy to head and neck in childhood significantly increases risk of papillary carcinoma of thyroid

Endocrine (1 decks)

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