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STEP > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Thyroid diverticulum arises from the

A

Floor of primitive pharynx and descend into neck

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2
Q

Thyroid connected to tongue via

A

Thyroglossal duct – persistence –> thyroglossal duct cyst or pyramidal lobe of thyroid

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3
Q

Ectopic thyroid tissue often found on

A

Tongue (removal can –> hypothyroidism if only thyroid tissue)

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4
Q

Persistent cervical sinus

A

Branchial cleft cyst in lateral neck

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5
Q

Thyroglossal duct cyst

A

Midline in neck that moves w/ swallowing

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6
Q

Derivation of thyroid

A

Endoderm

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7
Q

Adrenal cortex derivation

A

Mesoderm

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8
Q

Adrenal medulla derivation

A

Neural crease

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9
Q

Zona Glomerulosa

A

Outer layer – aldosterone (mineralocorticodid), regulated by Ang II

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10
Q

Zona fasciculata

A

Middle layer – cortisol (glucocorticoid), reg by ACTH, CRH

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11
Q

Zona reticulata

A

Inner layer – androgens – DHEA, reg by ACTH, CRH

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12
Q

Medulla

A

Chromafin cells regulated by preganglionic sympathetic fibers –> release catecholamines NE/E

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13
Q

Anterior pituitary aka

A

Adenohypophysis

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14
Q

Anterior pituitary secretes

A

FSH, LH, ACTH, TSH, PRL, GH, MSH (FLAT PiG)

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15
Q

Derivation of anterior pituitary

A

Rathke’s pouch (oral ectoderm)

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16
Q

Alpha subunit is common to

A

TSH, LH, FSH, hCG

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17
Q

B subunit

A

Determines hormone specificity

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18
Q

Acidophils produce

A

GH, PRL

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19
Q

Basophiles produce

A

FSH, LH, ACTH, TSH

B-FLAT

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20
Q

Posterior pituitary hormones

A

ADH, oxytocin

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21
Q

Post pituitary hormone synthesis

A

Synthesis is in hypothalamus in supraoptic/paraventricular nuclei –> post. pituitary via neurophysins

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22
Q

Post. pituitary derivation

A

Neuroectoderm

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23
Q

Alpha cells of pancreas make

A

Glucagon (peripheral in islet)

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24
Q

Beta cells of pancreas make

A

Insulin (central in islet)

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25
Q

Delta cells of pancreas make

A

Somatostatin (interspersed in islet)

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26
Q

Insulin synthesis

A

Preproinsulin from RER –> cleave presignal to proinsulin (stored in secretory granules) –> cleave proinsulin –> exocytose equal amounts of insulin and C peptide

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27
Q

Insulin receptors are…

A

Tyrosine kinase –> PIP3 and RAS/MAP

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28
Q

PIP3 pathway in response to insulin results in

A

GLUT4 vesicles translocated to membrane and glycogen, lipid and protein synthesis

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29
Q

RAS/MAP pathway leads to

A

Cell growth, DNA synthesis

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30
Q

Effects of insulin

A 
Anabolic --
Increased glc transport in skeletal m/adipose tissue
Increased glycogen synth/storage
Increased trig synthesis
Increased Na retention (kidneys)
Increased protein synth (mms)
Increased cellular uptake of K and amino acids
Less glucagon release
Less lipolysis in adipose tissue
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31
Q

Does insulin cross placenta?

A

No

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32
Q

Insulin dependent glucose transporters and location

A

GLUT4 – adipose tissue, striated muscle (increased by exercist)

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33
Q

Insulin independent glucose transporters and location

A

GLUT1: RBCS, brain, cornea, placenta
GLUT2 (bidirectional): B islet cells, liver, kidney, SI
GLUT3: brain, placenta
GLUT5 (fructose): spermatocytes, GI tract

Insulin independent glucose uptake in BRICK L
Brain, RBCs, Intestine, Cornea, Kidney, LIver

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34
Q

Insulin release related to sympathetic stimulation

A

Decreased by alpha2

Increased by beta2

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35
Q

Process of excreting insulin in response to glucose

A

Glucose enters B cells –> more ATP made from metabolism of glc –> closes K channels (target of SUs) –> depolarization –> voltage gated Ca channels open –> Ca influx –> insulin exocytosis

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36
Q

Glucagon function

A

Glycogenolysis, gluconeogenesis, lipolysis, ketone prodxn – secreted in response to hypoglycemia, inhib by insulin, hyperglycemia, somatostatin

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37
Q

CRH –>

A

Increases ACTH, MSH, B-endorphin, lower in chronic exogenous steroid use

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38
Q

Dopamine–>

A

Less PRL, TSH (dopamine antagonists –> galactorrhea due to hyper prolactinemia

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39
Q

GHRH–>

A

Increased GH

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40
Q

Tesamorelin

A

GH analog used to tx HIV assc lipodystrophy

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41
Q

GnRH–>

A

Incereased FSH, LH –> suppressed by hyperprolactinemia
Tonic GnRH–>suppresion of HPG axis
Pulsatile GnRH –>puberty, fertility

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42
Q

PRL—>

A

Less GnRH

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43
Q

Pituitary prolactinoma–>

A

Amenorrhea, osteoporosis, hypogonadism, galactorrhea via suppression of GnRH

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44
Q

Somatostatin–>

A

Decreases GH, TSH –> analogs can treat acromegaly (octreotide)

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45
Q

TRH–>

A

Increased TSH, PRL; increased TRH in 1o/2o hypothyroidism (trying to compensate) may increase prolactin secretion –> galactorrhea

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46
Q

PRL fxn–>

A

Stimulates milk prodxn in breast, inhib ovulation in females/spermatogenesis in males by inhib of GnRH synth/release (increase assc w/ decreased libido)

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47
Q

Dopamine and PRL

A

Dopamine inhibits PRL secretion via tuberoinfundibular pathway of hypothalamus

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48
Q

Dopamine agonists

A

Bromocriptine –> inhib PRL secretion –> tx of prolactinoma

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49
Q

Dopamine antagonists and estrogens–>

A

stimulate PRL secretion

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50
Q

GH aka

A

Somatotropin

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51
Q

Fxn of GH

A

Stimulates linear growth/muscle mass via action of IGF-1 from liver, increases insulin resistance (diabetogenic)

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52
Q

IGF-1 aka

A

Somatomedin C

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53
Q

GH regulation

A

GHRH –> pulsatile release of GH esp during exercise, deep sleep, puberty, hypoglycemia
Inhibition of secretion by glc, somatostatin (negative feedback on somatomedin)

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54
Q

Excess GH

A

Gigantism in children, acromegaly in adults – tx w/ stomatostatin analogs (octreotide) or surgery

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55
Q

Ghrelin–>

A

Hunger stimulation (orexigenic) and GH release

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56
Q

Ghrelin produced by

A

Stomach

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57
Q

Ghrelin increased by

A

Sleep deprivation or Prader Willi

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58
Q

Leptin–>

A

Satiety

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59
Q

Leptin made by

A

Adipose tissue

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60
Q

Leptin mutations–>

A

Congenital obesity

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61
Q

Leptin reduced by

A

Sleep deprivation, starvation

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62
Q

Endocannabinoids

A

Act at cannabinoid receptors in hypothalamus and nuc accumbens –> homeostatic/hedonic control of food intake –> increased apptite

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63
Q

ADH synthesis

A

Hypothalamus (supraoptic nuclei)

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64
Q

ADH fxn

A

Regulates serum osmo via V2 and BP via V1

Decreases serum osmo, increases urine osmo

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65
Q

How ADH works

A

Regulates aquaporin channel insertion in principle cells of collecting duct

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66
Q

When is ADH lower?

A

Central DI (can be normal or high in nephrogenic DI)

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67
Q

Cause of nephrogenic DI

A

Mutatio in V2

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68
Q

Desmopressin acetate

A

ADH analog – tx of central DI and nocturnal enuresis

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69
Q

Regulation of ADH

A

Osmoreceptors in thalamus, hypovolemia

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70
Q

17alpha hydroxylase def – effect on mineralocorticoids, cortisol, sex hormones, BP, K+, assc labs, presentation

A 
Mineralocorticoids: increased
Cortisol: decreased
Sex hormones: decreased
BP: increased
K+: decreased
Labs: low androstendione
Presentation:
XY-->ambiguous, undescended testes
XX-->lacks 2o sexual development
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71
Q

21 hydroxylase def – effect on mineralocorticoids, cortisol, sex hormones, BP, K+, assc labs, presentation

A 
Most common
Mineralocorticoids: Decreased
Cortisol: Decreased
Sex hormones: increased
BP: low
K+: High
Labs: High renin, high 17-hydroxy progesterone
Presentation: Salt wasting in infancy, precocious puberty in childhood, XX: virilization
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72
Q

11 B hydroxylase def – effect on mineralocorticoids, cortisol, sex hormones, BP, K+, assc labs, presentation

A 
Mineralocorticoids: Decreased aldo, but high 11-deoxycorticosteron (-->increase in BP)
Cortisol: Decreased
Sex hormones: Increased
BP: Increased
K+: Low
Labs: Low renin activity
Presentation: XX: virlization
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73
Q

Common features of multipl CAH

A

Enlargement of adrenal (increased ACTH), skin hyperpigmentation

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74
Q

Cortisol binds to

A

Cortisol binding globulin

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75
Q

Cortisol fxns

A

Increased appetite
Increase BP
- Upreg of alpha 1 on arterioles –> increased sens to NE/Epi
-High conc. binds to mineralocorticoid (aldo) receptors
Increase insulin resistance
Increase gluconeogenesis, lipolysis, proteolysis (less glc utilization)
Decrease fibroblast activity (–>poor wound healing, decreased collagen synth, increase in striae)
Decreased inflam/immuni response
- Inhib prdxn of leukotriences/PGs
- Inhib WBC adhesion (–>neutrophilia)
- Blocks histamine release from mast cells
- Eosinopenia, lymphopenia
- Blocks IL-2 prodxn
Less bone formation (decreases activity of osteoblasts)
A BIG/FIB

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76
Q

Regulation of cortisol

A

CRH–>ACTH–>cortisol prodxn –> excess downregs CRH, ACTH, and cortisol
BUT chronic stress –>prolonged secretion of cortisol

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77
Q

Calcium in plasma forms

A

Ionized/free>albumin>anions

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78
Q

Calcium in plasma change in binding…

A

Increased pH –> more affinity of albumin for Ca (increased neg charge) –> binding of Ca –> hypocalcemia (cramps, pain, paresthesias, carpopedal spasm)

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79
Q

Regulation of PTH

A

Ionized/free Ca

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80
Q

Vit D action

A

Increased absorption of dietary Ca and PO4, enhances bone mineralization

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81
Q

Vit D reg

A

Increased by PTH, low Ca and low PO4

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82
Q

Deficiency of vit D

A

Ricket in kids
Osteomalacia in adults
Due to malabsorption, low sunlight, poor diet, CKD

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83
Q

24 hydroxylase and Vit D

A

Makes 24,25 OH2 D3 – inactive

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84
Q

PTH action

A

Increased Ca/PO4 reabsorption from bone
Increased kidney reabsorption of Ca in DCT
Decreased reabsorption of PO4 in PCT
Increased dihydroxy vit D by stim of kidney 1alpha hydroxylase in prox tubule
NET LOSS OF serum PO4, increase in urine cAMP, increase in serum Ca

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85
Q

PTH secreted by

A

Chief cells of parathyroid

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86
Q

PTH action on bone –

A

Stimulates RANKL on osteoblasts/osteocytes

–> binds RANK on osteoclasts to stimulate them to resorb bone

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87
Q

Intermitten PTH release –>

A

Bone formation

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88
Q

Malignancies of PTHrP

A

SCC of lung, RCC

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89
Q

Regulation of PTH

A

Secretion sim: low Ca, high PO4, low Mg

Secretion inhib: REALLY low Mg

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90
Q

Causes of low Mg

A

Diarrhea, aminoglycosides, diuretics, EtOH abuse

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91
Q

What cells secrete calcitonin?

A

Parafollicular of thyroid

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92
Q

Action of calcitonin

A

Decreases bone resorption of Ca (stim by increased Ca); not really significant in normal Ca homeostasis

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93
Q

Thyroid hormone is produced in

A

Follicles of thyroid (t3 conversion in tissues mostly)

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94
Q

Fxn of thyroid hormones

A

Bone growth (GH synergism)
CNS maturation
Increases B1 receptors in heart (Increases CO, HR, SV, contractility)
Increased BMR by increase of Na/K ATPase activity –>more O2 consumption, RR, body temp
Increase in glycogenolysis, gluconeogenesis, lipolysis

(4 B’s – brain mat, bone growth, beta adrenergic, BMR)

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95
Q

Reg of thyroid hormone

A

TRH from hypothalamus–>TSH from ant pituitary–>stimulation of follicular cells (also via TSI in graves)
Negative feedback of T3/T4 on hypothalamus and ant pituitary

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96
Q

Wolff Chaikoff effect

A

Excess iodine –> temporary inhib of TPO –> less iodine organification –> less T3/4 prodxn

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97
Q

Thyroid hormone synthesis

A

Iodine/Na transporter into thyroid foll cell–>goes into colloid–>I gets oxidized to I2 via TPO –> organification of I2+TG by TPO resulting in –> MITs and DITs –> TPO causes coupling so some DIT/MITs combine to make T3/T4 (still attached to TG) –> endocytosed back into follicular cell–> proteases cleave thryoid hormones from TG (gets recycled) –> released into circ (5’ deiodinase catalyzes T4–>T3 in tissues

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98
Q

Cases of low TBG

A

Hepatic failure, steroids

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99
Q

Cases of high TBG

A

Pregnancy, OCP (increased by estrogen!)

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100
Q

Action of glucocorticoids on thyroid hormones

A

Inhibition of peripheral T4–>T3

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101
Q

cAMP signalling pathway hormones

A

FSH, LH, ACTH, TSH, CRH, h-CG, ADH (V2), MSH, PTH, calcitonin, GHRH, glucagon, histamine (H2)

FLAT ChAMP +calcitonin, GHRH, glucagon, histmine

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102
Q

cGMP signalling pathway hormones

A

BNP, ANP, EDRF (NO)

BAD GraMPa (vasodilators)

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103
Q

IP3 signalling pathway hormones

A

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

GOAT HAG

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104
Q

Intracellular receptor hormones

A

Prog, E2, Testosterone, Cortisol, Aldosterone, T3/T4, Vit D

PET CAT on TV

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105
Q

Receptor TK homones

A

Insulin, IGF-1, FGF, PDGF, EGF (MapK pathway, growth factors)

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106
Q

Nonreceptor TK hormones

A

Prolactin, Immunomodulators (cytokines, IL2, IL6, IFN), GH, G-CSF, EPO, TPO
(Jak-STAT, acidophils and cytokines)
PIGGlET

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107
Q

Effect of SHBG in men

A

Increased –> more bound Test –> lowers free T –> gynecomastia

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108
Q

Effect of SHBG in women

A

Low –> more free T –> hirsuitism

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109
Q

Effect of OCPs/pregnancy on SHBG–>

A

Increases it

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110
Q

Causes of Cushing syndrome

A

Increased cortisol:

  • Exogenous corticosteroids
  • 1o adrenal adenoma, hyperplasia, carcinoma
  • ACTH secreting pituitary adenoma and paraneoplastic ACTH secretion
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111
Q

Exogenous corticosteroids labs

A

Low ACTH, bilat adrenal atrophy – most common cause

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112
Q

1o adrenal adenoma, hyperplasia, carcinoma labs

A

Low ACTH, atrophy of uninvolved gland, can present w/ pseudohyperaldosteroneism via stim of aldor

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113
Q

ACTH secreting pituitary adenoma and paraneoplastic ACTH secretion labs

A

High ACTH, bilat adrenal hyperplasia

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114
Q

Majority of endogenous ACTH cushings syndrome

A

Cushings disease (ACTH pituitary adenoma)

115
Q

Findings in cushings syndrome

A

HTN, wt gain, moon facies, abdominal striae, truncal obesity, buffalo hump, skin changes (thinning, striae), osteoporosis, hyperglycemia (due to ins resistance), amenorrhea, immunosuppression

116
Q

Screening algorithm for Cushings

A
  1. ACTH measured via 24 hr free urine, late night salivary, inadequate suppression via 1 mg dexamethasone
    IF SUPPRESSED – ACTH indepented like exogenous or adrenal tumor
    IF ELEVATED – ACTH dependent
  2. Do CRH stimulation test or 3. High dose dex
    Ectopic secretion – CRH doesn’t affect ACTH and no suppression w/ high dose dex (do CT of chest/abdomen/pelvis)
    Pituitary adenoma – CRH will increase ACTH and cortisol, high dose dex will suppress (MRI of pituitary)
117
Q

Adrenal insufficiency sx

A

Weakness, fatigue, orthostatic hypotension, muscle aches, wt loss, GI disturbances, sugar/salt cravings

118
Q

Tx of adrenal insufficiency

A

Supplement glucocorticoids/mineralocorticoids

119
Q

Diagnosis of adrenal insufficiency

A

Measure serum lytes, cortisol, ACTH; metyrapone stim – blocks last step of cortisol synth (11-deoxycort–>cort)

120
Q

Diagnosis results in 1o adrenal insufficiency

A

Low cort, high ACTH, metyrapone –> increased ACTH but low 11-deoxycortisol

121
Q

Diagnosis results in 2o/3o adrenal insufficiency

A

Low cort, low ACTH, metyrapone –> low ACTH and 11 deoxycortisol

122
Q

1o adrenal insufficiency

A

Def of aldo and cortisol due to loss of gland fxn –> hypotension (hyponatremic volume contraction), hyperkalemia, metabolic acidosis, skin/mucosal hyperpigmentation (increased MSH from ACTH prodxn)

123
Q

Acute 1o adrenal insufficency

A

Suden onset (e.g. massive hemorrhage) –> shock

124
Q

Chronic 1o adrenal insufficiency aka

A

Addison disease

125
Q

Chronic 1o adrenal insuff due to

A

Adrenal atrophy/destruction by diease (autoimmune in west, TB in developing world)

126
Q

Associated with 1o adrenal insuff

A

Autoimmune polyglandular syndromes

127
Q

Waterhouse-Friedrichsen syndrome

A

Acute adrenal insuff due to adrenal hemorrhage assoc w septicemia (N. gonorrhea), DIC, endotoxic shock

128
Q

2o adrenal insuff

A

Decreased pituitary ACTH prodxn – no skin pigmentation, no hyperkalemia (aldo is fine bc of intact RAAS)

129
Q

3o adrenal insuff

A

Chronic exogenous steroid use – precipitated by abrupt w/drawal (No effect on aldo synth)

130
Q

Hyperaldosteronism –

A

Increased aldo –> HTN, decrease/normal K

131
Q

1o hyperaldosteronism

A

Adrenal adenoma (Conn syndrome) or bilateral adrenal hyperplasia –> high aldo and low renin

132
Q

2o hyper aldo seen in…

A

Pt w/ renovascular HTN, JG cell tumors that make renin, edema

133
Q

Neuroendocrine tumors

A

Originate from Kulchitsky and enterochromaffin like cells – thyroid medullary carcinoma, lung small call carcinoma, islet cell tumor of pancreas, pheochromocytoma

134
Q

Neuroendocrine tumors contain and secrete

A

Contain – APUD

Secrete: 5HIAAA, NSE, chromogranin A

135
Q

Neuroblastoma demographics..

A

Most common adrenal medulla tumor in children under 4

136
Q

Origin of neuroblastoma

A

Neural crest

137
Q

Neuroblastoma location

A

Anywhere in sympathetic chain

138
Q

Presentation of neuroblastoma

A

Abdominal distension, firm/irregular mass (can cross midline unlike Wilms), opsoclonus-myoclonus syndrome (dancing eyes, dancing feet)

139
Q

Lab tests in neuroblastoma

A

Increased HVA and VMA in urine

140
Q

Histology of neuroblastoma

A

Homer Wright rosettes (also in medulloblastoma), NSE and Bombesin +

141
Q

Genetics of neuroblastoma

A

Overexpression of N-myc

142
Q

Classification of neuroblastoma

A

APUD tumor

143
Q

Pheochromocytoma demographics

A

Most common tumor of adrenal medulla in adults

144
Q

Derivation of pheochromocytoma

A

Chromaffin cells (from neural crest)

145
Q

Germline mutations associated w/ pheochromocytoma

A

NF1, VHL, RET (MEN2A/B)

146
Q

Rule of 10s

A 
In pheochromocytoma
10% malignant
10% bilat
10% extra adrenal (bladder wall, organ of Zuckerkandl)
10% calcify
10% kids
147
Q

Sx of pheochromocytoma

A

Due to secretion of Epi. NE, and Dop –> episodic HTN, headache, perspiration, palpitations, pallor in spells (relapse/remit)

148
Q

Labs in pheochromocytoma

A

Increased catecholamines and metanephrines in urine/plasma

149
Q

Tx of pheochromocytoma

A

Irreversible alpha ant – prevent hypertensive crisis (phenoxybenzamine) followed by B blockers and then resection

150
Q

Hair in hypothyroid

A

Coarse brittle

151
Q

Hair in hyperthroid

A

Fine

152
Q

Myopathy in hyper vs hypothyroid

A

Both proximal, but hypothyroid can have low CK and hyper has NL CK

153
Q

Causes of smooth/diffuse goiter

A

Graves, Hashimoto, Iodine def, TSH secreting pit adenoma

154
Q

Causes of nodular goiter

A

Toxic multinodular goiter
Thyroid adenoma
Thyroid cancer
Thyroid cyst

155
Q

Cholesterol in hypo vs hyperthyroid

A

Hypercholesterolemia (decreased LDLr expression) in hypo

Hypocholesterolemia (increased LDLr expression) in hyper

156
Q

Myxedema in hypo vs hyperthyroid

A

Hypo – facial/periorbital

Hyper – pretibial

157
Q

Hashimoto thyroiditis abs

A

Anti TPO or anti TG

158
Q

Clinical course of hashimotos

A

Early hyperthyroid (follicular rupture) –> hypothyroid

159
Q

Histology of hashimotos

A

Hurthle cell change, lymphoid aggregates w/ germinal centers

160
Q

Hashimoto presentation

A

Moderately enlarged nontender thyroid

161
Q

Congenital hypothryoidism causes

A

Maternal hypothyroid, thyroid agenesis, iodine def, dyshormonogenetic goiter

162
Q

Congenital hypothyroidism findings

A

Pot bellied, Pale, Puffy faces w/ Protruding umbilicus, Protuberant tongue, Poor brain dev (6Ps)

163
Q

Subacute granulomaous thyroiditis (de Quervain) clinical course

A

Self limited after flu like illness (e.g. viral infxn) hyperthyroid–>hypothyroid

164
Q

Histology of de Quervain thyroiditis

A

Granulomatous inflam

165
Q

Findings in de Quervain thyroiditis

A

Increased ESR, jaw pain, TENDER thyroid

166
Q

Subacute lymphocytic thyroiditis

A

Autoimmune rxn in young/middle aged women post partum – mild enlargement of thyroid w/ patchy destruction of follicles; transient mild thyrotoxicosis–>hypothyroid
PAINLESS

167
Q

Riedel thyroiditis

A

Thyroid replaced by fibrous tissue w/ inflamm inflitrate, can extend to local structures (trachea/esophagus); 1/3 are hypothyroiid
Assc w/ IgG4 systemic disease (autoimmune pancreatitis, retroperitoneal fibrosis, noninfectionaortitis)
Fixed, hard, painless goiter

168
Q

Graves disease abs

A

TSI – stimulates TSHr on thyroid and dermal fibroblasts (–>pretibial myxedema)

169
Q

Pathophys of exopthalmos

A

T cell infiltration of retroorbital space by activated T cells –> increased cytokines (TNFalpha, IFN gamma) –> fibroblasts secrete GAGs –>osmotic muscle swelling, finlamm, increased adiopocytes –> exopthalmos

170
Q

Graves HLA associations

A

HLA DR3, HLA B8

171
Q

Toxic multinodular goiter

A

Patches of hyperfunctioning follicular cells distended w/ colloid working independent of TSH (usually TSHr mutation) –> more T3 T4 released

172
Q

Thyroid storm

A

Untreated/undertreated hyperthyroidism + stress (infxn, trauma, etc) –> agitation, fever, delirium, fever, diarrhea, coma, tachyarrhythmia (can cause death)

173
Q

Thyroid storm tx

A 
B blockers (Propanolol), PTU, corticosteroids (Prednisone), Potassium iodide (Lugol idoine)
(4Ps)
174
Q

Jod-Basedow phenomenon

A

Thyrotoxicosis if pt w/ iodine def and partiallly autonomous thyroid tissue is made iodine replete (opp of Wolff Chaikoff)

175
Q

Thyroid adenoma

A

Benign solitary growth of thyroid, usually cold

Rarely can cause hyperthyroidism

176
Q

Thyroid adenoma histology

A

Follicular usually – no capsular/vascular invasion (see in follicular carcinoma)

177
Q

Thyroid cancer diagnosis

A

Fine needle aspiration, tx is thyroidectomy

178
Q

Thyroidectomy complications

A

Hoarseness (recurrent laryngeal n. injury), hypocalcemia (parathyroid removal), transection of recurrent/sup laryngeal n during ligation of inf thyroid a. and sup thyroid a. respectively

179
Q

Papillary carcinoma incidence, prognosis

A

Most common, good prognosis

180
Q

Papillary carcinoma histology

A

Empty-appearing nuc w/ central clearing (oprhan annie), psammoma bodies, nuclear grooves

181
Q

Papillary carcinoma associations/genetics

A

RET, BRAF, childhood irradiation

182
Q

Follicular carcinoma prognosis

A

Good

183
Q

Follicular carcinoma histology

A

Invades thyroid capsule/vasculature, has uniform follicles

184
Q

Spread of follicular carcinoma

A

Hematogenous!

185
Q

Genetics of follicular carcinoma

A

RAS

186
Q

Medullary carcinoma origin cells

A

Parafollicular C cells

187
Q

Medullary carcinoma makes…

A

Calcitonin –> amyloid

188
Q

Medullary carcinoma histology

A

Sheets of cells in amyloid stroma, stains w/ congo red

189
Q

Mutations assoc w/ medullary carcinoma

A

MEN2A/2B RET

190
Q

Undifferentiated/anaplastic carcinoma demographic

A

Older patients

191
Q

Undifferentiated/anaplastic carcinoma prognosis

A

Poor – invades local structures

192
Q

What disease is lymphoma associated w/?

A

Hashimoto’s

193
Q

1o hypoparathyroidism causes

A

Surgical, resection, autoimmune, DiGeorge

194
Q

hypoparathyroid findings

A

Hypocalcemia –> tetany, hyperphosphatemia

195
Q

Chovstek sign

A

Tapp facial nerve –> facial mm contraction

196
Q

Trousseau sign

A

Occlusion of brachial a w/ BP cuff –> carpal spasm

197
Q

2o hypoparathyroidism causes

A

Vit D deficiency, low Ca intake, chronic renal failure

198
Q

1o hyperparathyroidism causes

A

Hyperplasia, adenoma, carcinoma

199
Q

PTH independent hypercalcemia

A

Excess Ca intake, cancer, high vit D

200
Q

Pseudohypoparathyroidism 1A aka

A

Albright hereditary osteodystrophy

201
Q

Pseudohypoparathyroidism 1A pathophys

A

Defective Gs protein alpha subunit–> Unresponsiveness of kidney to PTH –> hypocalcemia despite high PTH

202
Q

Pseudohypoparathyroidism 1A findings

A

Short 4/5 digits, short stature

203
Q

Pseudohypoparathyroidism 1A genetics

A

AD, must be inherited from mother due to imprinting

204
Q

PseudoPSEUDOhypoparathyroidism

A

Phyical exam features like Albright’s but no end-organ PTH resistance — defect inherited from father

205
Q

1o hyperparathyroidism findings

A

Hypercalcemia, hypercalciuria (–>kidney stones), polyuria, hypophosphatemia, high PTH, high ALP, high cAMP in urine; usually asymptomatic, but may have weakness/constipation, abdominal/flank pain (kidney stones, acute pancreatitis), depression

206
Q

Osteitis fibrosa cystica

A

Cystic bone spaces filld w/ brown fibrous tissue made of osteoclasts and hemosiderin from hermorrhages; due to high PTH (esp 1o)

207
Q

2o hyperparathyroidism findings

A

Hypocalcemia, hyperphosphatemia in chronic renal failure (low in other cases), high ALP, high PTH

208
Q

3o hyperparathyroidism causes

A

Refractory (autonomous) hyperparathyroidism resulting from chronic renal disease, high Ca, really high PTH

209
Q

Renal osteodystrophy

A

Renal disease –> 2o/3o hyperparathyroidism –> bone lesions

210
Q

Familial hypocalciuric hypercalcemia

A

Defective Gcoupled Ca sensing receptors –> higher than normal Ca levels to suppress PTH; excessive renal Ca reuptake –> mild hypercalcemia and hypocalciuria w/ normal/increased PTH levels

211
Q

Nelson syndrome

A

Enlargement of existing ACTH secreting pituitary adenoma after bilateral adrenalectomy for refractory Cushin disease (removal of cortisol feedback mechanism)

212
Q

Nelson syndrome findings

A

Hyperpigmentation, headaches, bitemporal hemianopia

213
Q

Tx of Nelson syndrome

A

Pituitary irradiation or surgical resection

214
Q

Acrogmegaly cause

A

Usually pituitary adenoma

215
Q

Acromegaly findings

A

Large tongue w/ deep furrows, deep voice, large hands/feet, coarsening of facial features, frontal bossing, diaphoresis, impaired glc tolerance, increased risk of colorectal polyps/cancer

216
Q

Dianosis of acromegaly

A

High IGF-1, failure to suppress serum GH following oral glc, pituitary mass on brain MRI

217
Q

Tx of acromegaly

A

Pituitary adenoma resection, octreotide (somatostatin analog), pegvisomant (GHr antagonist), dopamine agonists (cabergoline)

218
Q

Laron dwarfism pathophysiology

A

Defective GHr –> less linear growth, high GH, low IGF-1

219
Q

Laron dwarfism clinical features

A

Short height, small head circumfrence, facies w/ saddle nose and prominent forehead, delayed skeletal maturation, small genitalia

220
Q

Di symptoms

A

Intense thirst and polyuria, no ability to concentrate urine

221
Q

Central DI causes

A

Pituitary tumor, autoimmune, trauma, surgery, ischemic encephalopathy, idopathic

222
Q

Findings in central Di

A

Low ADH, low urine specific grav, high serum osmo (>290), hyperosmotic volume contraction

223
Q

Water deprivation in central DI

A

> 50% increase in urine osmo ONLY AFTER ADH analogue admin

224
Q

Tx of central DI

A

Desmopressin acetate, hydration

225
Q

Nephrogenic DI etiology

A

Hereditary (ADHr mutation), 2o to hypercalcemia, hypokalemia, lithium, demeclocycline (ADH ant)

226
Q

Nephrogenic DI findings

A

Normal or increased ADH, low urine SG, high serum osmo (>290), hyperosmotic volume contraction

227
Q

Water deprivation test in nephrogenic DI

A

Minimal change in urine osmo even after admi of ADH analog

228
Q

Tx of nephrogenic DI

A

HCTZ, indomethacin, amiloride, hydration, dietary salt restriction, avoidance of offending agent

229
Q

SIADH findings

A

Excessive free water retention, euvolemic hyponatremia w/ continued urinary Na excretion, urine osmo>serum osmo

230
Q

SIADH body response

A

Water retention –> lower aldo and increase ANP?BNP –> increase Na secretion in urine –> normal ECF volume –> euvolemic hyponatremia

231
Q

Result of low serum Na

A

Cerebral edema, seizures, correction too quickly –> osmotic demyelination syndrome (Central pontine myelinolysis)

232
Q

SIADH causes

A

Ectopic ADH (small cell lung cancer), CNS disorders/headtrauma, pulmonary disease, drugs (e.g. cyclophosphamidee)

233
Q

Tx of SIDADH

A

Fluid restriction, salt tablets, IV hypertonic saline, diuretics, conivaptan, tolvaptain, demeclocycline

234
Q

MOA of vaptans

A

Vasopressin receptor antagonists

235
Q

Ddx between SIADH and psychogenic polydipsia

A

Increased urine osmo in water deprivation test –> psychogenic polydisia

236
Q

Causes of hypopituitarism

A

Nonsecreting pituitary adenoma, craniopharyngioma, sheean syndrome, empty sella syndrome, pituitary apoplexy, brain injury, radiation

237
Q

Tx of hypopituitaryism

A

HRT

238
Q

Sheehan syndrome

A

Ischemic infarct of pituitary after postpartum bleeding, pregnancy induces growth of pituitary –> more susceptible to hypoperfusion; present w/ failure to lactate, absent menstruation, cold intolerance

239
Q

Empty sella syndrome

A

Atrophy or compression of pituitary (in sella turcica), obese women, idiopathic

240
Q

Pituitary apoplexy

A

Sudden hemmorhage of pituitary – usually in presence of existing pituitary adenoma; presents w/ sudden severe headache, visual impairment (bitemporal hemianopia, diplopia due to CN III palsy), feats of hypopituitarism

241
Q

DKA in..

A

DM 1

242
Q

Hyperosmolar coma in

A

DM2

243
Q

Complications of diabetes

A

Small vessel disease (diffuse thickening of basement membrane) -> retinopathy (hemorrhage, exudates, microaneurysms, vessel proliferation), glaucoma, neuropathy, nepropathy (nodular glomerulosclerosis, aka Kimmelstiel Wilson nodules –> progressive proteinuria [initially microalbuminuria, ACE inhibitors are renoprotective] and arteriolosclerosis–>HTN; both lead to chronic renal failure)

Large vessel atherosclerosis, CAD< peripheral vascular occlusive disease, gangren –> limb loss, cerebrovascular disease. MI most common cause of death

Osmotic damage (sorbitol accumulates in organs w/ aldose reductase/absent sorbitol DH) –> nephropathy (motor, sensory [glove and stocking distribution] and autonomic degen as well as cataracts

244
Q

HbA1C DM cutoff

A

> 6.5%

245
Q

Fasting plasma glucose DM cutoff

A

> 126 (fasting >8hrs)

246
Q

2 hour OGTT DM cutoff

A

> 200

247
Q

Abs in type 1 DM

A

Glutamic acid decarboxylase abs, destroy B cells

248
Q

HLA association in type 1 DM

A

HLA DR3/4

249
Q

Histology of type 1 DM

A

Islet leukocytic infiltrate

250
Q

Histology of type 2 DM

A

Islet amyloid polypeptide (IAPP) deposits

251
Q

Pathophysiology of ketoacidosis

A

Excess fat breakdown and increased ketogenesis from increased free fatty acids made into ketone bodies

252
Q

Signs/sx of DKA

A

Delirium/psychosis, Kussmaul respirations, Abdominal pain/nausea/vom, dehydration, fruity breath odor

253
Q

Labs in DKA

A

Hyperglycemia, high H+, low HCO3 (anion gap met acidosis), high blood ketones, leukocytosis, hyperkalemia (but depleted intracell K due to transcellular shift from low insulin and acidosis – so total body K is actually depleted)

254
Q

Complications of DKA

A

Life threatening mucormycosis (by Rhizopus), cerebral edema, cardiac arrhythmias, heart failure

255
Q

Tx of DKA

A

IV fluids, IV insulin, K+ to replete IC stores, glucose to prevent hypoglycemia if necessary

256
Q

Hyperosmolar hyperglycemic state

A

Profound hyperglycemia and dehydration –> increased serum osmo –> elderly T2D w/ limited ability to drink

Hyperglycemia -_> excesive osmotic diuresis –>dehydration –>eventually onset of HHNS

257
Q

Sx of hyperosmolar hyperglycemic state

A

Thirst, polyuria, lethargy, focal neuro deficits (seizures), can progress to coma and death

258
Q

Labs in HHGS

A

Hyperglycemia (like >600), high serum osmo (>320), no acidosis

259
Q

Tx of HHGS

A

Aggressive IV fluids, insulin

260
Q

Glucagonoma

A

Tumor of pancreatic alpha cells –>make glucagon –> dermatitis (necrolytic migratory erythema), diabetes (hyperglycemia), DVT, declining weight, depression

261
Q

Tx of glucagonoma

A

Ocretotide, surgery

262
Q

Insulinoma

A

Tumor o B cells –> make too much insulin –> hypoglycemia

Will have low glc but high C peptide, ~10% cases assc w/ MEN 1, tx by resection

263
Q

Whipple triad

A

Low blood glucose, symptoms of hypoglycemia (lethargy, syncope, diplopia), and resolution of symptoms after normalization of glucose lvls (in insulinoma)

264
Q

Somatostatinoma

A

Tumor of delta cells –> too much somatostatin –> less secretion of secretin, CCK, glucagon, insulin, gastrin, GIP

Present w/ diabetes/glc intolerance, steatorrhea, gallstones, achlorhydria

265
Q

Tx of somatostatinoma

A

Surgical resect, octreotide

266
Q

Carcinoid syndrome caused by

A

Carcinoid tumores from neuroendocrine cells

267
Q

Property of neuroendocrine tumors by histology

A

Rosettes

268
Q

Cause a lot of carcinoid syndrome

A

Metastatic small bowel tumors (secrete high serotonin)

269
Q

Sx of carcinoid syndrome

A

Recurrent diarrhea, cutaneous flushing, asthmatic wheezing, right sided valvular heart disease (tricuspid regurg, pulmonic stenosis

270
Q

Labs in carcinoid syndrome

A

High 5HIAA in urine, niacin def

271
Q

Tx of carcinoid syndrome

A

Surgical resection, somatostatin analog (octreotide)

272
Q

Rule of 1/3s

A

1/3 of carcinoid tumors metastasize, 1/3 present w/ 2nd malignancy, 1/3 are multiple

273
Q

Most common malignancy in SI

A

Carcinoid tumor

274
Q

Z-E syndrome

A

Gastrin secreting tumor (gastrinoma) of pancreas or duodenum –> acid hyper secretion –> recurrent ulcers in duodenum and JEJUNUM
Presentation: abdominal pain (PUD, distal ulcers)< diarrhea (malabsorption)

275
Q

Z-E Syndrome test

A

Positive secretin stim test – gastrin levels elevated after admin of secretin which normally inhibs gastrin

276
Q

Z-E association

A

MEN1

277
Q

MEN syndrome inheritance

A

AD

278
Q

MEN 1 disease

A 
Pituitary tumors (prolactin or GH)
Pancreatic tumors (Z-E, insulinomas, VIPomas, glucagonomas)
parathyroid adenomas
279
Q

MEN 1 genetics

A

Menin mutation – tumor suppressor on chr 11

280
Q

MEN 2A disease

A

Parathyroid hyperplasia
Medullary thyroid carcinoma (C cells – req prophylactic thyroidectomy)
Pheochromocytoma

281
Q

MEN 2A genetics

A

RET in cells of neural crest origin

282
Q

MEN 2B disease

A

Medullary thyroid carcinoma
Pheochromocytoma
Mucosal neuromas (oral/intestinal ganglioneuromatosis)
Marfanoid habitus

283
Q

MEN 2B genetics

A

RET mutation

STEP (15 decks)

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