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Endo > Islet Cell Tumors and MEN Syndromes (Nichols) > Flashcards

Islet Cell Tumors and MEN Syndromes (Nichols) Flashcards

1
Q

the most common type of pancreatic neuroendocrine tumor to produce an endocrine syndrome is a tumor making ….manifested by ….

A

insulin with hypoglycemia

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2
Q

What are the symptoms of hypoglycemia

A

shaky, sweaty, nervous, hunger, weak, visual disturbances, palpitations

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3
Q

most common visual dist seen w/ hypoglycemia

A

blurred vision

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4
Q

Why don’t you get a history of an episode of hypoglycemia from the pt?

A

many of these episodes are assc with amnesia ∴ ask family and friends

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5
Q

signs of hypoplgycemia

A

diaphoresis, tachycardia, systolic hypertension, tremulousness, pallor, confusion, unusual behavior

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6
Q

what are the body’s defenses against hypoglycemia

A

at glc below 80…↓ insulin

at glc below 70… ↑glucagon, epi, and cortisol

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7
Q

At what blood glc level do symptoms of hypoglycemia manifest (

A

below 50

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8
Q

how does fibrosis and amyloid impair the body’s defenses against hypoglycemia

A

disrupts intra-islet signaling (via insulin) that would cause the pancreas to ↑glucagon secretion

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9
Q

previous episodes of hypoglycemia impair the body’s defenses against hypoglycemia by …

A

lowing the threshold for sympathoadrenal response ∴ glc must fall even lower for epi and cortisol to be released

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10
Q

alcohol impairs hepatic (gluconeogeneis or glycogenolysis)

A

gluconeogenesis

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11
Q

in terms of hypoglycemia, what is the effect of a 1 day vs 2 day vs 3 day binge drinking event without eating
(duh, why waste space in your stomach with mac n cheese when you can polish off that 4th bottle of vodka?!?!–sidebar, how many bottles of vodka could one conceivably finish in a 3 day prd… i couldn’t decide on a good number, 1/day didn’t sound like enough but 5 seemed excessive? so I settled on 4. Aaand I just rewrote the broken-adult version of goldilocks and the 3 bears… anyway, back to science…)

A

1 day is unlikely to cause hypoglycemia due to liver glycogen stores (glycogenoslysis is fine) but around day 2 or 3, you run out of glycogen stores. Since the alcohol inhibits gluconeogenesis, the pt will become hypoglycemic!

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12
Q

serious consequences of hypoglycemia

A

seizures, arrhythmias, and DEATH (muahahaha)

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13
Q

I think Nichols is rubbing off on me… im including colorful writing in my notes…

A

please don’t tell anyone

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14
Q

(Better or worse) control of blood sugar leads to more episodes of hypoglycemia

A

better/tighter

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15
Q

when are insulin dept diabetic pts more prone to attacks of hypoglycemia

A

during sleep

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16
Q

What are additional factors that can contribute the the development of hypoglyemia

A

renal failure (↓Cx insulin)
missed meals
weight loss
exercise

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17
Q

the cycle of recurrent iatrogenic hypoglycemia can be reversed in ____ weeks of …

A

2 weeks of careful avoidance of hypoglycemia

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18
Q

what do you give all comatose pts

A

glucose

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19
Q

Most NETs are (functional or non-functional)

A

non-functional

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20
Q

____ is elevated in 70% of NETs

A

serum chromogranin A

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21
Q

80-100% of pts with MEN-1 will develop…

A

pancreatic NET with endocrinopathy?

i couldn’t decide what he meant by “one” on that slide, pg. 5

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22
Q

salt and pepper chromatin arranged in nests or trabeculae

A

histo of pancreatic NETs, especially islet cells

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23
Q

T or F: malignant vs benign pancreatic NETs are easily differentiated under the microscope

A

F: they look the same

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24
Q

What are the most common sites of metastases for pancreatic NETs

A

liver > retroperitoneal LN > bone

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25
Q

grossly, how can you tell if a tumor is benign or malignant

A

look to see if it is invading nearly organs/tissue

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26
Q

most common presentation of a non-functional pancreatic NET

A

asymptomatic

some abd pan, obstructive jaundice, anorexia/nausea, palpable mass

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27
Q

What are 5 pancreatic NETs discussed (ID 2 most common)

A
  1. insulinoma
  2. gastrinomas
    somatostatinoma
    glucagonoma
    VIPoma
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28
Q

episodic hypoglycemia

A

insulinoma

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29
Q

insulinomas are generally (aggressive or indolent)

A

indolent (87% are single benign tumors)

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30
Q

histo of insulinoma:

A

trabeculae + immunostain for insulin

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31
Q

causes Zollinger-Ellison Syndrome

A

gastrinomas

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32
Q

What is Zollinger-Ellison Syndrome

A

unrelenting PUD w/ abd pain and diarrhea

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33
Q

Can gastrinomas appear outside the pancreas?

A

yes, 40% do

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34
Q

DM, painful glottis, inflammed lip (cheilitis),

+ weight loss, GI dist, normocytic anemia, thromboembolism, neurophychiatric dist,

A

glucagonoma

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35
Q

erythematous, painful, puritic rash that begins as macules which coalesce, develop central bullae and then erode (leaving hyperpigmentation, and crusting at periph)

A

Necrolytic Migratory Erythema

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36
Q

describe the spread of Necrolytic Migratory Erythema

A

perirectum → perineum, thighs, butt, legs

37
Q

Necrolytic Migratory Erythema is assc with what pancreatic NET

A

glucagonoma

*but is not specific to glucagonoma

38
Q

Assc with DM and weight loss

A

glucagonoma

39
Q

Why are glucagonomas assc with DM and weight loss

A

glucagon opposes the action of insulin (~resistance)

and it is lipolytic

40
Q

use of glucagon in ER

A

resuscitation of hypoglycemic pt when there is no vascular access

overdose of BB and CCB
*Glucagon activates adenyl cyclase and exerts an inotropic and chronotropic effect (↑cAMP) by a pathway that bypasses the b receptors

41
Q

if glucagon fails to reverse BB and CCB OD, what can be used

A

insulin + glc

42
Q

DM + Cholelithiasis + steatorrhea

A

somatostatinoma syndrome (this seen in only 10% of somatostatinoma cases…)

43
Q

explain pathyphys behind the sydrome assc with somatostatinoma syndrome

A
  1. DM: stomatostatin ↓insulin release
  2. Cholelithiasis: stomatostatin ↓cholecystokinin release → ↓gallbladder emptying
  3. steatorrhea: inhibits pancreatic sectrion and lipid absorption
44
Q

treatment forpancreatic NETs

A
  1. surgical resection
  2. sunitinib and everolimus if unresectable
  3. octreotide to control symptoms if unresectable
45
Q

parathyroid, pancreas, pituitary

A

MEN-1:

46
Q

hypoglycemia hypoglycemia hypoglycemia

A

insulinoma

47
Q

severe watery diarrhea, achlorydria, hypokalemia, acidosis

A

VIPoma

48
Q

PUD, diarrhea

A

gastrinoma

*Zollinger-Ellison Syndrome

49
Q

3 words to remember for…

tumor secreting vasoactive intestinal peptide

A

VIPoma

50
Q

DM, cholelitiasis, steatorrhea

A

somatostatinoma

51
Q

pancreatic cholera

verner-morrison syndrome

A

VIPomas

52
Q

most common symptoms of somatostatinomas

A

abd pain and weight loss

53
Q

thyroid medullary, pheocromocytoma

A

MEN-2

54
Q

necrolytic migratory erythema

A

glucagonoma

55
Q

watery diarrhea, achlorhydria

A

VIPoma

56
Q

DM, painful glottis, inflammed lip (cheilitis),

A

glucagonoma

57
Q

serum chromogranin A

A

pancreatic NETs

58
Q

DM and weight loss

A

glucagonoma

59
Q

how can MEN cause hyperCa?

A

MEN is a parathyroid adenoma causing hyper PTH which ↑Ca CHRONICALLY

60
Q

urinary pain + endocrinopathy think…

A

chronic Ca elevation

*if fever, UTI

61
Q

epidemiolgy for primary hyperPTH

A

inc incidence with age
women > men
blacks and asians

62
Q

hypercalcemia + bilateral hilar lymphadenopathy + non-caseating granulomas

A

sarcoid

63
Q

why can sarcoid present with hyperCa?

A

macrophages in granulomas convert vitD to mature form (NO FEEDBACK REG) → ↑bone resorption → ↑Ca

**only 20% of sarcoid pts have hyperCa

64
Q

can mimic islet cell tumor or MEN

A

paraneoplastic syndrome

65
Q

most common paraneoplastic syndrome

A

hyper Ca

66
Q

Acute vs chronic hyperCa presentation

A

chronic: mostly asymptomatic, maybe mild anxiety, depression or cognitive difficulties

acute:
muscle weakness, ↓muscle reflexes,
confusion, lethargy → seizure → coma → death
constipation → nausea and vomiting
polyuria and polydipsia (interfere with ADH)
shortened OT and bradycardia

67
Q

asymptomatic and primary hyperPTH

A

chronic hyperCa

68
Q

confusion, lethargy, obtundation, and paraneoplastic

A

acute hyperCa

69
Q

amenorrhea and galactorrhea

A

prolactinoma

70
Q

prolactinoma is the most common …

A

pituitary adenoma

71
Q

lactation failure, amenorrhea, asthenia, apparent pre-mature aging, dryness and hypopigmentation of skin, genital and axillary hair loss
*post-partum

A

sheehan syndome

72
Q

what is the predomidant manifestation of acute adrenal insufficiency?

A

shock
*+nonspecific symptoms, weight loss, fatigue, nausea, vom, abd pain, weak, fatigue, fever, confusion

CANNOT HANDLE STRESSES TO BODY

73
Q

what color are adrenal cortical tumors? why?

A

yellow/gold

Cortisol/cholesterol

74
Q

postpartum hypopit due to necrosis of the gland from peripartum hemorrhagic shock

A

sheehan syndrome

75
Q

hypertension and hypokalemia

A

Conn syndrome seen in aldosterone secreting adrenal cortical tumors

76
Q

majority of adrenal cortical tumors are (functional or non-functional)

A

nonfunctional

77
Q

catecholamine secreting tumor of the adrenal medulla

A

pheochromocytoma

78
Q

what are 2 substances adrenal cortical tumors can secrete

A

cortisol and aldosterone

79
Q

HTN, episodic headaches, sweating, tachycardia

A

pheochromocytoma

80
Q

A 35-year-old black female presents with the acute onset of painful urination associated with increased urination, constipation, anorexia, fatigue, depressed mood and confusion. She most likely has…

A

hypercalcemia

81
Q

symptoms of acute hyperCa and hypoCa

A

Hyper: Stones, (abdominal) Moans, (psychic), Groans, Bones, constipation

hypo:parasthesias (esp lips), muscle cramps, irritability, depression

82
Q

symptoms of acute hyperglycemia and hypoclycemia

A

hyper: polyuria, polydipsia,polyphagia, fatigue, weight loss

Hypoglycemia: shakiness, sweatiness,nervousness, hunger, weakness

83
Q

symptoms of acute hyperK and hypoK

A

Hyperkalemia: fatigue, weakness, nausea,
parathesias, confusion

Hypokalemia: fatigue, weakness, constipation,
irritability, myalgias

84
Q

symptoms of acute hyperNa and hypoNa

A

Hypernatremia: lethargy, confusion,
irritability, seizures, coma

Hyponatremia: lethargy, confusion,
irritability, seizures, coma*

85
Q

Urolithiasis is suggestive of (acute or chronic) hypercalcemia

A

chronic

86
Q

what makes an presentation of hypercalcemia more severe?

A

↑# symptoms and more severe neurological impariment

87
Q

how can you differentiates parathyroid adenoma from hyperplasia

A

hyperplasia is in more than one glad

adenomas are uni-focal

88
Q

pre-mature menopause in a person wil DM for 15+ years

A

accelerated aging

89
Q

tumors of parathyroid, pancreas, pituitary

A

MEN-1

Endo (28 decks)

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