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x Pathoma > 15. Endocrine Pathology > Flashcards

15. Endocrine Pathology Flashcards

1
Q

what is a good way to think of the pancreas?

A

can think of it as 2 organs in 1:

  • exocrine pancreas (digestive enzymes to GI tract)
  • endocrine pancreas (subject of this section)
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2
Q

what are the major functional cells in the endocrine pancreas?

A

cell clusters - islets of Langerhans

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3
Q

what does a single islet cluster contain?

A

multiple cell types, each producing one type of hormone

alpha -> glucagon

beta -> insulin

delta -> somatostatin

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4
Q

what is secreted by beta-cells?

A

insulin

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5
Q

beta cells: where are they located in relation to the islets?

A

center

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6
Q

what is the main function of insulin? what tissues does it most affect?

A

major anabolic hormone.

upregulates GLUT4 on skel muscle and fat tissue

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7
Q

what is the result of increased GLUT4 receptors on skel muscle and fat tissue?

A

increased glucose uptake by tissues.

increased glycogen synthesis, protein synthesis, lipogenesis

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8
Q

what do alpha cells secrete?

A

glucagon

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9
Q

what does glucagon do?

A

opposes insulin in order to increase blood glucose levels via glycogenolysis and lipolysis

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10
Q

is glucagon most active in fed or fasting state?

A

fasting state

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11
Q

Type I DM: what is the main characteristic?

A

insulin deficiency leads to a metabolic disorder characterized by hyperglycemia

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12
Q

what causes the destruction of beta cells in Type I DM?

A

autoimmune destruction of beta cells by T lymphocytes

Type 4 hypersensitivity reaction.

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13
Q

which HLAs are associated with Type I DM destruction of beta cells?

A

HLA-DR3 and HLA-DR4

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14
Q

at what life stage does Type 1 DM present?

A

childhood

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15
Q

treatment for Type I DM?

A

lifelong insulin

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16
Q

why is there high serum glucose in Type I DM?

A

lack of insulin leads to decr glucose uptake by fat and skel muscle

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17
Q

what will be some qualities of the urine in a pt with Type I DM?

A

polyuria, glycosuria.

(hyperglycemia exceeds renal ability to resorb glucose; excess filtered glucose leads to osmotic diuresis)

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18
Q

what happens to body weight and muscle mass of a pt with (untreated) Type I DM? what accounts for these?

A

weight loss, low muscle mass.

due to unopposed glucagon which leads to gluconeogenesis, breakdown of glycogen, breakdown of fat.

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19
Q

what condition are people with Type I DM at risk for?

A

diabetic ketoacidosis

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20
Q

what is the primary characteristic of diabetic ketoacidosis? (lab finding)

A

excessive serum ketones

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21
Q

how can stress/infection lead to a state of diabetic ketoacidosis?

A

stress leads to increased epinephrine, which leads to increased glucagon, which increases lipolysis. Also increase in cortisol.

–> relative lack of insulin compared to quantities of counter-reg hormones. this increases FFAs which can be converted to ketone bodies in the liver

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22
Q

what are Kussmaul respirations?

A

type of hyperventilation: deep/labored breathing, seen in T1DM, attempt to reduce acidosis by breathing out volatile acid (Co2)

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23
Q

what are 3 lab abnormalities that result from diabetic ketoacidosis?

A
  1. hyperglycemia (>300 mg/dL)
  2. anion gap metabolic acidosis
  3. hyperkalemia
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24
Q

what does insulin do to serum potassium levels? what happens to K in the absence of insulin? what will happen in diabetic ketoacidosis?

A

drives K into cells

without insulin the serum potassium will be high.

DKA: the H+/K+ exchanger brings H+ into cells and K+ into serum -> hyperkalemia

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25
Q

what is the status of potassium in diabetic ketoacidosis (high/low)?

A

has been driven out of cells by H+/K+ exchanger, so serum K+ levels are high.

but OVERALL BODY potassium will be LOW because the K+ is excreted via urine.

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26
Q

what is the clinical presentation of diabetic ketoacidosis?

A

Kussmaul respirations, dehydration, nausea, vomiting, mental status changes, fruity breath (acetone)

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27
Q

treatment of diabetic ketoacidosis?

A

fluids (correcting polyuria-induced dehydration)

insulin

replacement of electrolytes (K+)

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28
Q

Type 2 DM: what is the fundamental problem?

A

end-organ insulin RESISTANCE leading to metabolic disorder characterized by hyperglycemia

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29
Q

what is the most common type of diabetes in US?

A

Type 2. 5-10% of US population, incidence is rising

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30
Q

Type 2 DM: onset?

A

middle-aged, obese adults

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31
Q

how does obesity lead to Type 2 DM?

A

leads to decr numbers of insulin receptors on muscle and adipose tissue

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32
Q

Type 2 DM vs Type 1: genetic predisposition is higher for which?

A

T2 stronger than for Type 1 DM

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33
Q

Type 2 DM: what happens to insulin levels over the course of the disease?

A

initially insulin levels increase, but later in the disease insulin deficiency develops due to beta cell exhaustion.

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34
Q

Type 2 DM: on pathology, what is found in the islets?

A

amyloid deposition

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35
Q

Type 2 DM: clinical presentation?

A

polyuria, polydipsia, hyperglycemia. but disease may be clinically silent

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36
Q

Type 2 DM: how is diagnosis made?

A

by measuring glucose levels: random, fasting, or glucose tolerance test

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37
Q

if doing a random glucose test, what level will dx Type 2 DM?

A

> 200

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38
Q

if doing a fasting glucose test, what level will dx Type 2 DM?

A

>126

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39
Q

if doing a glucose tolerance test, what level will dx Type 2 DM?

A

> 200, 2 hrs after glucose loading

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40
Q

Type 2 DM: treatment?

A
  • weight loss
  • drug therapy to counter insulin resistance
  • exogenous insulin due to beta cell exhaustion
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41
Q

Type 2 DM: pts are particularly at risk for what condition?

A

HONK: hyperosmolar non-ketotic coma

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42
Q

describe HONK

A

high glucose (>500) leads to life threatening diuresis with hypotension and coma

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43
Q

HONK: will this be accompanied by diabetic ketoacidosis?

A

no: ketones are absent in this condition, because there are small amounts of circulating insulin. just enough to counter glucagon and avoid ketone generation

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44
Q

define pituitary adenoma. functional or non-functional?

A

benign tumor of anterior pituitary cells

can be functional or non functional

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45
Q

what is the biggest problem with non-functional pituitary adenomas?

A

mass effect: bitemporal hemianopsia due to compression of the optic chiasm

headache, hypopituitarism due to compression of the normal pit tissue

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46
Q

what are the most likely types of functional pituitary adenomas?

A

-prolactinomas & growth hormone adenomas

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47
Q

prolactinomas: how do they present in males? females?

A

males: decr libido
females: amenorrhea, galactorrhea

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48
Q

why does a prolactinoma cause anemmorrhea, galactorrhea (females), decr libido (males)?

A

prolactin prevents synthesis and release of GnRH, which causes release of FSH/LH

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49
Q

treatment for prolactinoma?

A

dopamine agonists (bromocriptine) to suppress prolactin production

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50
Q

growth hormone adenoma of pituitary: how will it present in children?

A

gigantism if it presents before closure of the epiphyseal plates

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51
Q

growth hormone adenoma of pituitary: presentation in adults?

A

acromegaly

52
Q

signs of acromegaly?

A

enlarged jaw, frontal bossing, enlarged tongue

growth of visceral organs may lead to cardiac failure

53
Q

given high levels of GH, what can a growth hormone adenoma cause?

A

secondary diabetes due to counter-reg hormone effect of GH

54
Q

how to dx a growth hormone adenoma by simple blood test?

A

elevated GH, elevated IGF-1

55
Q

how to dx growth hormone adenoma by stimulus test?

A

glucose bolus: should cause GH suppression.

If GH is not suppressed, probably overproduction

56
Q

pharm treatment for GH adenoma?

A

octreotide: somatostatin analog, suppresses GH

57
Q

ACTH adenomas secrete what, leading to what syndrome?

A

secrete ACTH, leading to Cushing Sx

58
Q

causes of hypopituitarism?

A
  • pituitary adenomas
  • craniopharyngioma (kids)
  • Sheehan sx (preg women)
  • empty sella sx
59
Q

how do pituitary adenomas or craniopharyngiomas lead to hypopituitarism?

A

mass effect, compression of normal tissue, or bleeding into gland

60
Q

pathophys of Sheehan syndrome?

A

pregnancy-related infarction of the pituitary. gland normally doubles during preg, and its blood supply doesn’t increase very much. if blood is lost during delivery, may become ischemic and infarct.

61
Q

presentation of Sheehan syndrome?

A

poor lactation, loss of pubic hair (bc this is androgen-dependent)

62
Q

What is Empty Sella syndrome?

A

Congenital defect of the sella: herniation of the arachnoid and CSF into the sella. Compresses/destroys pituitary. Pituitary = absent on imaging. FA: May be due to idiopathic atrophy of pituitary, common in obese women.

63
Q

what 2 hormones are made in the hypothal, then released from the posterior pit?

A

ADH, oxytocin

64
Q

ADH does what?

A

acts on distal tubules and collecting ducts of kidney, promotes free water retention

65
Q

oxytocin does what?

A

mediates uterine contraction during labor, mediates release of breast milk during lactation

66
Q

Central Diabetes Insipidus: deficiency of what?

A

ADH

67
Q

reasons for central diabetes insipidus?

A
  • hypothalamic pathology
  • pituitary pathology: tumor, trauma, infection
68
Q

Central DI: serum and urine status?

A

Serum: concentrated, hypernatremic

Urine: dilute, low specific gravity

69
Q

central DI: why hypernatremia?

A

due to loss of free water due to lack of ADH

70
Q

how to test for central DI?

A

water deprivation test. if central DI, patient will fail to concentrate urine as they should

71
Q

how to treat central DI?

A

desmopressin (ADH analog)

72
Q

Nephrogenic DI: define

A

impaired renal response to ADH

73
Q

Nephrogenic DI: response to desmopressin

A

none, because problem is non-response to ADH

74
Q

Nephrogenic DI: causes?

A

inherited mutations

drugs (lithium, demeclocycline = ADH inhibitor, treatment for SIADH)

75
Q

SIADH: define

A

inappropriate ADH secretion

76
Q

SIADH: cause?

A

ectopic production of ADH due to small cell carcinoma;

CNS trauma

pulm infection

some drugs

77
Q

SIADH: symptoms?

A

excessive retention of free water. hyponatremia and low serum osmolality.

mental status changes due to neuronal swelling from hyponatremia

78
Q

SIADH: treatment

A

water restriction

demeclocycline (blocks effect of ADH, caution: can cause Nephrogenic DI)

79
Q

what is non-enzymatic glycosylation?

A

sugar sticks to basement membranes of vasculature, no enzymes required.

80
Q

what does NEG of large and medium sized vessels lead to?

A

atherosclerosis

81
Q

what are some of the leading causes of complications in diabetics?

A
  • cardiovascular disease
  • peripheral vascular disease (leading cause of non traumatic amputations)
82
Q

NEG of small vessels leads to what?

A

hyaline arteriosclerosis (thickened vessel membrane, decr size of lumen)

83
Q

NEG of renal arterioles leads to what?

A

glomerulosclerosis –> small, scarred kidneys with granular surface

84
Q

NEG preferentially involves which renal arterioles?

A

efferent; leading to glomerular hyperfiltration injury with microalbuminemia.

85
Q

what will glomerular hyperfiltration injury with microalbuminenia eventually lead to?

A

nephrotic syndrome, with K-W nodules in glomeruli

86
Q

what is pathongmonic of diabetic nephropathy?

A

Kimmelstiel-Wilson nodules in glomeruli

87
Q

what causes HbA1c?

A

HbA1c = glycated hemoglobin

caused by NEG of red blood cells

88
Q

how can high serum glucose can cause damage to retinal vessels and schwann cells?

A

via osmotic damage: retinal blood vessel pericytes freely take in glucose, which is converted to sorbitol; osmolarity increases, water comes into cells and weakens vessel wall -> rupture and micro hemorrhage Similar for schwann cells -> peripheral neuropathy

89
Q

in general, what kinds of problems does osmotic damage due to high serum glucose lead to?

A
  • peripheral neuropathy
  • impotence
  • blindness
  • cataracts
90
Q

what is MEN1? what does it present with?

A

Multiple Endocrine Neoplasia (genetic)

Presents with pancreatic neoplasms, parathyroid hyperplasia, pituitary adenomas (3 Ps)

91
Q

Insulinoma: presentation?

A

epidosic hypoglycemia with mental status changes that can be relieved with administration of glucose

92
Q

how do we dx an insulinoma?

A

low serum glucose levels, high insulin, high C-peptide

93
Q

besides an insulinoma, what are the other two types of pancreatic tumors?

A

gastrinoma

somatostatinoma (delta cells in islets)

94
Q

gastrinoma: from what organ? presentation?

A

Pancreas.

presents as treatment-resistant peptic ulcers. may be multiple ulcers, may extend into jejunum. Called Zollinger-Ellison syndrome

95
Q

somatostatinoma: from what organ? presentation?

A

Pancreas.

presents as achlorhydria (?due to inhibition of gastrin) and chloelithiasis with steatorrhea (due to inhibition of CCK from gallbladder)

96
Q

what cells regulate Ca? how do they do this?

A

chief cells in the parathyroid gland. they secrete PTH

97
Q

Chief cells regulate what type of Ca in the blood?

A

free/ionized, as opposed to Ca that is bound to proteins

98
Q

if serum Ca is low, what are the 3 actions of PTH?

A
  1. Bone: incr. osteoclast activity, releasing Ca and phosphate
  2. GI: incr absorption of Ca and P
  3. Kidney: incr Ca reabsorption; decr phosphate reab
99
Q

how does PTH cause an incr in GI reab of C and P?

A

by activating Vit D

100
Q

how does PTH cause an incr in bone osteoclast activity?

A

by activating osteoblasts, which then activate osteoclasts

101
Q

PTH: what is the neg feedback for its secretion?

A

increased serum ionized Ca levels

102
Q

what are the most common causes of Primary HyperPTH?

A
  • parathyroid adenoma
  • sporadic parathyroid hyperplasia
  • parathyroid carcinoma
103
Q

parathyroid adenoma: benign or malig? what does it secrete?

A

benign, secretes PTH

104
Q

parathyroid adenoma most commonly causes what?

A

asymptomatic hypercalcemia

105
Q

parathyroid adenoma and incr PTH may cause what? (6 items)

A
  • hypercalcemia
  • nephrolithiasis
  • nephrocalcinosis
  • CNS disturbances
  • acute pancreatitis
  • osteitis fibrosa cystica
106
Q

what causes nephrolithiasis?

A

kidney stones made of calcium oxalate, due to high serum Ca

107
Q

what is nephrocalcinosis? what can it cause?

A

metastatic calcification of renal tubules; deposition of Ca on tissues. can cause renal insufficiency and polyuria

108
Q

how can hyperPTH cause acute pancreatitis?

A

high Ca, think of Ca as sort of an enzyme activator that will activate the cells of the pancreas. Not accurate but a way to remember.

109
Q

what is osteitis fibrous cystic?

A

resorption of bone, leading to fibrosis and cystic spaces. due to hyperPTH

110
Q

hyperPTH: what are lab findings? (5)

A

incr serum PTH

incr serum Ca

decr serum phosphate

incr urinary cAMP

incr serum alkaline phosphatase

111
Q

why does hyperPTH cause incr serum alkaline phosphatase?

A

this is a sign of osteoblast activity, and it creates an alkaline environment at the bone, which is needed to lay down Ca.

112
Q

why does hyperPTH cause incr urinary cAMP?

A

PTH binds its receptor, which stimulates a G-coupled protein receptor pathway, upreg Adenylate Cyclase, ATP –> cAMP.

when this process occurs in kidney cells, cAMP is increased in the urine

113
Q

define secondary hyperparathyroidism

A

excess production of PTH due to a disease process extrinsic to the parathyroid gland

114
Q

what is the most common cause of 2’ hyperPTH?

A

chronic renal failure

115
Q

how does chronic renal failure lead to 2’ hyperPTH?

A
  • renal insuff leads to decr phosphate excretion
  • incr serum phosphate binds free calcium
  • decr free calcium stimulates parathyroid glands
  • incr PTH leads to bone resorption
116
Q

lab findings in 2’ hyperparathyroidism? (4)

A

incr PTH

decr serum Ca

incr serum P

incr alkaline phosphatase

117
Q

what can lead to hypoPTH?

A
  • autoimmune damage
  • surgical excision
  • DiGeorge syndrome
118
Q

what is DiGeorge syndrome?

A

failure to develop the 3rd and 4th pharyngeal pouches, so failure to develop PTH glands.

119
Q

hypoPTH: 2 symptoms?

A
  • muscle spasms/tetany
  • numbness/tingling, esp periorally
120
Q

what are two tests for muscle spasms due to hypoPTH?

A

Trousseau: BP cuff, see if distal limb spasms

Chvostek: tap on facial nerve -> spasm

121
Q

hypoPTH: labs? (2)

A

decr PTH, decr Ca

122
Q

what is pseudohypoPTH?

A

due to end organ resistance to PTH

123
Q

pseudohypoPTH: lab findings? (2)

A

decr Ca, incr PTH

124
Q

pseudohypoPTH: what does the auto dom form present with?

A

short stature short 4th/5th digits

125
Q

pseudohypoPTH: what is mech for end organ resistance?

A

could be associated with a defect in the Gstim pathway

126
Q
A

x Pathoma (19 decks)

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