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Pathology I > Endocrine Pathology > Flashcards

Endocrine Pathology Flashcards

1
Q

what are the functions of the endocrine system

A
  • maintain metabolic equilibrium (homeostasis)
  • secrete chemical messengers (hormones)
  • regulate activity of various organs
  • process of feedback inhibition
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2
Q

what does the process of feedback inhibition do

A

-increased activity of target tissue
- typically down regulates activity of gland secereting stimulating hormone

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3
Q

what are the types of endocrine diseases

A
  • disease of under/over production of hormones
  • diseases associated with development of mass lesions
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4
Q

what are functional tumors

A

tumors that secrete the hormone native to the gland

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5
Q

what organs are affected by endocrinopathies

A

-anterior pituitary
- posterior pituitary
- thyroid
- parathyroid
- pancreas
-adrenal

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6
Q

where is the pituitary gland

A
  • base of brain sella turcica
  • connected to the hypothalamus via a stalk composed of axons
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7
Q

what is the central role of the pituitary gland

A

regulation of other endocrine glands

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8
Q

what are the two components of the pituitary gland

A
  • anterior lobe/ adenohypophysis
  • posterior lobe/ neurohypophysis
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9
Q

how big is the pituitary gland

A

1 cm

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10
Q

what are the cells types in the anterior pituitary and what hormones do they produce

A
  • somatotrophs: GH
  • lactotrophs: prolactin
    -corticotrophs: ACTH
  • thyrotrophs: TSH
  • gonadotrophs: FSH and LH
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11
Q

what are the cell types in the posterior pituitary and what hormones do they produce

A
  • ADH/vasopressin
  • oxytocin
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12
Q

what are the diseases of the anterior pituitary

A
  • decreased/increased secretion of trophic hormones
  • hypopituitarism/hyperpituitarism
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13
Q

describe hypopituitarism

A

-destructive lesions- ischemia, radiaiton, inflammation and neoplasms

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14
Q

what is hyperpituitarism

A
  • functional adenoma within anterior lobe
  • local mass effects- enlargement of sella turcica, visual field abnormalities, increased intracranial pressure
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15
Q

what are the causes of hypopituitarism

A
  • pituitary adenomas
  • radiation treatment
  • neurosurgery
  • sheehan syndrome
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16
Q

what is sheehan syndrome

A

ischemic necorsis of pituitary gland

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17
Q

what are the clinical manifestation of hypopituitarism

A
  • pituitary dwarfism
  • amenorrhea and infertility
  • decreased libido and impotence
  • postpartum lactation failure
  • hypothyroidism
  • hypoadrenalism
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18
Q

what are the causes of hyperpituitarism

A
  • pituitary adenomas
  • pituitary hyperplasia
  • pituitary carcinomas
  • hypothalamic disorders
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19
Q

what are the clinical manifestations of hyperpituitarism

A
  • gigantism
  • acromegaly
  • cushing disease
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20
Q

describe hyperpituitarism

A

-primary tumor
- excess GH
-adenoma of anterior pituitary
-2nd most common
- affects all growing tissues

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21
Q

when does gigantism occur

A

when excesss GH is secreted before epiphyseal plates close

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22
Q

describe gigantism

A
  • generalized overgrowth more than 3 standard deviations
  • headaches
  • chronic fatigue
  • arthritis, osteoporosis
  • muscle weakness
  • hypertension
  • CHF
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23
Q

describe acromegaly

A
  • late diagnosis
  • poor vision: photophobia
  • enlarges skull, hands, feet and ribs
    -soft tissue and viscera enlarged
  • enlarged maxilla, mandible, nasal, frontal bones and maxillary sinus
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24
Q

what are the intraoral manifestations of acromegaly

A
  • diastemas
  • malocclusion
  • macroglossia
  • enlarged lips
  • sleep apnea
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25
Q

what are the diseases of the posterior pituitary

A
  • diabetes insipidus (Central)
  • secretions of inappropriately high levels of ADH (SIADH)
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26
Q

what are the manifesations of diabetes insipidus in posterior pituitary pathology

A
  • polyuria, dilute urine
  • polydipsia
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27
Q

what are the manifesations of SIADH in posterior pituiary pathology

A
  • hyponatremia
  • cerebral edema
  • neurologic dysfunction
  • increase in total body water: blood volume normal and no peripheral edema
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28
Q

where is iodide stored and what is it bound to

A

in the thyroid gland bound by thyroglobulin

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29
Q

what is the difference between T3 and T4

A

one iodide

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30
Q

T4 is exclusively produced by:

A

the thyroid

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31
Q

majority of T3 is result of:

A

T4 conversion

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32
Q

what is the activator for the synthesis of TSH

A

TRH

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33
Q

what is the activator for T3 and T4 production

A

TSH

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34
Q

what 3 glands are responsible for the thyroid function

A
  • hypothalamus
  • pituitary
  • thyroid
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35
Q

how do T3 and T4 circulate

A
  • mostly bound to thyroxine
  • some are free in circulation
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36
Q

which form of T3 and T4 are metabolically active

A

free hormones, not bound

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37
Q

what is primary hypothyroidism

A
  • intrinsic abnormality in the thyroid
  • surgery
  • radiotherapy
  • autoimmune
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38
Q

what is secondary hypothyroidism

A

pituitary failure

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39
Q

what are the 2 manifestations of hypothyroidism

A
  • myxedema
  • cretinism
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40
Q

describe myexedma

A
  • in adults
  • generalized fatigue
  • apathy
  • mental slugishness
  • listless
  • cold intolerance
  • overweight
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41
Q

describe cretinism

A
  • childhood
  • impaired skeletal development
  • severe mental retardation
  • short stature
  • course facial features
  • delayed tooth eruption
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42
Q

what are symptoms of hypothyroidism

A
  • cold intolerance
  • fatigue, lethargy
  • weight gain
  • constipation
  • bradycardia
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43
Q

what are the levels of TSH, T3 and T4 in primary hypothyroidism

A
  • high TSH
  • low T4
  • low T3
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44
Q

what are the levels of TSH, T3 and T4 in secondary hypothyroidism

A
  • low TSH
  • low T4
  • low T3
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45
Q

what is the treatment for hypothyroidism

A

supplements

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46
Q

describe hashimoto thyroiditis

A
  • autoimmune
  • painless enlargement- systemic and diffuse
  • risk of B cell non hodgkins lymphoma
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47
Q

what are the clinical signs and symptoms of hyperthyroidism

A
  • goiter (small)
  • exopthalmus (frequent)
  • heat intolerance
  • weight loss
  • malabsorption and diarrhea
  • tachycardia
  • irritability and anxiety
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48
Q

what are the most common causes of hyperthryoidism

A

autoimmune-graves disease

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49
Q

what are the lab values for hyperthyroidism

A
  • T4 and free T4 elevatde
  • T3 and free T3 elevated
  • TSH and TRH supressed
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50
Q

what are the symptoms of hyperthyroidism

A
  • weight loss
  • nervousness
  • rapid pulse
    -goiter
  • muscle wasting
  • tachycardia
  • increased appetite
  • exopthalmos
  • intolerance to heat
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51
Q

what is the mechanism of hyperthyroidism

A

autoantibodies stimulate the thyroid hormone production

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52
Q

what is the treatment for hyperthyroidism

A

ablation

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53
Q

what is the significance of hyperthyroidism

A
  • thyroid storm
  • caused by infection, stress, trauma
  • elevated body temp
  • tachycardia
  • 20-40% mortality
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54
Q

what is diffuse and multinodular goiter

A
  • thyroid enlargement
  • impaired synthesis of thyroid hormone
  • iodine deficiency
  • hyperplasia of follicle from pituitary stimulation
  • maintenance of minimal function: euthyroid
  • diffuse early on then nodular
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55
Q

what is the sequence of events in endemic goiter

A
  • diet deficient in iodine
  • decreasd output of T3 and T4 by thyroid
  • pituitary responds by secreting TSH
  • thyroid hyperplasia
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56
Q

what are the thyroid neoplasms

A
  • adenoma
  • papillary carcinoma
  • follicular carcinoma
  • medullary carcinoma
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57
Q

describe thyroid adenomas

A
  • solitary
  • males
  • younger
  • warm/ cold nodules
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58
Q

describe thyroid papillary carcinomas

A
  • 75-85%
  • all ages
  • radiation
  • 10 year = 95%
  • worse in elderly
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59
Q

describe thyroid follicular carcinoma

A
  • 10-20%
  • older
  • iodine deficiency
  • cold nodules
60
Q

describe thyroid medullary carcinoma

A
  • 5%
  • neuroendocrine
  • calcitonin (C cells)
  • amyloid
  • MEN 2 A/B 20%
61
Q

what are the parathyroid glands derived from

A

pharyngeal pouches

62
Q

what do parathyroid glands do

A

secrete PTH which regulates calcium homeostasis

63
Q

what is parathyroid gland regulated by

A

level of free calcium

64
Q

what does PTH do

A
  • activates osteoclast activity
  • increases Ca renal tubular absorption
  • increases conversion of vitamin D into the active dihydroxy form in the kidneys
  • increases urinary excretion of phosphates
  • increases Ca absorption by the GI tract
  • increases serum calcium
65
Q

what is hypoparathyroidism caused by

A
  • surgically induced: iatrogenic, most common
  • congenital absence: :DiGeorge Syndrome
  • autoimmune: APECED
66
Q

what is seen in hypoparathyroidism

A
  • hypocalcemia: tetany
  • Chvostek sign: tapp on CN VII causes muscle contraction of eye mouth and nose
  • trosseau sign: occluding circulation of forearm causes carpal spasm
67
Q

how does hypoparathryoidism affect teeth

A
  • hypoplastic enamel
  • delayed tooth eruption
68
Q

what are the primary hyperparathyroid pathologies and their incidence

A
  • adenoma:75-80% one gland
  • hyperplasia: 10-15%, multiglandular, MEN 1 and 2 a,b
  • carcinoma: less than 5%
69
Q

what are the secondary hyperparathyroidism pathologies

A
  • renal failure causing:
  • hyperphosphatemia
  • chronic hypocalcemia
  • vitamin D deficient
70
Q

what are the morphologic changes in primary hyperparathyroidism

A
  • skeletal changes: bone resorption, formation of bone cysts and hemorrhages, brown tumors, urinary tract stones, metastatic calcification
  • serum calcium levels are high - especially ionized calcium levels
71
Q

what are the levels of calcium and phosphate in primary hyperparathyroidism

A
  • hypercalcemia
  • hypophosphatemia
  • increased urinary excretion of both calcium and phosphate
72
Q

what are the levels of calcium and phosphate in secondary hyperparathyroidism

A
  • calcium is low leading to hyperactivity of parathryoid
  • phosphate levels are high
73
Q

what are the causes of secondary hyperparathyroidism

A
  • chronic renal failure
  • vitamin D deficiency
  • inadequate dietary calcium
  • steatorrhea
74
Q

what is the morphology of secondary hyperparathyroidism

A
  • hyperplastic parathyroid glands
  • bone changes
  • metastatic calcification
75
Q

what are the clinical features of secondary hyperparathyroidism

A
  • not as severe as primary
  • related to symptoms secondary to chronic renal failure
  • bone abnormalities
  • calciphylaxis
  • tertiary hyperparathryoidism
76
Q

what is seen in hyperparathyroidism

A
  • osteomalacia and loss of lamina dura
  • brown tumor
  • nephrolithiasis
  • peptic/duodenal ulcers
  • mental changes
77
Q

what is similar radiographically and histologically to a brown tumor and how do you tell them apart

A
  • central giant cell granuloma
  • brown tumor blood panel will show hyperPTH
  • central giant cell granuloma blood panel will be normal
78
Q

how should you remember clinical symptoms of hyperparathryoidism

A

stones, bones, moans and groans

79
Q

what are the oral manifestations of hyperparathyroidism

A
  • nodules on gingiva
  • expansion of palate
80
Q

what is the histology of hyperparathyroidism

A
  • lots of multinucleated giant cells
81
Q

what does the adrenal medulla make

A

epinephrine and norepinephrine

82
Q

what are the 3 zones of the adrenal cortex and what do each of them make and what are they regulated by

A
  • zona glomerulosa: aldosterone, regulated by ANGII
  • zona fasiculata: cortisol/glucocorticoids, regulated by ACTH
  • zona reticularis: androgens, no feedback with ACTH
83
Q

what is the pathology of too little adrenal cortex hormones

A
  • acute: waterhouse- Friderichsen
  • primary chronic: addision disease
84
Q

what is the pathology of too much adrenal cortex hormones

A
  • hyperaldosterism
  • hypercortisolism: Cushings disease
  • adrenogenital syndrome
85
Q

what is addisons disease

A
  • destruction of adrenal cortex leads to decreased production of adrenal corticosteroid hormones
  • autoimmune
  • metastatic carcinoma
  • infections: TB and deep fungal , AIDS
  • secondary hypoadrenocorticism: disorder of hypothalamus or pituitary gland
86
Q

what are the symptoms of addisons disease

A
  • appear late
  • weakness and fatigue
  • hypotension
  • GI distrubances: nausea, vomitting, anorexia, diarrhea, weight loss, salt cravings
  • hyperpigmentation: ACTH stimulates melanocytes
  • adrenal crisis (Acute)- abdominal pain, hypotension, vascular collapse
87
Q

what is primary hypercortisolism

A
  • too much endogenous steroid
  • females 5x
  • 3rd decade
  • pituitary adenomas (ACTH) 50%, cushing disease
  • adrenal hyper/neoplasia: 10-20%
  • neuroendocrine tumors: produce ACTH, small cell lung carcinoma
88
Q

what is secondary hypercortisolism

A
  • most common
  • exogenous
  • rule of 2s
  • can become hypocortisol without taper of steroids
89
Q

what is the clinical presentation of hypercortisolism

A
  • central obesity
  • peripheral wasting
  • buffalo hump
  • moon facies
  • abdominal striae
  • hirsutism
  • poor wound healing
  • diabetes
  • hyperglycemia
  • osteoporosis
  • hypertension
90
Q

what are the adrenal neoplasma of the cortex

A
  • adenomas: cushings, hyperaldosteronism, incidentalomas
  • carcinomas: rare, virilizing adenoma, Li-Fraumeni and Beckwith- Wiedemann
91
Q

what are the adrenal neoplasms of the medulla

A
  • pheochromocytoma
  • neuroblastoma
  • 10% tumor: 10% familial (MEN 2A, B), 10% extra adrenal, 10% are bilateral, 10% are malignant
92
Q

what are the types of multiple endocrine neoplasias

A
  • MEN-1 AD; Chr 11q (TSG)
  • MEN 2A-AD; Chr10q (RET proto onco gene)
  • MEN2B
93
Q

what is affected in MEN1- AD

A
  • pancreas (95%): insulinomas, gastrinomas
  • parathyroid (40%): hyperplasia
  • pituitary(30%): prolactinomas
94
Q

what is affected in MEN 2A- AD

A

adrenal medulla 50%

95
Q

what is affected in MEN 2B

A

MEN 2A + marfinoid habitus and mucosal neuromas

96
Q

describe MEN 2B

A
  • AD
  • marfinoid body type
  • medullary thyroid carcinoma
  • pheochromocytomas
  • neuromas
97
Q

describe the neuromas in MEN 2B

A
  • can be first sign
  • soft painless papules
  • lips, conjunctiva, tongue, palate, buccal mucosa
  • sentinel neuromas
98
Q

what is mccune albright syndrome

A
  • skin pigmentation with border that looks like the coast of maine
  • ## fibrous dysplasia
99
Q

what does the exocrine pancreas do

A
  • secrete enzymes for digestion and inactive proenzymes
100
Q

what are the pathologies of the exocrine pancreas

A
  • acute pancreatitis
  • chronic pancreatitis
  • cancer
101
Q

what does the endocrine pancreas do

A
  • secretes hormones
  • glucose homeostasis
  • other metabolic activities
102
Q

what is the pathology of the endocrine pancrease

A

diabetes mellitus

103
Q

what happens in acute pancreatitis

A
  • injury to acinar cells
  • interstitial or edematous pancreatitis: mild, reversible
  • acute hemorrhagic pancreatitis: alcoholism, chronic biliary disease
104
Q

what is the metabolic etiology of acute pancreatitis

A
  • alcoholism
  • hyperlipoproteinemia
  • hypercalcemia
  • drugs: thiazide diuretics
  • genetic
105
Q

what is the mechanical etiology of acute pancreatitis

A
  • trauma
  • gallstones
  • iatrogenic injury: perioperative injury, endoscopic procedures with dye injections
106
Q

what is the vascular etiology of acute pancreatitis

A
  • shock
  • atheroembolism
  • polyarteritis nodosa
107
Q

what is the infectious etiology of acute pancreatitis

A
  • mumps
  • cocksackievirus
  • mycoplasma pneumoniae
108
Q

describe chronic pancreatitis

A
  • destruction of pancreatic parenchyma
  • intermittent acute attacks
  • alcoholism
  • obstruction of pancreatic duct
  • chronic injury to acinar cells
109
Q

what can cause obstruction of pancreatic duct

A
  • mechanical blockage
  • congenital defects
  • cancer
  • insipissated mucous
110
Q

what are the exocrine pancreas neoplasms

A
  • pancreatic cystic neoplasm
  • pancreatic cancer
  • acinar cell carcinoma
111
Q

what are the islet cell tumoes

A
  • insulinoma
  • glucagonoma
112
Q

what is the syndrome of pancreatic gastrinoma

A
  • zollinger- ellison syndrom
  • hypersecretion of gastric acid
  • peptic ulcers
  • high blood gastrin
113
Q

what is in the endocrine pancreas

A
  • islets of langerhans
  • alpha cells- glucagon
  • beta cells- insulin - DM
114
Q

what does insulin cause in adipose tissue

A
  • increase glucose uptake
  • increase lipogenesis
  • decreased lipolysis
115
Q

what does insulin cause in striated muscle

A
  • increased glucose uptake
  • increased glycogen synthesis
  • increased protein synthesis
116
Q

what does insulin do in the liver

A
  • decreased gluconeogenesis
  • increased glycogen synthesis
  • increased lipogenesis
117
Q

loss of insulin results in:

A

catabolic state affecting glucose, fat, protein metabolismd

118
Q

describe type 1 diabetes mellitus

A
  • absolute deficiency
  • destruction of beta cells
  • only 10% diabetics
  • average onset 14 years old
119
Q

what are the emergencies of DM

A
  • acute: hypoglycemia
  • chronic: ketoacidosis
120
Q

what causes type 1 DM

A
  • destruction of beta cells
  • autoimmune
  • T cell mediated
  • auto antibodies
  • genetic: 30-70% twin concordance
  • environmental: infectious
121
Q

how is type 1 diagnosed

A
  • WNL = 70-120 mg/dL
  • any of these: > 200 mg/dL + S/S
  • fasting >126 mg/dL
  • OGTT > 200 mg/dL in 2 hours
122
Q

what is the pathogenesis of type 1 DM

A
  • genetic factors
  • autoimmunity
  • environmental factors: viruses- cocksackie B and chemicals
123
Q

what is the diagnosis of DM

A
  • fasting plasma glucose greater than 140
  • following ingestion of 75 grams of glucose: 2 hr glucose is greater than 200, at least one glucose value during that period is over 200
124
Q

describe type 2 DM

A
  • relative lack of insulin
  • 80-90% diabetics
  • insulin resistance: early normal blood insulin level, target tissue resistance, B cell dysfunction fails to compensate
  • demographic are changing
  • ketoacidosis is rare
  • reduced tissue sensitivity to insulin
125
Q

what causes DM type 2

A
  • obesity
  • genetics: 50-90% of twins and 20-40% of 1st degree
  • only 5-7& of population
126
Q

what is the pathogenesis of type 2 DM

A
  • genetic: family hx, obesity, HTN
  • glucose metabolism
  • beta cell function
127
Q

what is the clinical progression of diabetes

A
  • polyuria
  • polydipsia
  • polyphagia
  • fatigue/wasting
  • ketosis: ketone bodies
128
Q

what ketosis is present in DM1 and DM2

A
  • DM1: ketoacidosis and diabetic coma
  • DM2: hyperosmolar non ketotic coma
129
Q

what tissues do not require insulin for glucose transport

A
  • nerves, lens, kidney, blood vessles
130
Q

metaboslim of intracellular glucose depletes:

A

NADPH, compromising regeneration of GSH

131
Q

what is diabetic neuropathy

A

persistent hyperglycemia is a major underlying cause

132
Q

what is glycosylated hemoglobin and what does it reflect

A
  • the fraction of glycosylated hemoglobin in circulating red blood cells
  • reflects the degree of hyperglycemia during the preceding 6-8 weeks
133
Q

what are the complications of DM and describe both

A
  • macrovascular disease: large and medium sized arteries
  • microvascular disease: capillary dysfunction in target organs
134
Q

describe macrovascular disease

A
  • heart: MI, atherosclerosis
  • brain: stroke
  • peripheral vascular disease: lower extremity gangrene
135
Q

describe microvascular disease

A
  • retina: diabetic retinopathy
  • kidneys: nephropathy
  • peripheral nerves: neuropathy
136
Q

great variability in DM patients in:

A

-time of onset
- severity
- organs involved

137
Q

in most DM patients chagnes are likely to be found inL

A
  • arteries
  • basement membrane of small vessels
  • kidneys
  • retina
  • nerves
138
Q

what are the late complications of DM

A
  • macrovascular disease
  • hyaline artiolosclerosis
  • microangiopathy
139
Q

what is microangiopathy

A

thickened basement membrane

140
Q

what does microangiopathy cause

A
  • nephropathy
  • retinopathy
  • neuropathy
141
Q

diabetes is the leading cause of:

A
  • end stage renal disease
  • blindness
  • non traumatic amputation
142
Q

DM is a major contributor to:

A
  • peripheral neuropathy
  • increased risk of cardiovascular disease
  • neutrophil chemotaxis impairment
143
Q

what is acanthosis nigricans

A
  • a dermatosis characterized by velvety, papillomatous, brownish black, hyperkaratotic plaques, typically of the intertriginous surfaces and neck
144
Q

what could acanthosis nigricans be associated with

A

insulin resistance
- internal malignancy

145
Q

what are the oral complications of DM

A
  • infections: candida, mucormycosis, bacterial
  • slow healing
  • gingiva: enlargement, erythema
  • subjective xerostomia
  • parotid gland enlargement
146
Q
A

Pathology I (24 decks)

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