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Pathology IV > Quiz 3 > Flashcards

Quiz 3 Flashcards

1
Q

Hormones released by the anterior pituitary gland:

A
  • thyroid-stimulating hormone (TSH)
  • prolactin (PRL)
  • adrenocorticotropin hormone (ACTH)
  • growth hormone (GH)
  • follicle-stimulating hormone (FSH)
  • luteinizing hormone (LH)
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2
Q

In pituitary histology, the pink staining acidophils (eosinophilic cytoplasm) release ______ and ______. The purple staining basophils secrete __________, ___________, __________, and ________.

A 
Pink:
* GH
* PRL
Purple: 
* FSH
* LH
* TSH
* ACTH
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3
Q

Histologically, the posterior pituitary resembles _______ tissue.

A

Neural

  • glial cells
  • nerve fibers
  • nerve endings
  • intra-axonal neurosecretory granules
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4
Q

The 2 hormones secreted by the posterior pituitary, ______ and _______, are synthesized __________.

A

ADH and oxytocin

in the hypothalamus, stored in the post pit

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5
Q

__________ occurs as a result of excess secretion of trophic pituitary hormones.
Causes include:

A

Hyperpituitarism

  • pituitary adenoma (MC)
  • hyperplasia
  • carcinomas of ant pit
  • secretion or hormones by non-pit tumors
  • certain hypothalamic d/o’s
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6
Q

Result of deficiency in one or more of the hormones produced by the pituitary gland:

A

Hypopituitarism

  • ischemic injury
  • surgery
  • radiation
  • inflammatory reactions
  • non-functioning adenoma
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7
Q

Pituitary-related changes that may be referred to as mass effect:

A
  • sellar expansion
  • bony erosion
  • disruption of the sella
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8
Q

Pituitary lesions of a sufficient size often compress:

leading to:

A

the optic nerve at the optic chiasm

visual field abnormalities, usu lateral visual field deficits
“bitemporal hemianopsia”

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9
Q

MC pituitary tumor:

A

Pituitary adenoma

Also MC brain tumor!
15% of all intracranial lesions

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10
Q

How do you differentiate a macro- and microadenoma?

A

Macro - >/=10mm

Micro -

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11
Q

How are pituitary adenomas classified?

A

By hormone secreted (MC - PRL)

formerly by staining, still use “chromophobic” for non-fxn tumors

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12
Q

Describe the typical pituitary adenoma (gross):

A

soft
well-circumscribed
mb confined to sella, or extend superiorly

larger:
erode sella
infiltrate neighboring tissues (cavernous/sphenoid sinuses, dura)

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13
Q

Histology of pituitary adenoma:

A
  • small round cells
  • uniformly round nuclei
  • pink to blue cytoplasm
  • nest or cords
  • prominent vascularity
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14
Q

Mass effect sx:

A
  • HA
  • visual field deficit
  • cranial nerve defect
  • cavernous sinus syndrome (rare)
  • sx specific to excess hormone (if fxn)
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15
Q

MC functioning pituitary adenoma:

A

prolactinoma (lactroph adenoma)
30%

underlies ~25% of cases of amenorrhea

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16
Q

Adenomas of the anterior pituitary are a (major/minor) clinical feature of ______, a form of inherited endocrine disorder.

A

major
multiple endocrine neoplasia type 1 (MEN 1 )

MEN causes various combos of benign or malignant tumors in endocrine glands or may cause glands to enlarge w/o forming tumors

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17
Q

MEN syndromes MC affect:

A
  • parathyroid glands
  • pancreatic islet cells
  • anterior pituitary (25% of MEN1)
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18
Q

MEN1 may cause non-endocrine tumors likes:

A
  • facial angiofibromas
  • collagenomas
  • lipomas
  • meningiomas
  • ependymomas
  • leiomyomas
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19
Q

Acute hemorrhage into an adenoma or pituitary infarction:

A

pituitary apoplexy - rapid enlargement of the lesion

80% not previously dx - although usu pre-existing

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20
Q

MC initial sx of pituitary apoplexy:

A

sudden HA

  • often w/rapidly worsening visual field defect
  • double vision
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21
Q

Necrosis of the pituitary gland due to blood loss and hypovolemic shock during and after childbirth:

A

Sheehan’s syndrome (postpartum hypopituitarism)

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22
Q

Hypertrophy and hyperplasia of lactotrophs (PRL cells) during pregnancy results in:

A

enlargement of the anterior pituitary, without a corresponding increase in blood supply.

agalactorrhea - MC initial sx
may go undetected, mb found later upon hypothyroid or 2° adrenal insufficiency dx

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23
Q

An empty sella contains:

A

only CSF w/o visible pituitary tissue on MRI

pituitary stalk typically visible, extends to floor of sella

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24
Q

Hypothalamic suprasellar tumors may induce:

A

hypo- or hyperfunction of the anterior pituitary, diabetes insipidus, or combinations of these manifestations.

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25
Q

MC implicated hypothalamic suprasellar lesions:

A

gliomas and craniopharyngiomas

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26
Q

The craniopharyngioma is thought to be derived from vestigial remnants of _______________.

A

Rathke’s pouch

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27
Q

Craniopharyngiomas are (fast/slow) growing tumors with a (early/late/bimodal) onset.

A

slow
bimodal
* 5-15
* 65+

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28
Q

Diagnostic histopathology of craniopharyngiomas:

A
  • compact lamellar keratin formation “wet keratin”

also see:

  • peripheral palisading
  • cords of squamous epithelium

less important:

  • dystrophic calcification
  • cyst formation
  • fibrosis
  • chronic inflammatory reactions
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29
Q

Malignant anterior pituitary tumors (1°) are defined by:

A

ability to metastasize

although many are widely invasive, destructive to adjacent tissues, and lethal, they are not classified as malignancy (H-ras and p53 have been noted in association, but not in tumor)

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30
Q

MC cancers that mets to the pituitary:

A

breast and lung

but mets to pituitary = rare

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31
Q

Newborn screening for congenital hypothyroidism, which can cause __________, is performed by __________ test. If tx is delayed by ___ (weeks/months), development is impaired and full function is not possible.

A

cretinism
heel-pad test
6 months

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32
Q

____ from the ant pituitary binds a specific receptor on the thyroid surface. This with ______________ increase formation of ______ in the thyroid, which initiates exocytosis and release of _________ hormone.

A

TSH
adenylate cyclase
cAMP
thyroid

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33
Q

A decrease in pituitary and circulating ____ stimulates production of TRH from the ___________. TRH serves to stimulate release of _____ and subsequent release of ___ and ___ until (negative/positive) feedback causes diminished release of TRH.

A 
T3
hypothalamus
TSH
T3 and T4
negative
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34
Q

Metabolic functions increased by T3:

A
  • protein synthesis/degradation
  • drug metabolism
  • catecholamine receptor sensitivity
  • glucose absorption
  • gluconeogenesis
  • O2 consumption
  • heat production
  • metabolic rate
  • lipid synthesis/oxidation
  • cholesterol synthesis/degradation
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35
Q

Target tissue effects of excess T3:

A
  • heart - inc HR
  • vascular - vasodilation
  • skin - warm, smooth, moist
  • GI - inc motility
  • bone - inc turnover
  • neuromuscular - hyperactivity, inc contraction
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36
Q

At a cellular level, thyroid hormone action is initiated by binding to a (specific/non-specific) receptor from a family of _______ factors that regulate specific genes. These receptors preferentially bind ____, which is why it has a greater biologic effect than ____.

A

specific
transcription
T3
T4

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37
Q

Normal thyroid histology consists of:

A

follicles lined by epithelium, and filled with colloid.
The interstitium may contain “C” cells (parafollicular cells) and has a rich vascular supply, into which hormone is secreted.

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38
Q

C cells secrete:

A

calcitonin

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39
Q

The conditions most notable for causing a hypothyroid state:

A
  • Hashimoto’s thyroiditis
  • acute thyroiditis
  • subacute thyroiditis (DeQuervain’s)
  • infiltrative thyroid dz
  • post-op hypothyroidism
  • iatrogenic hypothyroidism
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40
Q

MC cause of autoimmune lymphocytic thyroiditis:

A

Hashimoto’s thyroiditis

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41
Q

_______ is essential for the production of thyroxine. When lacking from the diet, this can lead to thyroid gland (shrinking/enlargement), resulting in what is termed _______________.

A

Iodine
enlargement
endemic goiter

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42
Q

Adding iodine to ____ has eliminated __________ in most developed countries.

A

salt

endemic cretinism

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43
Q

Condition due to excess amount of free thyroid hormone:

mb the result of increased ________ and _______ of thyroid hormone by:

A 
hyperthyroidism
synthesis and secretion
* serum stimulators
* autonomous thyroid hyper function
* over secretion of TSH w/o inc synthesis of T3/T4
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44
Q

Another major cause of hyperthyroidism is thyrotoxicosis factitia, which is:

A

conscious or accidental ingestion of excess quantities of thyroid hormone

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45
Q

The principle conditions responsible for causing a hyperthyroid state include:

A
  • Graves dz
  • toxic thyroid nodule
  • toxic multinodular goiter (Plummer’s dz)
  • iatrogenic hyperthyroidism
  • thyroid storm (usu Graves + infx)
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46
Q

In relation to thyroid, “toxic” refers to:

A

producing excess hormone

taking up more iodine

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47
Q

Autoimmune dz where thyroid gland is attacked by a variety of cell- and antibody-mediated immune processes:

A

Hashimoto’s thyroiditis (chronic lymphocytic thyroiditis)

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48
Q

In Hashimoto’s, the thyroid gland becomes:

But dz develops w/o:

A

firm
large
lobulated

w/o visible or palpable change to thyroid gland

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49
Q

First dz recognized to be an autoimmune dz:

A

Hashimoto’s

in 1912

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50
Q

Thyroid enlargement in Hashimoto’s is due to:
A. tissue hypertrophy
B. lymphocytic infiltration and fibrosis

A

B. lyphocytic infiltration and fibrosis

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51
Q

In Hashimoto’s, antibodies against ______ and/or __________ cause gradual destruction of _________ in the thyroid gland.

A

TPO (thyroid peroxidase)
thyroglobulin
follicles

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52
Q

Cells that often appear in thyroid tissue of pts with Hashimoto’s or follicular thyroid cancer:

A

Hürthle cells

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53
Q

Histologically, Hürthle cells appear:

A
  • enlarged epithelial cells
  • generally stain pink
  • abundant eosinophilic granular cytoplasm as a result of altered mitochondria.
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54
Q

Form of thyroiditis that can cause both hypo- and hyperthyroidism:

A

subacute thyroiditis

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55
Q

Subacute thyroiditis manifests as:

A
  • sudden, painful enlargement of the thyroid gland
  • fever
  • malaise
  • muscle aches
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56
Q

Types of subacute thyroiditis:

A
  • DeQuervain’s (subacute granulomatous) thyroiditis
  • subacute lymphocytic thyroiditis
  • postpartum thyroiditis
  • palpation thyroiditis
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57
Q

Features of DeQuervain’s thyroiditis:

A
  • multi-nucleated giant cells
  • ESR >100mm/hr
  • painful enlarged thyroid gland
  • fever, malaise, neck soreness
  • low uptake of tracer on scan
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58
Q

Subacute thyroiditis can be distinguished from Graves’ disease by:

A

the low uptake of tracer on a thyroid uptake scan

- vs increased uptake in Graves’ disease

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59
Q

MC location for a thyroglossal cyst:

A

btw isthmus of the thyroid and hyoid bone

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60
Q

MC type of congenital neck malformation:

A

thyroglossal duct cyst = persistent duct becomes fluid filled, 2-4% of neck masses

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61
Q

The thyroglossal duct connects the _______ to the _______ during fetal development, and usu atrophies at ___ weeks gestation.

A

tongue
thyroid
9

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62
Q

About ___% of thyroid nodules are malignant.

A

5%

prevalence of nodules is 5% clinically, but much higher on US or autopsy

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63
Q

Most thyroid cancers are _________________________ with (poor/good/excellent) prognosis.

A

well-differentiated papillary or follicular tumors

excellent

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64
Q

Most cost-effective dx tool for thyroid nodules:

A

fine-needle aspiration biopsy

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65
Q

A thyroid gland that contains autonomously functioning thyroid nodules, resulting in hyperthyroidism:

A

toxic nodular goiter (TNG)

TNG represents a spectrum of dz, from single hyperfunctioning nodule (toxic adenoma) w/in a multinodular thyroid to a gland with multiple areas of hyperfunction.

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66
Q

What is Graves’ dz?

A

autoimmune dz caused by long acting thyroid autoantibodies (LATS-Ab) which activate TSH-receptors, stimulating thyroid hormone synthesis/secretion and thyroid growth - causing a diffusely enlarged goiter.

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67
Q

MC cause of hyperthyroidism:

A

Graves’ dz

60-90% of all cases

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68
Q

Graves’ dz usu presents during ________, has a powerful hereditary component, and is more prevalent in (men/women).

A 
adolescence
women (5-10:1)
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69
Q

The exophthalmos assoc w/Graves’ is caused by:

A

inflammation of the eye muscles by attacking autoantibodies and glycoprotein deposition.

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70
Q

Histopathology of Grave’s:

A
  • hyperplastic epithelium
  • prominent infoldings
  • tall columnar thyroid epithelium lining
  • clear vacuoles in the colloid
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71
Q

T/F: It is sometimes difficult to tell a follicular adenoma from a well-differentiated follicular carcinoma.

A

True

thus, pts with follicular neoplasms are usu treated with subtotal thyroidectomy.

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72
Q

Four main types of thyroid cancer:

A
  • Papillary
  • Follicular
  • Medullary
  • Undifferentiated / Anaplastic
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73
Q

The majority of thyroid cancers are (benign/malignant) and are (generally/not) responsive to treatment.

A

highly malignant

generally responsive to tx

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74
Q

Thyroid nodule findings that might suspect malignancy:

A
  • feels hard
  • solitary nodule
  • cold nodule on scan
  • Hx of radiation exposure to head/neck/chest, esp as youth
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75
Q

MC thyroid cancer:

A

Papillary carcinoma

60-70%

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76
Q

Papillary carcinoma is dx more frequently in the (young/elderly) but when dx in the other, it is more likely (benign/malignant) with a (better/worse) prognosis.

A

Young - more frequent
Elderly - malignant, worse prognosis
F:M 2 or 3:1

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77
Q

Papillary tumors develop in cells that produce:

Metastasis occurs via:

A

thyroid hormones
lymph

the cells grow slowly, and form tiny mushroom-shaped patterns in the tumor

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78
Q

Histopathology of papillary carcinoma:

A
  • fronds of tissue in papillary (finger-like) pattern
  • thin fibrovascular core
  • clear nuclei
  • psamomma bodies
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79
Q

T/F: Papillary adenomas are common and benign, but lead to carcinoma.

A

FALSE!!

There is NO such thing! ALL papillary neoplasms should be considered malignant.

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80
Q

Follicular carcinoma accounts for ___% of thyroid cancers, more frequent in __:__, and is more commonly noted in the (young/elderly).

A

15%
MC F:M
elderly

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81
Q

Follicular carcinoma is (more/less) malignant than papillary carcinoma with (lymph/hematogenous) spread causing (local/distant) metastases.

A

more
hematogenous
distant

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82
Q

Follicular tumors develop in cells that produce:

A

iodine-containing hormones

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83
Q

On gross exam, follicular carcinoma appears:

A
  • encapsulated
  • solitary
  • found in necrotic/hemorrhagic areas
84
Q

Histopathology of follicular carcinoma:

A
  • mb encapsulated
  • well-defined follicles
  • colloid-containing
85
Q

T/F: Follicular adenoma and carcinoma can be readily differentiated histologically.

A

False

86
Q

Medullary carcinoma may occur as a ________ (usually unilateral) condition or as a _______ (frequently bilateral) condition that is transmitted as an autosomal (recessive/dominant) trait.

A

sporadic
familial
dominant

1 in 10 is hereditary

87
Q

Medullary tumors develop in cells that produce:

A 
calcitonin
C cells (parafollicular)
88
Q

T/F: The excess calcitonin produced by medullary tumors significantly lowers serum calcium and phosphate levels.

A

False

concentration is rarely high enough to alter serum levels

89
Q

T/F: Although medullary tumors are slow growing, they mb harder to control than papillary and follicular d/t tendency to metastasize.

A

True

90
Q

Familial medullary carcinomas are associated with:

syndrome

A

multiple endocrine neoplasia syndrome

91
Q

The fastest growing thyroid tumors are:

A

anaplastic tumors

92
Q

Anaplastic carcinoma tumors are characterized by:

A 
rapid growth
painful enlargement of the thyroid gland
80% die w/in 1 year of dx
MC in elderly
>F:M
93
Q

4+ glands located on the posterior thyroid:

Typical weight:

A

parathyroid glands

25-40mg (each is the size of a grain of rice)

94
Q

Microscopically, the parathyroid glands are (easy/hard) to differentiate. Surgically, they are (easy/hard).

A

easy microscopically - densely packed cells

hard surgically - visibly similar to thyroid and fat

95
Q

The activity of the parathyroid glands is controlled by the level of free _________ in the bloodstream, rather than ___________ secreted by the hypothalamus and pituitary.

A

(ionized) calcium (neg feedback)
trophic hormones

decreased serum calcium stimulates synth/release of PTH

96
Q

Summarize the metabolic functions of PTH in regulating serum calcium levels:

A
  • Inc renal tubular reabsorption of Ca2+, conserving free Ca2+.
  • Inc conversion of vit D to active dihydroxy form in Ki.
  • Inc urinary phosphate excretion, lowering serum phos levels.
  • Augments GI Ca2+ absorption.
97
Q

(Similar/in contrast) to the mechanism that most secretory cells use, calcium (increases/inhibits) vesicle fusion and release of PTH.

A

In contrast
inhibits

In parathyroids, Mg plays role of stimulus-secretion coupling. Hypomagnesia may result in paralysis of PTH secretion, leads to a reversible form of hypoparathyroidism.

98
Q

Parathyroid stimulators:

A
  • dec serum Ca2+
  • mild dec serum Mg2+.
  • inc serum phosphate (inc phosphate causes complex w/ serum Ca2+, forming calcium phosphate -> reduces stimulation of Ca-sensitive receptors that dont sense Calcium phosphate. lack of stimulation triggers inc in PTH)
99
Q

Parathyroid inhibitors:

A
  • Inc serum Ca2+

* Severe dec in serum Mg2+ (mb produce sx of hypoparathyroidism, such as hypocalcemia)

100
Q

PTH is secreted by the _____ cells in the glands, and acts to increase concentration of _____ in the bloodstream. This is in contrast to the effects of _______ which is produced by the _______________ cells that act to decrease concentrations.

A

chief
calcium

calcitonin
parafollicular C cells (of the thyroid)

101
Q

PTH inc the concentration of Ca2+ in blood by acting upon ____ receptors which are found in high concentrations in the ____ and ______. It also works on _____ receptors found in __________________________.

A

PTH1
bone and kidney

PTH2
CNS, pancreas, testes, and placenta

102
Q

Avg PTH levels in serum:

A

10-60pg/ml

103
Q

PTH enhances the uptake of phosphate from the ______ and _______ into the blood.

A

intestine and bones

slightly more calcium than phosphate is released from the breakdown of bone.

104
Q

Oxyphil cells are (larger/smaller) than the chief cells, (more numerous/fewer) in number and stain more (lightly/darkly). The function of Oxyphil cells is:

A

larger
fewer
lightly
not yet known

105
Q

Histology of parathyroid chief cells:

A
  • abundant
  • stain light to dark pink
  • polygonal
  • eosinophilic staining cytoplasm
  • centrally located, uniformly round nuclei
  • secretory granules containing PTH
  • sometimes appear clear d/t lg amt of stored glycogen
106
Q

One of the MC endocrine d/o’s and an important cause of hypercalcemia:

A

primary hyperparathyroidism

107
Q

Underlying condition in 85-95% of parathyroid hyperfunction:

A

adenoma

5-10% primary hyperplasia
1% parathyroid carcinoma

108
Q

80% of pts w/1° hyperparathyroidism are dx:

A

incidentally on a serum electrolyte panel

  • most 50+
  • F:M 4:1
109
Q

Parathyroid adenomas are almost always (solitary/multiple) lesions

A

solitary

110
Q

T/F: Dx of parathyroid carcinoma based on cytologic detail is unreliable, and invasion of surrounding tissues and metastasis are the only reliable criteria.

A

True

111
Q

What morphological changes to the skeletal system occur with hyperparathyroidism?

A
  • skeletal - inc # of osteoclasts to mobilize Ca2+ salts, inc osteoblast activity w/widely spaced trabeculae, thinned cortex (late stage) w/fibrous marrow, hemorrhage foci, cyst formation.
112
Q

2° hyperparathyroidism is caused by _____________, which leads to ___________________.

A

any condition that gives rise to chronic hypocalcemia

compensatory over activity of the parathyroid glands -> inc cell division, cell number -> eventual hyperplasia

113
Q

MC cause of 2° hyperparathyroidism:

A

renal failure

other:
inadequate dietary intake of calcium
vitamin D deficiency
steatorrhea
malabsorption syndromes
114
Q

In 2° hyperparathyroidism the parathyroid glands are:

A

hyperplastic

115
Q

Do you see the same bone changes in 2° hyperparathyroidism?

A

yes. Mb also metastatic calcifications - lungs, heart, stomach, blood vessels.

116
Q

Mechanisms - renal failure -> 2° hyperparathyroidism:

A
  • dec phosphate excreted in urine -> hyperphosphatemia
  • inc serum phosphate depresses serum Ca2+ -> stimulate parathyroid activity
  • dec Vit D3 synthesis in affected kidneys -> dec GI absorption of Ca2+
117
Q

Histopathology of parathyroid hyperplasia:

A
  • little/no adipose
  • all normal cell types
  • pink oxyphil cells
118
Q

T/F: The onset of hypercalcemic symptoms in parathyroid carcinoma is usu more abrupt and more severe than hyperparathyroidism from non-malignant causes.

A

True

esp severe bone and renal sxs!

119
Q

Common clinical findings of parathyroid carcinoma:

A
  • bone pain, pathologic fracture (90%)
  • renal stones (80%)
  • fatigue
  • weakness
  • confusion
  • depression
  • constipation
120
Q

Parathyroid carcinoma is (common/rare).

A

rare

1.25 cases per 10M people

121
Q

Malignancy related to hypercalcemia MC results from:

A

ectopic production of PTHrP from tumor cells [PTH related protein]

less common: skeletal cancer infiltration, lysis of bone

122
Q

PTHrP can be secreted by many types of cancer cells but is seen MC with:

A

breast cancer

certain types of lung cancer

123
Q

T/F: PTHrP is always abnormal.

A

False

tooth eruption
mammary gland development
co-regulates lactation

124
Q

A dz or sx that is the consequence of the presence of cancer in the body, but not d/t local presence of cancer cells:

A

para-neoplastic syndrome [mediated by humoral factors or immune response to tumor]

i.e. PTHrP-related hypercalcemia

125
Q

T/F: The two functional parts of the adrenal glands are derived from the same tissue type but function as separate glands.

A

false - derived from different tissues, function separate

outer cortex
inner medulla

126
Q

Describe the HPA axis.

A
  • hypothalamus releases CRH in response to stress
  • CRH stimulates ant pit to release ACTH
  • ACTH stimulates adrenals to release cortisol
  • CRH under neg feedback by ACTH and cortisol
127
Q

ACTH is produced by __________ cells which make up ___% of the pituitary. It is released in a _______ fashion throughout the day and in a normal ______ rhythm. Peak levels occur at _______, trough at _________.

A 
corticotroph
15%
pulsatile
circadian
peak: 4-6am
trough: 12-2am
128
Q

3 types of steroid hormones produced by the adrenal cortex:

Overproduction of any is MC result of:

A
  • glucocorticoids (cortisol)
  • mineralcorticoids (aldosterone)
  • sex steroids (DHEA)
    ALL DERIVED FROM CHOLESTEROL

functional adenoma in one cell line

129
Q

The zona __________ is the outermost layer of the adrenal cortex. It produces ______________. Regulation of production is via the _______.

A

glomerulosa
mineralcorticoids (aldosterone)
RAS (renin-angiotensis system)

130
Q

The zona ___________ is the middle layer. It produces __________. Regulation is via _________.

A

fasciculata
glucocorticoids (cortisol, sm amts of androgen)
CRH and ACTH

131
Q

The zona _________ is the innermost layer. It produces ___________. Regulation is via __________.

A

reticularis
sex steroids (adrogens, sm amt of estrogens/cortisol)
CRH and ACTH

132
Q

The adrenal medulla is essentially a ________________ and 80% of cells produce __________. The rest produce _________.

A

gland within a gland
epinephrine
norepinephrine

adrenal medulla also produces sm amts of dopamine

133
Q

Renin is produced by the ___________ cells. It converts:

A

juxtaglomerular cells of the kidney

angiotensin I to angiotensin II

134
Q

Aldosterone production/release is controlled by:

A

** RAS system via Angiotensin II **

also by:

  • ACTH
  • sympathetic nervous system
  • inc serum K+
135
Q

Conn’s syndrome is _______________________, MC d/t presence of a ______________.

A

1° hyperaldosteronism
functional adrenal adenoma
mb d/t adrenal hyperplasia

136
Q

Clinical findings in Conn’s syndrome:

A
    • HTN often the only sign **
  • cortisol usu normal
  • unexplained hypokalemia/hypernatremia
137
Q

Describe the mechanism for HTN in Conn’s:

A

Aldosterone -> sodium retention by the kidney -> fluid retention -> increased intravascular volume -> elevation of blood pressure.

138
Q

A (majority/minority) of adrenocortical adenomas are functional - ___%.

A

minority

15%

139
Q

Abn labs seen in Conn’s:

A
  • high aldosterone
  • high sodium
  • low potassium
  • dec plasma renin
140
Q

Work up for Conn’s:

Usu treatment:

A

CT or MRI
Surgical - if adenoma
Aldosterone agonist - if hyperplasia

141
Q

Adrenal hyperfunction, MC d/t long term use of pharma doses of glucocorticoids:

A

Cushing’s syndrome

drugs like prednisone act as exogenous glucocorticoids -> suppress CRH and ACTH production

142
Q

When Cushing’s is non-iatrogenic, it is usu d/t:

A

tumors

  • pituitary (corticotrophin cell line -> ACTH)
  • adrenal (zona fasciculata)
  • ectopic (lung MC)
143
Q

T/F: Ectopic ACTH production and resultant excess serum cortisol is dependent on negative feedback inhibition.

A

False

Independent of negative feedback inhibition!

144
Q

The majority of Cushing’s syndrome is ACTH (in/dependent).

A

Dependent (80%)

  • pituitary tumors
  • lung cancer and other tumors

Independent (20%)

  • benign adrenal tumors / adenoma
  • malignant adrenal tumors / ACC
145
Q

Features of Cushing’s:

A
  • Moon facies
  • truncal obesity
  • striae
  • buffalo hump
  • flushed appearance
  • easy bruising
  • muscle wasting
  • weakness
146
Q

Addison’s dz is a condition of _________ insufficiency.

A

adrenocorticoid

1° - adrenal gland damaged
2° - insufficient ACTH -> adrenal cortex atrophy

147
Q

MC cause of Addison’s dz is:

Often found in assoc with:

A

autoimmune destruction of the adrenal cortex

  • type 1 DM
  • Hashimoto’s thyroiditis
  • Vitiligo
148
Q

Features of Addison’s:

A
  • hypotension
  • hyperpigmentation (high ACTH -> inc melanin)
  • weakness
  • anorexia
  • dehydration
149
Q

Secondary Addison’s mb d/t:

A
  • **usu from inadequate secretion of ACTH by the ant pit
  • withdrawal of long term exogenous glucocorticoid use
  • pituitary tumors
  • damage to pituitary by surgery, trauma, irradiation
  • adrenal function loss from trauma or hemorrhage
150
Q

Adrenal gland failure d/t hemorrhage from sepsis is called:

A

Waterhouse-Frederickson syndrome

MC - Neisseria meningitidis

151
Q

What is a differentiating skin symptom for 2° Addison’s?

A

skin pallor instead of hyperpigmentation

d/t diminished ACTH, no stimulation of melanocytes

152
Q

Describe the etiology of Addisonian crisis.

A

Abrupt removal of exogenous glucocorticoid drugs leaves pts low on ACTH, pituitary is unable to compensate with adequate production, and adrenals may not produce sufficient cortisol.
* may also occur in great stress (surgery, infx)

153
Q

Sx of Addisonian crisis:

A 
Extreme weakness
Nausea/vomiting
Dehydration
Hypotension – often life threatening
Hypoglycemia
Hyponatremia
154
Q

Inborn error of metabolism with a specific deficiency of one or more enzymes involved in cortisol synthesis:

A

Congenital adrenal hyperplasia (CAH)

a group of autosomal recessive disorders that each result in an enzyme deficiency

155
Q

MC example of CAH enzyme deficiency:

A

21-hydroxylase - 95%

CYP21A mutation or deletion

156
Q

21-hydroxylase deficiency results in blockage of ________ production, with subsequent increase in _____ levels. _______________ is also increased with subsequent increase in _______________.

A

cortisol
ACTH
17-hydroxyprogesterone
androstenedione (virilization in females)

157
Q

How is 21-hydroxylase CAH diagnosed?

A

measure 17-hydroxyprogesterone and 17-ketosteroids

both elevated in pt w/21-hydroxylase enzyme deficiency

158
Q

Embryologically, adrenal medulla tissue is derived from _____________ cells which migrate from the ____________.

A

pheochromoblast
neural crest

This tissue also secretes amine hormones, epinephrine, norepinephrine, and dopamine.

159
Q

All catecholamines are derived from the amino acid:

A

tyrosine

160
Q

Most significant pathology assoc w/ the adrenal medulla:

A

pheochromocytoma

catecholamine-secreting tumor of the chromaffin cells

161
Q

Hallmark sx of pheochromocytoma:

A

variable and very labile HTN

162
Q

MEN IIa assoc with:

A
  • pheochromocytoma
  • medullary carcinoma of the thyroid
  • hyperparathyroidism
163
Q

MEN IIb assoc with:

A
  • pheochromocytoma
  • mucosal neuromas
  • hyperparathyroidism
164
Q

T/F: Adrenocortical incidentalomas are relatively uncommon.

A

False

relatively common - mb 5-15% of adults
small number are functional
only 1% of tumors found to be malignant

165
Q

1° adrenal cancers:

A
  • neuroblastomas
  • adrenocorticoid carcinomas
  • adrenal pheochromocytomas
166
Q

MC solid extra-cranial malignancy in infants and children:

A

neuroblastoma
90% by 8y.o.
50% by 2y.o.
10% of childhood cancers in US

167
Q

Histopathology of neuroblastomas reveals:

A

rosettes - circular groupings of dark cells surrounding a pale center composed of neurofibrils

168
Q

The pancreas is both an ________ gland, producing hormones like __________________ and a ________ organ.

A 
endocrine
hormones
- insulin
- glucagon
- somatostatin
- pancreatic polypeptide
digestive
169
Q

Insulin is produced by the ___ cells in the _____________. These make up the _______ portion of the pancreas.

A

beta
islets of Langerhans
endocrine (1% of mass)

170
Q

Surrounding the islets are darker staining ______ cells, which make up the ________ portion of the pancreas which secrete ____________.

A

acinar
exocrine
digestive enzymes

171
Q 
The islets contain several types of cells - that secrete:
alpha cells - 
beta cells - 
delta cells - 
D1 cells - 
PP cells - 
Enterochromaffin cells -
A 
alpha - glucagon
beta - insulin, amylin
delta - somatostatin
D1 - VIP (vasoactive intestinal polypeptide)
PP - pancreatic polypeptide
enterochrom - serotonin
172
Q

Staining used to help ID the nature of islet cells:

A

immunoperoxidase

173
Q

Paracrine feedback system of the islets of Langerhans:

A

Insulin - activates beta; inhibits alpha
Glucagon - activates alpha -> activate beta and delta
Somatostatin - inhibits alpha and beta

174
Q

GLUT receptors require _______ to begin the process of moving glucose into the cell. In its absence, transporters remain ______________.

A

insulin

in cytoplasmic vesicles

175
Q

T/F: Diabetes mellitus is a single disease notable for marked hyperglycemia.

A

false

it is a group of metabolic disorders with hyperglycemia being the common underlying feature, mb d/t defects of secretion, action, or both

176
Q

Diabetes causes secondary damage in:

A
  • kidneys
  • eyes
  • nerves
  • blood vessels
    others
177
Q

Lab criteria for dx of DM:

A
  • fasting glucose >126mg/dL
  • non-fasting glucose >200mg/dL w/sx
  • positive OGTT w/>200mg/dL 2-3 post-bolus
  • Hgb A1C >6.5%
178
Q

A sugar molecule bonding to a protein or lipid without enzyme:

A

glycation (vs. glycosylation w/enzyme)

179
Q

DM I accounts for _____% of cases, whereas DM II accounts for ______%.

A

I - 5-10%
II - 85-95%
1.5 - ~5%

180
Q

Type __ DM is an autoimmune disease in which islet destruction is caused by immune effector cells reacting against endogenous β-cell antigens.

A

1 - islet cell abs and anti-insulin abs

MC develops in childhood, manifest in puberty, progresses w/age

181
Q

In DM type 1, most islet cell abs are directed against:

A

GAD (glutamic acid decarboxylase) within pancreatic beta cells

182
Q

Histopathology finding of DM I:

A

leukocyte infiltration of islet cells - “insulitis”

183
Q

The 2 metabolic defects that characterize DM II:

A
  • peripheral insulin resistance

* beta cell dysfunction manifest as inadequate secretion

184
Q

Insulin resistance assoc w/obesity is induced by:

A
  • adipokines
  • FFAs
  • chronic inflammation in adipose
185
Q

Histopathology of DM II:

A
  • pink hyalinization

* amyloid deposition

186
Q

What is LADA?

A

late-onset autoimmune diabetes of adulthood

estimated 20% of non-obesity related type 2 mb LADA

187
Q

How is diabetic retinopathy best controlled?

A

blood glucose control and early tx of HTN

occurs in 15% of pts w/diabetes x10-15 yrs +1%/yr

188
Q

Frequency of neuropathy in DM II:

A

70-80%
* sensorimotor
* autonomic
[slide 39]

189
Q

Non-proliferative diabetic retinopathy is characterized by:

A

dilated capillaries that leak RBCs and plasma into retina

  • hemorrhage
  • edema
  • exudative deposits
  • neovascularization
  • cotton wool spots
190
Q

MC cause of vision loss d/t diabetic retinopathy:

A

macular edema

191
Q

Histopathology of diabetic glomerulonephropathy:

A
  • thickening of capillaries (earliest) -> microalbuminuria
  • diffuse inc in mesangial matrix
  • acellular PAS-positive nodules
192
Q

Pancreatic endocrine tumors (PETs) are (common/uncommon) and present as _______________.

A

uncommon

functional or non-functional

193
Q

Functional PETs are commonly assoc with:

A

specific hormonal syndromes

  • Zollinger-Ellison
  • hyperinsulinemia
194
Q

Histopathology of pancreatic islet cell adenoma:

A

“monotonous” appearance

  • minimal pleomorphism
  • minimal mitotic activity
  • amyloid deposition
195
Q

An insulinoma is a pancreatic tumor derived from ___ cells.

A

beta

insulin secretion is not properly controlled by feedback mechanisms, thus continue to secrete -> hypoglycemia

196
Q

What is Whipple’s triad?

A
  • sx of hypoglycemia

* serum glucose of

197
Q

MC location for insulinoma to arise:

A

pancreas - 99%

5% assoc w/parathyroid, MEN I

198
Q

Dx for insulinoma made on:

A
  • low serum glucose
  • high serum insulin, proinsulin, C-peptide

confirm by MRI or angiography, then biopsy

199
Q

Tumor of the pancreas or duodenum that secretes excess gastrin, leading to excess gastric production of HCl -> subsequent development of GI ulcerations:

A

gastrinoma

HCl also causes hyperperistalsis, inhibits lipase

200
Q

Sx of gastrinoma:

A
  • hypergastrinemia
  • GI ulcers
  • severe diarrhea
  • cancer sx - anorexia, wt loss, fatigue, malaise
201
Q

Most gastrinomas are found as (single/multiple) tumor(s) and are found to be (benign/malignant). Most are found in the (pancreas/duodenum/jejunum).

A

single (notes contradictory)
malignant
duodenum

202
Q

Malignant gastrinomas MC spread to:

A

liver

lymph nodes near pancreas and sm intestine

203
Q

Gastrinomas are frequently the cause of excess gastrin in:

A

Zollinger-Ellison syndrome (25% MEN I)

204
Q

Zollinger-Ellison triad:

A
  • gastric acid hypersecretion
  • severe peptic ulceration
  • gastrinomas (pancreas or duodenum)
    self-perpetuating, leading to multiple ulcers
205
Q

Laughter is the best medicine,

A

unless your diabetic, then insulin might be better.

THE END

Pathology IV (6 decks)

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