Exam 1 Flashcards

Question

Anterior pituitary hormone targets:

Answer 1

• GnRH —> FSH/LH —> ovary/testis • GHRH —> GH —> liver/all tissue • somatostatin —| GH • TRH —> TSH —> thyroid • TRH —> prolactin —> breast • dopamine —| prolactin • CRH —> ACTH —> adrenal cortex

Answer 2

• synthesis/secretion stimulated by TRH from hypothalamus • stimulates growth of the thyroid gland and secretion of thyroid hormones such as T3 and T4

Answer 3

• synthesis/secretion stimulated by GnRH from the hypothalamus • promotes estrogen/progesterone synthesis in ovaries and promotes testosterone synthesis in testes

Answer 4

• synthesis/secretion stimulated by gonadotropin releasing hormone (GnRH) from hypothalamus • stimulates follicle growth in ovaries and spermatogenesis in testes

Answer 5

• synthesis/secretion stimulated by corticotropin releasing hormone (CRH) in the hypothalamus • stimulates corticosteroid production by the adrenal cortex (cortisol, etc.)

Answer 6

Precursor polypeptide POMC (proopiomelanocortin)

Answer 7

Alpha-MSH (melanocyte-stimulating hormone) ~ this would be considered a secondary hypercortisolism

Answer 8

• structurally homologous to growth hormone, its **secretion is under tonic inhibition by dopamine** • secretion stimulated by infant sucking and TRH • promotes breast development, lactation, inhibits ovulation via inhibition of GnRH

Answer 9

Placental progesterone

Answer 10

• most common functioning pituitary tumor leading to a hyper secretion of prolactin —> induces lactation, inhibits GnRH, decreases FSH and LH, leads to decreased progesterone/estrogen and testosterone —> amenorrhea, infertility, impotence, gynecomastia

Answer 11

1. Dopamine agonist is the first line **(bromocriptine, cabergoline)** because it inhibits prolactin secretion 2. Surgery due to increased to ICP/mass effect

Answer 12

• structurally homologous to prolactin, the main function is to promote linear growth • important in adolescence

Answer 13

• stimulated by release of GHRH, exercise, trauma, and acute hypoglycemia • inhibited by somatostatin • decreased by age, disease, glucose

Answer 14

**insulin like growth factor-1** • increased protein synthesis, fat utilization • decreased glucose uptake

Answer 15

Growth hormone (GH) • increases serum glucose levels by promoting glycogenolysis, gluconeogenesis, lipolysis, ketogenesis

Answer 16

**growth hormone, GH** • gigantism: in children, acting on epiphyseal plate • acromegaly: adults, acting on fused growth plate cartilage

Answer 17

• enlarged liver and heart • peripheral neuropathy secondary to nerve compression • glucose intolerance and diabetes • amenorrhea, impotence

Answer 18

• increased serum IGF-1 • Oral glucose tolerance test fails to suppress GH

Answer 19

• surgical removal of pituitary • octreotide: somatostatin analog • bromocriptine: DA agonist • pegvisomant: GH receptor antagonist

Answer 20

• promotes contractions of the uterine myometrium during labor • stimulates contractions of the mild epithelial cells in the breast (milk production)

Answer 21

• stimulate: cervix dilation, suckling of infant • inhibit: fear, pain, noise, fever

Answer 22

Anti-diuretic hormone: 1. Central DI: absent/insufficient ADH release (pituitary problem) 2. Nephrogenic DI: normal ADH secretion, kidneys unresponsive (renal resistance)

Answer 23

Central DI and nephrogenic DI. Central DI will respond positively to the administration of vasopressin (Tx), and nephrogenic will not (needs thiazide diuretics)

Answer 24

Syndrome of inappropriate secretion of antidiuretic hormone: ADH in the absence of hyperosmolarity—> inability to dilute urine—> euvolemic hyponatremia ~ tx: water restriction

Answer 25

1. Somatotropin: recombinant hGH 2. Mecasermin: recombinant IGF-1

Answer 26

1. Octreotide: somatostatin receptor agonist 2. Pegvisomant: GH receptor antagonist 3. Bromocriptine: dopamine D2 receptor agonist

Answer 27

• replacement in GH deficiency • increased final adult height in children with conditions of short stature • wasting associated with AIDS/malignancy • short bowel syndrome

Answer 28

• edema • hyperglycemia • decreased insulin sensitivity • thickening of bones, progression of scoliosis • carpal tunnel syndrome

Answer 29

• clinical application: replacement in IGF-I deficiency that is not responsive to somatotropin • side effects: hypoglycemia, intracranial HTN, increased liver enzymes

Answer 30

• acromegaly • hormone secreting tumors • acute control of bleeding from esophageal varices

Answer 31

• GI disturbances • gallstones • bradycardia, cardiac arrhythmias • thyroid disruption

Answer 32

• clinical application: acromegaly • side effects: minimal, liver enzyme increase on induction but not failure

Answer 33

Dopamine D2 receptor agonist suppresses pituitary secretion of: 1. prolactin 2. GH

Answer 34

• GH based: acromegaly • prolactin based: hyperprolactinemia

Answer 35

• psychiatric disturbances, confusion • G.I. disturbances • orthostatic hypotension • headache • vasospasm

Answer 36

• a GnRH analog that increases LH and FSH secretion with intermittent pulsatile administration (used for fertility) • continuous non-pulsatile administration reduces LH and FSH secretion (endometriosis, precocious puberty, trans medicine)

Answer 37

• induction and augmentation of labor • control of uterine hemorrhage post delivery

Answer 38

Desmopressin and vasopressin ~ used in central diabetes insipidus, hemophilia, and von Willebrand disease (Desmo)

Answer 39

Conivaptan ~ typically used for hyponatremia stabilization in hospitalized patients (infusion only)

Answer 40

• adenoma (lactotroph, somatotroph, corticotrophin, gonadotroph) • carcinoma • genetics

Answer 41

• apoplexy • Sheehan • empty sella • hypothalamic • inflammatory/infectious • genetic

Answer 42

Visual defects due to proximity of the optic chasm: bilateral temporal hemianopia

Answer 43

• most common functioning adenoma • secretes prolactin, stimulates breastmilk production, inhibits ovulation and spermatogenesis • more commonly seen in women of reproductive years

Answer 44

• excessive secretion of growth hormone, stimulation of hepatic secretion of insulin like growth factor-1 (IGF1) • can cause gigantism, acromegaly, secondary diabetes mellitus • tx: surgery, somatostatin analog (octreotide)

Answer 45

• excess ACTH production leading to adrenal hyper secretion of cortisol, hypercortisolism, and **cushing disease**

Answer 46

• highly basophilic/chromophobic • positive ACTH immunohistochemistry • densely granular EM • crooke hyaline changes

Answer 47

• secretes hormones inefficiently/not at all (LH, FSH) leading to decrease energy/libido in men and amenorrhea in women from decreased LH

Answer 48

• a very rare, one percent of pituitary adenomas • can cause hyper thyroidism by excessive TSH release

Answer 49

Mass effect causing other brain injuries/symptoms. Hypopituitarism which may lead to pituitary apoplexy

Answer 50

Macro is greater than 1 cm

Answer 51

• typically due to destructive processes such as tumors, trauma, subarachnoid hemorrhage, surgery, apoplexy, ischemia, TB/sarcoidosis

Answer 52

• acute hemorrhage into the pituitary, often pre-existing adenoma • sudden excruciating headache and diplopia, cardiovascular collapse, LOC, and death possible

Answer 53

• postpartum pituitary necrosis • **anterior pituitary** normally doubles and size during pregnancy without an increased blood supply from low pressure venous system (obstetric hemorrhage or shock may lead to infarction due to low blood supply) • Posterior pituitary uninvolved due to separate arterial blood supply, eventually replaced by fibroid tissue or empty sella

Answer 54

• defect of the diaphragma sella allows arachnoid and CSF to herniate into the sella, compressing the pituitary • most common in women with a history of multiple pregnancies • results in visual defects, aberrant hyperprolactinemia

Answer 55

• mass such as adenoma is surgically removed or infects lead to loss of function of the pituitary gland

Answer 56

• benign: craniopharyngioma • metastatic tumors (breast, lung) • radiation of other brain or nasopharyngeal areas

Answer 57

• gliomas (pilocytic astrocytoma, NF1) • craniopharyngioma (Rathke pouch remnant) ~ slow growing, **children typically have adamantinomatous type, adults have papillary type** with calcification

Answer 58

1. Palisading epithelium 2. Stellate reticulum 3. Wet keratin

Answer 59

Beta-Catenin and Wnt

Answer 60

Non-keratinizing squamous epithelium and capillary fibrovascular stroma

Answer 61

BRAF V600E

Answer 62

• sarcoidosis • tuberculosis • meningitis

Answer 63

mutation of pituitary specific PIT-1 gene

Answer 64

Pituitary dwarfism

Answer 65

Amenorrhea, infertility, decreased libido, impotence, loss of pubic and axillary hair

Answer 66

Hypothyroidism

Answer 67

Hypoadrenalism

Answer 68

Color deficiency— pallor

Answer 69

• peptides • proteins • glycoproteins

Answer 70

• steroids • thyroid hormone

Answer 71

• there are large protein molecules which dissolve well in the blood • they are broken down quickly by peripheral enzyme systems • bind surface membrane receptors and cause cellular response through signal transduction systems **(secondary messenger systems that are fast, and gene transcription which is slow)**

Answer 72

• lipophilic and easily cross membranes • bind carrier proteins in order to travel in the blood, have a longer half-life • cytoplasmic or nuclear receptors

Answer 73

Cholesterol

Answer 74

In the adrenal medulla

Answer 75

Water— even though they come from Tyrosine (like thyroid hormones that are lipid soluble)

Answer 76

Intracellular receptors

Answer 77

Beta adrenoreceptors (heart is more sensitive to catecholamines in the presence of thyroid hormone)

Answer 78

Growth hormone (GH)

Answer 79

Synergism: combined effect > sum of individually effects Permissiveness: need second hormone to get full effect Antagonism: one substance opposes the action of another

Answer 80

1. Hypothalamus (brain) releases hormones— GHRH, TRH, CRH, GnRH through portal system 2. Pituitary secretes stimulating hormones— GH, TSH, ACTH, LH, FSH 3. Peripheral target gland secrete peripheral hormones— IGF, thyroid hormone, cortisol, sex hormones

Answer 81

Negative feedback

Answer 82

1. Adrenal glands 2. Gonads (ovaries, testes) 3. Placenta

Answer 83

1. De Novo via acetyl-CoA in the endoplasmic reticulum 2. Uptake from dietary fat, lipoprotein particle

Answer 84

Progesterone (intermediate of all), cortisol, corticosterone, aldosterone, testosterone, estradiol

Answer 85

Steroid acute regulatory protein (StAR)

Answer 86

The conversion of cholesterol to pregnenolone by the mitochondrial matrix enzyme P450scc (CYP11A1)

Answer 87

Inherited mutations in lysosomal acid lipase (LAL). Characterized by cholesterol engorged macrophage infiltration of organs and death by organ failure in infancy

Answer 88

• caused by mutation in StAR. Characterized by steroid hormone insufficiency resulting in female external genitalia and genetic XY individuals, salt wasting, and destruction of tissue due to fat accumulation

Answer 89

* liver steatosis * crystals of cholesterol esters in Kupffer cells

Answer 90

• CYP450scc (carbons are hydroxylated, bonds cleaved) • 3 molecules of NADPH • 3 molecules of oxygen

Answer 91

Catecholamines: adrenal medulla Steroids: adrenal cortex

Answer 92

• determined by gradient of WNT/beta-catenin and cAMP/PKA

Answer 93

• loss of adrenal function • can be caused by TB/autoimmune reaction • symptoms: fatigue, weight loss, hypotension, nausea, vomiting, **hyperpigmentation due to increased ACTH activity in melanocytes**

Answer 94

Inherited mutations in P450c21 (CYP21) resulting in a less active enzyme **(21 hydroxylase)**—> this causes pregnonolone and progesterone to divert to androgen production

Answer 95

* decreased cortisol—> **increased ACTH** * decreased mineralcorticoids—> **hypotension, hyponatremia, hyperkalemia** * increased androgens—> **early puberty, masculinization infemales**

Answer 96

• decreased cortisol—> increased ACTH • increased mineralocorticoids—> hypertension, hypokalemia • decreased sex hormones—> XX, XY anatomically female without maturation

Answer 97

• decreased cortisol —> increased ACTH • increased 11 deoxycorticosterone—> hypertension • increased sex hormones—> masculinization in females

Answer 98

1. Follicular/principal cells 2. Parafollicular/C-cells

Answer 99

• structural unit of thyroid • simple epithelium: cuboidal, squamous, columnar depending on colloid/activate • colloid contains a thyroglobulin (gel)

Answer 100

• apical ends of cells adjacent to colloid, microvilli that extends into the colloid • basal end of cells rest on basement membrane • slightly basophilic cytoplasm, round nuclei, prominent nuclei • **synthesize thyroid hormones (T3, T4)**

Answer 101

• inactive: resting, basal level of thyroglobulin, squamous to cuboidal, few mitochondria/small Golgi, some rough ER • active: stimulated by TSH from pituitary, columnar cells, numerous mitochondria/enlarged Golgi/increased rough ER, lipid droplets and PAS positive, releases T3 and T4 on basal surface

Answer 102

• lining endothelial cells go from squamous/flat to large columnar filled with colloid

Answer 103

• occurs singly or in small groups between follicular cells and membrane • neuroendocrine cells that synthesize calcitonin

Answer 104

Parafollicular thyroid gland cell

Answer 105

• lowers blood calcium by inhibiting bone resorption • decreases osteoclast motility/numbers • promotes excretion of calcium and phosphate from the kidneys

Answer 106

In colloid in the thyroid gland (glycoproteins and tyrosine residues available available for iodination—> T3 and T4 precursors)

Answer 107

Iodine of thyroglobulin with tyrosine, stimulated by TSH produced by thyrotropes in the pars distalis of the pituitary • 1tyrosine = monoiodotyrosine • 2 tyrosine = diiodotyrosine • 1 MIT + 1 DIT = T3 • 1 DIT + 1 DIT = T4

Answer 108

**1. Lysosomal/physiologic:** endosomes fuse with lysosomes,T3/T4 is released from Tg, active hormone T2/T4 diffuses through the cell and released at basal surface to capillaries **2. Transepithelial pathway:** cell surface receptor megalin binds thyroglobulin and all allows it to skip the lysosome, iodinated thyroglobulin is released at the basal surface

Answer 109

1. Chief/principal cell 2. Oxyphil cells 3. Fat cells

Answer 110

• small cells, most numerous, slightly acidophilic cytoplasm • replicate when chronically stimulated by changes in blood calcium levels • **parathyroid hormone, PTH synthesis, storage and secretion to regulate circulating calcium**

Answer 111

• a peptide involved in the regulation of calcium and phosphate levels • it increases blood calcium by stimulating osteoblasts to produce osteoclast stimulating factor (RANKL)—> bone resorption increases blood calcium

Answer 112

• larger than chief cells, smaller and dark staining nuclei with no known secretory function • large eosinophilic cytoplasm that is finally granular due to numerous mitochondria

Answer 113

Derived from the pharyngeal endoderm of the the third and fourth pharyngeal pouch ~ principal cells differentiate first to regulate calcium, oxyphil cells differentiate at puberty

Answer 114

• a small pinecone shaped body with a Pia matter capsule attached by a stalk to the roof of third ventricle between the two hemispheres of the brain • contains pinealocytes and interstitial (glial) cells

Answer 115

• majority (95%) of pineal gland cells • resemble neuroendocrine cells • produce melatonin at night

Answer 116

• Astrocytes (supportive role) similar to the pituicytes of the posterior pituitary

Answer 117

• an area of the pineal gland that has concentrations of calcium phosphate and carbonate on carrier proteins • accumulates with age, no known function • **use as a radiological marker because it is opaque on x-rays**

Answer 118

Increase melatonin, reduced GnRH and GnIH, therefore reduced FSH, reduced LH

Answer 119

The pineal gland

Answer 120

Hyperthyroidism, a hypermetabolic state caused by excess circulating T3 and T4 • primary: excess production by the thyroid gland (most common) • secondary: extrathyroid source

Answer 121

TSH level (will be low)

Answer 122

1. Diffuse hyperplasia, Graves’ disease 2. Multinodular goiter 3. Hyperfunctional adenoma

Answer 123

• hypermetabolic and increased sympathetic tone: warm, flushed skin, heat intolerance, increase sweating, weight loss despite increased appetite • cardiac manifestations: increased cardiac contractility, tachycardia, palpitations, cardiomegaly, a fib, left ventricular dysfunction

Answer 124

* most common cause of endogenous hyperthyroidism: triad of thyroid toxicosis, ophthalmopathy, dermatopathy * autoimmune, secondary hypersensitivity reaction * glycosaminoglycan deposition in the ECM and lymphoid infiltrates * **lab findings: high serum free T3/T4 and low TSH**

Answer 125

* propylthiouracil: decrease synthesis of thyroid hormone (blocks T 4 5' deiodinase) * radioiodine ablation * surgery for large goiters compressing adjacent structures

Answer 126

Thyroid enlargement and impaired synthesis of thyroid hormone, usually due to dietary iodine deficiency. Results in compensatory increase in TSH, causing hyperplasia and hypertrophy of follicular cells and gross enlargement of the gland

Answer 127

• endemic- where soil, food, water have low iodine • sporadic- female predominance, puberty/young adults, unclear cause

Answer 128

• decrease production of thyroid hormone, increased with age, more common in females • **primary:** defect and thyroid gland (congenital, auto immune, iatrogenic) • **secondary:** defect elsewhere in the axis (division of TSH, TRH)

Answer 129

* hypothyroidism and infancy/early childhood typically in areas endemic of iodine deficiency, maternal hypothyroidism, agenesis, or dishormonogenic goiter * **impaired skeletal and CNS development, short stature, coarse facial features, mental deficiency**

Answer 130

Myxedema— general slowness, decreased metabolic rate. Caused by iodine deficiency, drugs (lithium), or thyroiditis ~ measuring TSH is the most sensitive screening test

Answer 131

• most common cause of hypothyroidism where iodine levels are sufficient • autoimmune **(autoantibodies to thyroglobulin and thyroid peroxidase)** characterized by progressive gland destruction, Hurthle cell change, mononuclear infiltrates with germinal centers with or without fibrosis

Answer 132

• painless, postpartum thyroiditis presenting with mild hyperthyroidism, goiter, or both • autoimmune, circulating **anti-thyroid peroxidase antibodies** • no hurthle cell metaplasia, otherwise similar to Hashimoto’s

Answer 133

• painful, age 40-50, women • triggered by viral infection, Coxsackie, mumps, measles, adenovirus • **most common cause of thyroid pain, transient hyperthyroidism (high T3, T4 and low TSH) that is self limiting and normal function returns in 6-8 weeks**

Answer 134

• rare, fibrous disease causing thyroid gland hardening • IgG4 related systemic disease • clinical features: hard, immovable thyroid mass, hypothyroidism, compression effect (difficulty swallowing, breathing, voice changes)

Answer 135

• discrete encapsulated solitary masses of follicular epithelium, typically non-functional • **GOF mutation in TSHR, GNAS • rare: RAS or PIK3C a mutations or a PAX8-PPARG fusion gene**

Answer 136

• gray/white two red/brown cut surface • hemorrhage, fibrosis, calcification seen • uniform small follicles with some colloid, follicle cell monotony, mitotic figures are rare

Answer 137

Entire tumor capsule must be examined because capsular and vascular invasion define carcinoma

Answer 138

• papillary, most common • follicular • anaplastic • medullary ~ mutations in RET gene, or MEN2 are common genetic predispositions

Answer 139

• women, 40-60 • acquired mutations that activate RAS or the PI3K/AKT arm of the receptor tyrosine kinase pathway (or LOF of PTEN)

Answer 140

• gross: single nodule, gray to pink/tan to yellow with hemorrhage/necrosis occasionally • microscopic: uniform cells forming small molecules, less colloid than normal, Hurthle variant occurs

Answer 141

Although slowly enlarging painless mass, total thyroidectomy followed by radioactive iodine and thyroid hormone treatment to suppress endogenous TSH is the treatment

Answer 142

* most common thyroid malignancy, 25-50 years old or childhood * exposure to ionizing radiation is a risk factor * **GOF mutation of RET or NTRK1 receptor tyrosine kinase or BRAF**

Answer 143

• gross: solitary/multifocal, cystic, fibrosis, calcification, papillae sometimes visible on surface • microscopic: branching Papillae with fibrovascular core, clear ground glass nuclear appearance (orphan Annie eye), calcified psammoma bodies

Answer 144

• **Tall cell:** older individuals, vascular invasion, BRAF, PTC/RET translocation • **diffuse sclerosing:** younger age, papillary growth, squamous nest simulating Hashimoto, lymph involvement • **follicular variant:** nuclear features of PTC but follicular architecture (can be infiltrative or encapsulated)

Answer 145

• rare, high mortality undifferentiated tumor of thyroid epithelium, around 65 • **RAS, PIK3CA mutations as well as TP53 in activation or activating beta-catenin**

Answer 146

• neuroendocrine neoplasm derived from parafollicular C- cells • excessive secretion of calcitonin (occasionally also serotonin, ACTH, VIP) which can lead to neck masses/dysphasia/hoarseness, diarrhea (VIP), and Cushing (ACTH)

Answer 147

* gross: sporadic solitary nodule, familial may be bilateral or multicentric * microscopic: polygonal to spindle shaped cells, nests, tuberculae, c-cell hyperplasia * stromal amyloid may be seen

Answer 148

• autonomous overproduction of PTH • adenoma or hyperplasia

Answer 149

• compensatory hyper secretion of PTH in response to a prolonged hypocalcemia • renal failure

Answer 150

• persistent secretion of PTH even after the cause of prolonged hypocalcemia is corrected • renal failure followed by a transplant with continued high PTH

Answer 151

1. Cyclin D-1 inversions leading to the overexpression of cyclin D-1 2. MEN-1 mutations

Answer 152

• sporadic or as a component of MEN syndrome • diffuse or nodular increase in cellularity with decreased intervening fat, no atrophic suppressed rim of tissue— typically increased cellularity of the chief cells

Answer 153

• diffuse and pervasive marked atypia and increased mitotic activity • invasion of surrounding tissues and metastasis

Answer 154

Typically asymptomatic, however can be symptomatic: **painful bones, renal stones, abdominal groans, and psychic moans** • osteoporosis, brown tumor, osteitis fibrosis cystica • nephrolithiasis • G.I. constipation, ulcer, pancreatitis, gallstone • neuromuscular weakness • aortic or mitral valve calcifications

Answer 155

• conversion of compact cortical bone to cancellous bone by osteoclast forming cutting cones, dissecting osteitis

Answer 156

• associated with hyperparathyroidism • can occur anywhere in the skeleton, non-specific pain/swelling • one or more lytic lesions, many osteoclast-like giant cells

Answer 157

• mild skeletal abnormalities • vascular calcification that can be life-threatening • calciphylaxis skin/organ involvement • cold necrotic plaque and eschar on abdomen/lower extremities

Answer 158

• tenany (neuromuscular irritability due to decreased calcium) • mental status change • intracranial calcification in the basal ganglia • ocular calcification of the lens/cataract • cardiovascular conduction defect/prolonged QT interval • dental abnormalities, hypoplasia/failure of eruption/defective enamel

Answer 159

• germline mutation in MEN one tumor suppressor gene menin—> block transcriptional activation by JunD **PPP** • parathyroid hyperplasia/adenoma • pituitary tumors: prolactinoma • pancreatic islet cell tumors: gastrinomas, insulinomas

Answer 160

• germline GOF RET pro-oncogene, extracellular domain mutation **PPM** • pheochromocytoma • medullary thyroid carcinoma • parathyroid hyperplasia, hypercalciuria and renal stones

Answer 161

• intracellular domain mutation **PMM** • pheochromocytoma • medullary thyroid cancer, multifocal and more aggressive • marfanoid habitus (neuromas or ganglion neuromas of skin, oral mucosa, eyes, respiratory, G.I.)

Answer 162

• MEN2: routine genetic test for RET mutation. Undergo thyroidectomy if positive

Answer 163

* iodine is uptaken and converted in the gut to iodide which is taken up by the thyroid gland * follicular cell via **PENDRIN** * undergoes oxidation to convert iodide to iodine

Answer 164

• carried on proteins: **thyroid binding globulin**, transtryetin, albumin, lipoproteins

Answer 165

In the thyroid with iodine— conjugating thyroglobulin

Answer 166

In the thyroid gland AND in other tissues via **T4,5’ deiodinase** • type 1: liver and kidney and thyroid (drug target) • type 2: muscle, brain, pituitary, placenta, skin

Answer 167

• bone growth and the closing of growth plates • CNS development, primarily in the first trimester (no fetal production, supplementation from mom)

Answer 168

• heart: increases beta2 receptors (increased heart rate, contractility) • lungs: stimulates respiratory centers • skeletal muscle: promotes gluconeogenesis and lipolysis • metabolism: increases O2 consumption

Answer 169

• bradycardia, weight gain, hair loss, decreased deep tendon reflexes, myalgia, increased depression

Answer 170

• obvious goiter • hx head and neck surgery • autoimmune disorders • family history • medication: lithium, amiodarone

Answer 171

• high TSH • low total T3, low to normal T4

Answer 172

Primary hypothyroidism due to antibodies to thyroid peroxidase **(TPO antibodies)** ~ pt cannot make T3/T4 because they cannot add iodine to thyroglobulin

Answer 173

• problem with the pituitary/hypothalamus—> no TRH/TSH • strokes, postpartum Sheehan syndrome, radiation, surgeries

Answer 174

TSH: low or normal (8% high) Total T3: low or normal Serum free T4: low or normal

Answer 175

Levothyroxine: normalized TSH, alleviates symptoms. Must take on empty stomach (calcium, PPI, iron can bind it) ~ in pregnancy, increased dose 30 to 50% and check every 2 to 4 weeks

Answer 176

• tachycardia, atrial fibrillation • new or worsening hypertension • weight loss • diarrhea, diaphysis • xalphthalmos (lid lag)

Answer 177

TSH: moderately decreased T3: increased or normal T4: increased or normal

Answer 178

• test for a thyrotropin receptor antibodies (TRAb) • radioactive iodine uptake (entire gland lights up in Graves’ disease) • ultrasonography for thyroidal blood flow

Answer 179

Granulomatous disease or infection

Answer 180

Drugs such as lithium, amiodarone or postpartum (17%)

Answer 181

1. Methanimazole: blocks thyroid peroxidase, cannot be used in pregnancy 2. Propylthiouracil: blocks T4,5’ deiodinase 3. Reactive iodine (can lead to hypothyroidism) 4. Surgery- nodule removal

Answer 182

Kidneys and bones. The goal is to increase serum calcium

Answer 183

Acts on osteoblasts —> RANKL —> osteoclasts —> calcium and phosphorus release from bone

Answer 184

* decreased Na-PO4 transporter in the proximal tubule * increased CaSR, and calcium absorption in the thick ascending limb

Answer 185

Indirect. PTH increases 1,25 dihydroxy Vit D leading to increased gut calcium absorption from food

Answer 186

Stimulates PO4 excretion and blocks 1-alpha hydroxylase

Answer 187

• elevated to PTH • elevated calcium • Elevated 24 hour urine calcium (>300mg) • 1, 25 -OH can be normal or high

Answer 188

1. cinecalcet (calcimimetic): blocks CaSR 2. Bisphosphonates: inhibits osteoclasts ~ AVOID thiazides, high calcium diet

Answer 189

• genetic disorder, FGF 23 mutation leading to an inactivation of the calcium sensing receptor (CaSR)

Answer 190

PTH: increased Vitamin D: normal, 1, 25-OH may be high 24 hour urine calcium: low

Answer 191

PTH: dramatically low, suppressed Vitamin D : normal to low PTHrP: parathyroid related peptide, mimics PTH, produced by some cancers. Can be increased or negative

Answer 192

• squamous cell carcinoma • renal cell carcinoma • lung cancer • ovarian cancer ~ multiple myeloma, and breast cancer can typically cause parathyroid hormone problems

Answer 193

• rehydrate • calcitonin (increase renal excretion of calcium) • furosemide (increase renal excretion of calcium) • bisphosphonates: stabilized bone, may cause AKI, especially without fluids

Answer 194

PTH: low 1,25-OH: normal to High 25-OH: normal to High ~ tx: discontinue supplementation

Answer 195

PTH: low Vitamin D: very elevated 1, 25-OH ~ lithium, thiazides, excessive vitamin A may cause this

Answer 196

**chronic kidney disease** • kidneys cannot filter, they cannot excrete what they do not see • PTH: extremely elevated • Phosphorus: extremely elevated • GFR: low ~tx: phosphorus binders to be given with food to lower the absorption

Answer 197

• bisphosphonates, citrates, calcium chelators, cisplatin, calcimimetics

Answer 198

• steroids secretion (aldosterone, cortisol) • partially regulated by anterior pituitary • mesoderm derived

Answer 199

• catecholamines (epi, NE) • neural crest derived (ectoderm)

Answer 200

1. Zona glomerulosa (secretes mineralocorticoids) 2. Zona fasciculata (secretes glucocorticoids and gonadocorticoids) 3. Zona reticularis (secretes glucocorticoids and gonadocorticoids)

Answer 201

“Go find Rex, make good sex”

Answer 202

Zona fasciculata (broadest, middle zone that is lightly stained)

Answer 203

• cortisol • hydrocortisone • some androgens, very little estrogen

Answer 204

* aldosterone * deoxycortisone

Answer 205

• primarily androgens, very little estrogen

Answer 206

• chromaffin cells • sinusoidal capillaries and nerves • sympathetic nerve fibers terminate on chromaffin cells (release acetylcholine—> trigger granule release of epi, NE, chromogranins, ATP, and Ca2+)

Answer 207

• modified postganglionic sympathetic neurons • lack axons or dendrites • neural crest origin • innervated by Pre ganglionic sympathetics • secrete direct directly into capillaries (instead of nerve terminals)

Answer 208

Chromaffin cells of the adrenal medulla

Answer 209

• 3 suprarenal arteries • three sets of capillaries: capsular plexus, cortical sinusoidal vessels, medullary capillaries

Answer 210

Capillary plexi —> medullary venules —> collecting veins —> medullary central vein —> suprarenal vein

Answer 211

• glucagon: polypeptide to raise blood sugar levels • most numerous at the periphery of the islet

Answer 212

• insulin to regulate protein, lower blood sugar levels • c peptide • amylin • more numerous towards the center of the islet, can have crystalline appearance of secretory vesicles • diseased = DM

Answer 213

• somatostatin, a polypeptide with paracrine and endocrine effects (suppression of insulin and glucagon, reduces contractions of alimentary tract and gallbladder smooth muscles)

Answer 214

• pancreatic polypeptide with paracrine and endocrine effects (inhibits and somatic secretion from exocrine pancreas, relaxes gallbladder resulting in decreased bile secretion) • predominant in the head of the pancreas

Answer 215

• Ghrelin, neuropeptide that regulates appetite (hunger hormone)

Answer 216

Thyroglobulin: it is only produced by thyroid tissue

Answer 217

Hashimoto thyroiditis (can also rarely be presented in Graves’ disease)

Answer 218

Graves’ disease

Answer 219

• graves: RAIU is elevated, the entire gland becomes “hot” • Hashimoto’s: uptake is usually low, with patchy hotspots in the gland

Answer 220

Cancer/malignancy

Answer 221

Primary hyperthyroidism

Answer 222

Primary hypothyroidism

Answer 223

Secondary hypothyroidism

Answer 224

Secondary (or tertiary) hyperthyroidism

Answer 225

Problem with the hypothalamus: TRH producing adenoma

Answer 226

Hashimoto’s (including anti-thyroid peroxidase antibodies) However: 1/3 of patients will have hyperthyroidism and hypothyroidism, 1/3 will have only hypothyroidism, 1/3 will have only hypothyroidism

Answer 227

• beta blockers (propanolol) • levothyroxine in the hypothyroidism state ~ hyperthyroidism is typically self limited

Answer 228

1-3 weeks following delivery, with symptoms including strong feelings of sadness, anxiety, despair. Having trouble coping with daily tasks, treatment and counseling recommended

Answer 229

• drastic changes in hormone levels • hx of depression • emotional factors relating to pregnancy/delivery • fatigue and lifestyle choices

Answer 230

The adrenal medulla

Answer 231

The adrenal cortex

Answer 232

Glucocorticoid receptors and mineralocorticoid receptors

Answer 233

Cholesterol to pregnenolone via cholesterol demolase/P450scc/ CYP11A1

Answer 234

Circadian rhythm and stress

Answer 235

11beta-hydroxysteroid dehydrogenase type 1 and type 2

Answer 236

Cortisol effectively increases blood glucose concentration

Answer 237

Rate of secretion adjusted depending on extracellular volume, [K+], [Na+], and arterial pressure ~ high serum K increases secretion, high serum Nadecreases secretion, RAAS system increases secretion

Answer 238

Kidney, colon, sweat glands, heart, hippocampus, brown adipose

Answer 239

11beta-HSD2 allows for specificity of mineralocorticoid receptor responding to MC

Answer 240

• fetal development • adrenarche • adult: maintain **female** axillary and pubic hair, contributory to female testosterone more than male • menopause

Answer 241

Glucocorticoid therapy (iatrogenic), and primary glandular excess production of cortisol (adrenal tumors)

Answer 242

Conn syndrome: benign adenoma in the Zona glomerulosa —> excess aldosterone and increased sodium reabsorption and potassium secretion

Answer 243

• primary adrenal insufficiency • idiopathic atrophy of the adrenal cortex, can be caused by autoimmune process, TB, AIDS

Answer 244

• 21- hydroxylase deficiency • 11beta- hydroxylase deficiency ~ autosomal recessive disorders causing cortisol deficiency, increased ACTH and bilateral adrenal gland hyperplasia result

Answer 245

• increase glucocorticoid potency (ratio of GCR to MCR effect) • less protein bound, slower metabolism

Answer 246

• They decrease arachidonic acid metabolites (leukotriene, prostaglandins, prostacyclins) • inhibition of phospholipase A2 • repression of COX2 expression • inhibition of NFkB

Answer 247

• Broadly immunosuppressive • inhibit inflammation that occurs at the boundary of donated tissue • inhibits antigen release from the grafted/donor tissue • SE: increase susceptibility to infection

Answer 248

They inhibit the synthesis of histamine by mast cells, limiting the duration of an allergy attack

Answer 249

• hyperglycemia • infection • cardiac: increased to contractility, increased blood pressure, increased sodium and water retention • CNS: lowers seizure threshold, behavioral changes (mood depression, elevation, anxiety/psychosis)

Answer 250

The inhibition of prostaglandin and prostacyclin increase the gastric acid and pepsin secretion. May suppress local immune response to H. pylori

Answer 251

Direct inhibition of osteoblasts —> secondary stimulation of PTH which stimulates osteoclasts —> osteoporosis risk

Answer 252

• inhibits side chain cleavage (P450scc) and other CYP enzymes used for Cushing syndrome/hypercortisolism

Answer 253

• inhibit 11beta-hydroxylase interfering with cortisol and corticosterone (and therefore aldosterone) production. Used for the treatment of Cushing syndrome/hypercortisolism

Answer 254

• somatostatin analog: **pasireotide** • D2 agonist: **cabergoline, bromocriptine** • GR antagonist: **mifepristone**

Answer 255

• 24 hour urine free cortisol • ACTH stimulation (short test to confirm low cortisol post stimulation, long test to distinguish between primary and secondary hypocortisolism)

Answer 256

• 24 hour urine free cortisol • resting ACTH levels • dexamethasone drug challenge (low-dose test to determine if HPA is normal/abnormal, high dose test to determine pituitary/non-pituitary)

Answer 257

Compare blood cortisol levels before and after IV tetracosactide (synthetic ACTH): 1. If serum cortisol has risen by 2x compared to normal, primary adrenal gland functioning is normal 2. If ACTH stimulation results in lower cortisol expected, hypo cortisol is occurring—> need long ACTH stimulation test

Answer 258

This test differentiates between primary and secondary adrenal insufficiency by using a larger dose of tetracosactide, and multiple administrations. Blood level is taken at one, four, eight, and 24 hours: 1. If primary hypocortisolism/Addison disease, cortisol level is reduced at all time points 2. Secondary hypocortisolism, the adrenal gland is still responsive to ACTH but has a delayed production of cortisol (normal response overtime)

Answer 259

Dexamethasone suppression test: • cortisol analog, administration should lead to reduction in CRH and ACTH. Cortisol level should also be reduced if the HPA is functional

Answer 260

• high ACTH level • low-dose dexamethasone suppression test: no change • high dose test: normal suppression

Answer 261

• ACTH is low • low-dose dexamethasone suppression test: no change • high dose test not needed

Answer 262

• ATH level is high • low-dose dexamethasone suppression test: no change • high dose test: no change

Answer 263

• decreased renal perfusion (renal artery stenosis, arterial nephrosclerosis) • arterial hypovolemia and edema (CHF, cirrhosis, nephrotic syndrome) • pregnancy (estrogen induces increases in plasma rennin)

Answer 264

• An acute adrenal cortical insufficiency due to overwhelming bacterial infection with Neisseria meningitidis (or pseudomonas, pneumococcal, haemophilus, staphylococcus) more common in children • rapid progressive hypotension and shock • DIC with widespread Purpura • massive adrenal hemorrhagic necrosis and adrenal cortical insufficiency

Answer 265

21-hydroxylase and 17-hydroxylase

Answer 266

• composed of chromaffin cells, releases catacholamines. Rare cause of surgically curable hypertension

Answer 267

• small blue cell tumor, primitive cells with scant cytoplasm and dark nuclei • mitotic activity and Karyorrhexis, pleomorphism prominent • Hommer-wright pseudorosettes can be seen

Answer 268

• complete maturation of neuroblastoma • no residual small blue cell component • ganglion (arrow) and Schwannn cells • schwannian stroma in a neuroblastoma is associated with a more favorable prognosis

Answer 269

**age and stage** 1. younger than 18 months 2. stage 1, 2, and 4S 3. Neuronal differentiation 4. Hyperdiploidy

Answer 270

MYC amplification

Answer 271

Deterioration of bone mass that is unassociated with other chronic illnesses. Related to aging and decreasing gonadal function.

Answer 272

Osteoporosis that results from chronic conditions that contribute significantly to accelerated bone loss. These chronic conditions include endogenous and exogenous thyroxine excess, hyperparathyroidism, malignancies, gastrointestinal diseases, medication, renal failure, and connective tissue diseases.

Answer 273

Interpretation of bone density in standard deviations when in comparison to a healthy 35-year-old of the same gender (peak bone mass)

Answer 274

Bone density scan in comparison to someone of approximately the same age, sex, ethnicity, height, and weight (similar cohort). Commonly used in menopausal and perimenopausal women

Answer 275

• endocrine (thyroid, hyperparathyroidism, DM, low testosterone) • G.I. (absorption, etc.) • renal disease • medication • nutrition (low calcium, anorexia, vitamin D deficiency, alcoholism) • malignancy (multiple myeloma) • collagen/genetic disorders

Answer 276

* CMP with calcium and phosphate * CBC * vitamin D (25-hydroxy vitamin D) * TSH * PTH * 24 hour urine calcium and creatinine

Answer 277

Excess production of PTH due to enlargement of one or more of the parathyroid glands. Excess PTH causes hypercalcemia

Answer 278

Excess production of PTH produced by the body because calcium levels are too low. Renal failure is the most common cause of secondary hyperparathyroidism. Also seen with low vitamin D levels, or calcium absorption in the gut

Answer 279

• calcium levels > 1 unit above normal • osteoporosis • CrCl (creatinine clearance) < 60 • 24 hour urine calcium > 250 mg/day in women or >300 mg/day in men • nephrolithiasis or nephrocalcinosis • age < 50

Answer 280

• increased risk of fracture • increased urinary tract infections due to kidney stones/blockage • PUD • pancreatitis • pseudogout • low blood calcium levels—> tetany (peripheral/mouth tingling and muscle twitching)

Answer 281

• **insulin sensitizer:** enhances the effects of insulin by decreasing hepatic glucose production, decreasing intestinal absorption of glucose, and improving insulin sensitivity • **MECH:** suppression of mitochondrial respiratory chain, activation of AMPK, increase insulin receptor TK activity, stimulation of GLUT4 transporter • **SE: lactic acidosis**, Caution in renal insufficiency patients, diarrhea

Answer 282

• **insulin sensitizers:** enhance the effects of insulin by increasing uptake and storage of glucose and skeletal muscle/adipose tissue • **MECH:** PPAR-gamma ligands that can modulate expression of genes involved in in lipid/glucose metabolism—> increase GLUT1, GLUT4, decreased FFA levels, decreased hepatic glucose output • **SE:** weight gain, LE edema, heart failure/CV events, bladder cancer **requires insulin presence for action**

Answer 283

• **insulin secretogogues:** promote pancreatic beta cell insulin secretion by binding to sulfonylurea receptor **(SUR1)** of beta cells **(ATP sensitive potassium channel)** causing an increased depolarization and release of insulin • **SE:** hypoglycemia and weight gain

Answer 284

• **insulin secretogogues:** promote pancreatic beta cell insulin secretion by binding to sulfonylurea receptor **(SUR1)** of beta cells **(ATP sensitive potassium channel)** causing an increased depolarization and release of insulin in a different binding site than that of sulfonylurea drugs • **SE:** hypoglycemia and weight gain

Answer 285

• **Incretin modulators:** promote pancreatic beta cell insulin aggregation by stimulating insulin and inhibiting glucagon secretion, delaying gastric emptying, and inducing safety • **SE:** pancreatitis, C-cell tumors in individuals with thyroid cancer/MEN2

Answer 286

• **Incretin modulators:** promote pancreatic beta cell insulin aggregation by inhibiting the breakdown of incretins (GIP, GLP1) • **SE:** GI, pancreatitis

Answer 287

• **Alpha-glucosidase inhibitor:** impair GI carbohydrate absorption by competitively inhibiting the intestinal alpha-glucosidase enzymes, delaying digestion and absorption of polysaccharides and diet • **SE:** GI

Answer 288

• **Amylinomimetics:** slows gastric emptying, promotes satiety by binding to amylin receptors leading to the inhibition of glucagon release and inhibition of glucose synthesis in the liver • **SE:** severe hypoglycemia in combination with insulin

Answer 289

• **Sodium glucose transporter-2 (SGLT2) inhibitors:** increase glucose excretion by the kidneys in the proximal tubule • **SE:** genital infections/urinary tract infections (due to increased glucose excretion) dehydration, polyuria **may have some renal benefits, decreased risk of dialysis, transplantation, death**

Answer 290

• analogues: insulin lispro, aspart, and glulisine • inhaled human regular insulin • typically given as a bolus during meal time to compensate for carbohydrates

Answer 291

• human regular insulin • typically given as a bolus during meal time for carbohydrate compensation

Answer 292

• human NPH insulin • given as a basal/background insulin modulator in diabetic patients

Answer 293

• **insulin glargine, detemir, and degludec** • have a flat peak of action and a long effective duration used for basal/background insulin modulation and diabetic patients

Answer 294

• hypoglycemia • weight gain • allergic reactions (injection site) • atrophy or hypertrophy of subcutaneous fat at injection site • insulin resistance

Answer 295

• rare, autosomal dominant, monogenetic disorders caused by mutations in single genes that disrupt pancreatic beta cell function

Answer 296

• insulin is not made because pancreatic beta cells are destroyed • auto immune process, T cell receptors recognizing self antigen are not eliminated because of genetic defect in immune system —> T cells expressing TCR which recognize beta cell peptides as antigen destroy beta cells

Answer 297

• auto antibodies to islet proteins in patients • insulitis: infiltration of T cells • recognize and proliferate in response to beta cell antigens

Answer 298

• DR4-DQ8 • DR3-DQ2

Answer 299

Anti-CD3 antibody, blocks TSS interaction with antigen presenting cell. It can delay the progression to clinical type one diabetes

Answer 300

Excess nutrients at cellular level leading to hyperglycemia, increased circulating free fatty acids —> inflammation, regulated lipid metabolism —> insulin resistance —> beta cell destruction, insufficiency (or compensation)

Answer 301

• TCF7L2 and PPAR-gamma — transcription factors • KCNQ1 — potassium ion channel • zinc transporter • insulin receptor substrate (IRS)

Answer 302

1. Adipocytes expand beyond limits of O2 diffusion 2. Extreme stress —> secretion of MCP-1 —> recruitment of macrophages —> **secretion of TNF alpha —> insulin resistance**

Answer 303

• inhibition of PPAR-gamma • activation of JNK leading to the inhibition of insulin receptor signaling • amplification of inflammatory response (activation of NFKB)

Answer 304

Insulin resistance and skeletal muscle

Answer 305

JNK, and AKT are inhibited—> GLUT4 does not move to cell surface in response to insulin

Answer 306

* ability of insulin to regulate metabolic pathways * gluconeogenesis increased (FOXO1) * glycogen synthesis decreased (GSK3, glycogen synthesis)

Answer 307

Insulin resistance amplifying hypernutrition —> oxidative stress, endoplasmic reticulum stress —> apoptosis (unfolded protein response, caspase 1, cytokine IL1-beta)

Answer 308

1. Oxidative and ER stress 2. Advanced glycation end products (AGE) 3. Polyol/sorbitol pathway

Answer 309

• non-enzymatic modification of proteins by sugar due to hyperglycemic environments • accumulates in vessel walls promoting cross-linking and additions of bulky non-functional modifications • binds RAGE on macrophages and causes ROS/release of inflammatory cytokines

Answer 310

Hyperglycemia leads to distorted glucose metabolism—> hexokinase is saturated and glucose can enter polyol pathway (creating sorbitol, and depleting NADPH leading to more oxidative stress and increased osmolality/swelling/tissue damage)

Answer 311

• accelerated atherosclerosis • stroke • myocardial infarction • lower extremity ischemia and peripheral vascular disease

Answer 312

• diabetic retinopathy • diabetic nephropathy • diabetic neuropathy

Answer 313

1. Formation of advanced glycation end (AGE) products 2. activation of protein kinase C 3. Oxidative stress and disturbances in the polyol pathways 4. Hexosamine pathways and generation of fructose-6-phosphate

Answer 314

1. Contraction bands at hours- 1-2 days 2. Neutrophil and then macrophages at 3-4 days 3. Granulation tissue at 7-10 days 4. Scar at weeks-months

Answer 315

• chronic arterial glomerulosclerosis and arterionephrosclerosis • granular surface, small kidney, thinned cortex • Kimmelstei-Wilson nodules peripherally • glomerular hyaline arteriosclerosis • tubular basement membrane thickening

Answer 316

• cataracts: opaque lens • glaucoma: increased intraocular pressure • retinal vasculopathy and neovascularization

Answer 317

Glutamic acid decarboxylase (GAD) -65

Answer 318

1. One hour test, if glucose > 140 mg/dL three hour test 2. Three hour test: One glucose check every hour, 2 reads > 190 mg/dL indicates gestational diabetes

Answer 319

• fasting plasma glucose greater than one 26 mg/dL on two separate occasions • random plasma glucose of 200 mg/dL with symptoms (polyuria, polydipsia, weight loss) • plasma glucose greater than 190 mg/dL three hours after a 75 g oral glucose load (pregnancy) • glycosylated hemoglobin (A1C) > 6.4%

Answer 320

**Lactic acidosis** especially when combined with IV contrast

Answer 321

• GLP-1 agonist and SGLT2 inhibitors

Answer 322

• steatohepatitis • elevated triglycerides/low HDL • hyperuricemia (gout) • acanthosis nigricans

Answer 323

• heart disease and stroke (2-4x) • kidney failure (44% of new cases) • blindness (leading cause) • lower limb amputations (over 60% of new cases)

Answer 324

Typically 100 mL/Kg — **fluid replacement is essential**

Answer 325

• hypertension > 130/80 • hypertriglyceridemia > 150 • low HDL cholesterol < 40 in men, < 50 in women • obesity (central-apple shaped) BMI > 30 • impaired glucose handling (insulin resistance) BG > 100 • microalbuminuria

Answer 326

• prothrombotic state • elevated fibrinogen, plasminogen activator inhibitor-1, and other coag factors • TX: low-dose aspirin, clopidogrel

Answer 327

Sleep deprivation— fewer than six hours per night

Answer 328

The liver via glycogenolysis and gluconeogenesis

Answer 329

• increased glycogen synthesis • increased fatty acid synthesis • increased triglyceride synthesis • increased liver glycolysis

Answer 330

• increased glycogenolysis • increased gluconeogenesis • increased lipolysis • decreased liver glycolysis

Answer 331

• autosomal dominant call by mutation and Glucokinase • insulin is not released appropriately when blood glucose increases

Answer 332

• glucose 6-phosphatase • PEP-CK ~ their expression is controlled by transcription factor FOX01

Answer 333

PKB (Akt), which is activated by insulin

Answer 334

* CREB * PGC1-alpha ~ glucagon stimulates protein kinase A (PKA) through cAMP —> PKA phosphorylates CREB —> CRE activates PGC1-alpha

Answer 335

• Somatostatin • IGF-1 (insulin-like growth factor) by inhibiting GHRH

Answer 336

promote gluconeogenesis, fatty acid biosynthesis, and bile acid synthesis

Answer 337

In the cortex

Answer 338

• oogonia enlarge and become primary oocyte • divide up until **prophase of meiosis 1** (arrested here until adulthood)

Answer 339

* first meiotic division completed just prior to ovulation (one oocyte per month) * secondary oocyte proceeds to **metaphase 2 of meiosis 2** (arrested here until fertilization)

Answer 340

* primary oocyte (arrested in prophase of meiosis 1) * follicular cells (single layer of flattened cells, germinal epithelial cells) * FSH receptors: responsive to maturation stimulus

Answer 341

• primary oocyte • follicular cells divide, become columnar and stratified (granulosa cells) —> these contribute to the zona pellucida (eosinophilic gel like neutral protein)

Answer 342

• primary oocyte still in prophase 1 • follicular fluid production (granulosa cells secrete GAGs/proteoglycans that generate osmotic gradient to draw water into the theca interna) • Antrum (fluid filled a space) begins to form

Answer 343

• highly vascular • epithelioid • smooth ER, produces androgens

Answer 344

• produce aromatase to convert hydrogen into estrogen • response to FSH by secreting inhibin (negative feedback) • estrogen increases FSH receptors

Answer 345

* **corona radiata:** granulosa cells in direct contact with the oocyte, cells radially arranged around zona pellucida * **cumulus oophorus:** granulosa cells that anchor the oocyte to the basal lamina * **theca folliculi:** reach their greatest development and produces androgens

Answer 346

Luteinizing hormone

Answer 347

• thinning of ovarian wall adjacent to tunica albuginea • decreased blood flow, protease released by follicle cells • rupture of epithelium and explosion of cumulus mass and follicular fluid—> captured by oviductal fimbriae

Answer 348

• stimulates granulosa cell growth and estrogen synthesis • stimulates the formation of LH receptors and augments responsiveness

Answer 349

• stimulates thecal cell growth and androgen production • stimulates progesterone production in granulosa cells

Answer 350

• temporary glandular structure derived from remnants of ruptured follicle following ovulation • granulosa sells become granulosa lutein cells • theca interna cells become theca lutein cells

Answer 351

• corpus luteum graviditatis • forms shortly after implantation (around nine days) • becomes large, around 5 cm • maintained by hCG produced by trophoblast of placenta and persists during first trimester

Answer 352

• produced primarily by growing follicles (theca makes androgen, granulosa converts to estrogen via aromatase) • induces maturation of female reproductive tract and mammary glands • directs the repair of the uterus following menstruation and influences growth of mammary glands in pregnancy

Answer 353

• produced primarily by corpus luteum (post ovulatory levels are high) • causes uterine gland to secrete and prepares uterus for implantation of fertilized ovum • aids in the growth of mammary glands • inhibits uterine contractions (allowing for pregnancy)

Answer 354

• produced by corpus luteum and decidual cells of the placenta • inhibits contractions of myometrium during pregnancy and promotes dilation of the cervix by softening it

Answer 355

• produced by granulosa cells, found in follicular fluid • negative feedback to anterior pituitary, **reduces FSH release**

Answer 356

• follicular atresia, oocyte degenerates first, then follicular cells and then theca interna (inside out) • entire structure replaced by scar tissue and can occur at any stage of oogenesis

Answer 357

**1. Infundibulum:** funnel shaped opening near the ovary with its fimbriae **2. Ampulla:** sight of fertilization **3. Isthmus:** narrowing **4. Intermural portion:** lies within uterine wall and opens into cavity of uterus

Answer 358

1. Mucosa (endosalpinx— simple columnar) 2. Muscularis (myosalpinx) 3. Serosa (peritoneal/mesothelial cells— simple squamous)

Answer 359

• simple columnar epithelium with ciliated cells stimulated by estrogen (transport) • secretory cells: non-ciliated, peg cells (fluid production, proteins, ions, stimulated by progesterone)

Answer 360

1. Endometrium (mucosa) 2. Myometrium (muscularis) 3. Perimetrium (serosa)

Answer 361

• **epithelium:** simple tubular glands (exocrine) and a simple columnar epithelium, and lamina propria • **basal layer:** deepest, not shed during menstruation (responsible for regeneration of the functional layer) • **functional layer:** superficial and deep layers, responsible for shedding during menstruation

Answer 362

1. Superficial compact layer: • narrow, ciliated cell • no edema • contains a straight portions of tubular glands 2. Deep spongy layer • thick, secretory cells • edematous • glance or tortuous and have large lumens

Answer 363

• shortest: the week after menstruation • longest: fourth week of the cycle ~ cyclical every 28 days, hormone responsive

Answer 364

1. Proliferative phase (estrogenic, follicular) 2. Secretory phase (progestational, luteal) 3. Premenstrual (ischemic) 4. Repair phase

Answer 365

• days 7-14 • begins at end of menstrual flow and repair • induced by estrogen, 2-3x increase in endometrial thickness • straight tubular glands increase in number and length, cells accumulate glycogen • coiled arteries elongate

Answer 366

• days 15-26 • ovulation precipitates formation of corpus luteum • progression increases dramatically, estrogen increases slightly • endometrial thickening continues (strum edema, gland dilate and become secular/tortuous) • glycogen salts and protein increase

Answer 367

• days 26-28 • corpus luteum regresses, decreases steroid output (decreased progesterone) • coiled arteries constrict intermittently leading to ischemia and necrosis • leukocyte infiltration occurs

Answer 368

• menstrual: days 1-4 • functional layer of endometrium undergo complete necrosis and his shed • repair phase: days 5-6 • Denuded surface is re-epithelialized and coiled arteries regrowth

Answer 369

• estrogenic: at ovulation, low viscosity, permits sperm migration, egg white consistency • gestrogenic: high viscosity, prevents fertilization of the wrong time by inhibiting particle passage

Answer 370

Simple columnar with occasional ciliation —> Stratified squamous non-keratinized epithelium ~ **squamocolumnar junction is site of most pre-cancerous lesions**

Answer 371

• estrogen stimulates epithelial cells to synthesize and store glycogen, which is metabolized by **lactobacilli** • produces lactic acid and an acidic environment **(low pH in vaginal lumen helps restrict pathogenic invasion)**

Answer 372

• neuropeptide, ligand of G protein coupled receptor 54 • mutation can cause hypogonadotrophic hypogonadism • pulsatile kisspeptin increase occurs at puberty onset

Answer 373

0.3-0.55 IU/L

Answer 374

• onset of adrenal androgen production, independent of the pubertal maturation of the HPG axis • secretes weak hydrogens DHEA and DHEAS, and androstenedione Beginning at age 6/7 in girls and 7/8 in boys

Answer 375

Onset of sexual hair growth (androgen effect)

Answer 376

Onset of breast development (estrogen effect)

Answer 377

Onset of menses

Answer 378

The onset of pubertal function of the gonads (sex hormone production, gametogenesis)

Answer 379

The appearance of spermatozoa in Seminal fluid

Answer 380

Tanner stage two classified by breast development in women, and testicular size in menis considered puberty onset

Answer 381

• genetics • nutritional status (higher BMI= earlier puberty onset. Malnutrition/illness= delayed puberty) • skeletal maturation (puberty stage correlates better with bone age than chronological age) • stress, trauma, ACEs

Answer 382

• reduced adult height • cancer: testicular/breast • metabolic syndrome • polycystic ovarian syndrome • risky behavior and substance use • depression and eating disorders

Answer 383

Girls: onset of breast development before age 8 Boys: increase testicular volume (>4mL) boys before age 9 ~ progressive and accompanied by acceleration of bone age and linear growth

Answer 384

The absence of somatic signs of puberty development at an age to standard deviations higher than the mean (approximately 14 for boys and 13 for girls)

Answer 385

Onset of Tanner stage 2: Girls: presence of visible breast buds Boys: testicular volume > 4mL or length of the ovoid testicle >2.5cm

Answer 386

• central precocious puberty involving HPG axis • true puberty, puberty levels of gonadotropins • producing sex steroids • normal puberty sequence of events happening earlier • isosexual (development aligned with biological sex)

Answer 387

• peripheral precocious puberty • pseudoprecocious puberty • pre-puberty levels of gonadotropins, sex steroids may be from gonads or non-gonadal sources (adrenal, exogenous, ectopic) • abnormal sequence of events • can be isosexual or contrasexual

Answer 388

• CNS lesions: hypothalamic hamartoma, tumors, cerebral malformation, CNS injury • idiopathic (most common) • genetic • internal adoption

Answer 389

• autonomous gonadal activation: McCune Albright syndrome, genetic disorder • tumors: gonads, liver, mediastinum • adrenal: congenital adrenal hyperplasia • exogenous sex steroids

Answer 390

• transient breast development between 6 to 12 months of age • spontaneously regressed by three years, no other secondary sex characteristic development • no height acceleration

Answer 391

• pubic and/or axillary hair before 8 years • no other secondary sex characteristic development • no height acceleration

Answer 392

• genetic: - Kleinfelter syndrome (47, XXY) - Turner syndrome (45, XO) - Female carriers of fragile X • acquired: - Chemotherapy, radiation - Infectious disease (mumps) - Autoimmune (oophiritis) - Gonadal trauma/surgery

Answer 393

• **pathologic: abnormal HPG** - Congenital GnRH deficiency - Acquired: trauma, tumor, infiltrative disease • **physiologic: functional issue with HPG** - secondary chronic illness: leukemia, anorexia - functional hypothalamic amenorrhea