Week One Day 2

Front 1

Adenodypophysis

Back 1

Anterior Pituitary

Front 2

Neurohypophysis

Back 2

Posterior Pituitary

Front 3

Connects the hypothalamus to the pituitary gland

Back 3

Infundibular stalk
COMPRESSION OF STALK will cause decreased dopamine-->Increased Prolactin!!!
Macroadenoma

Front 4

List the Anterior Pituitary Hormones (synthesized and secreted)

Back 4

Prolactin
Growth Hormone
ACTH
LH
TSH

Front 5

List the Posterior Pituitary Hormones that are STORED and secreted (Made in the hypothalmus: supraoptic and paraventricular nuclei)

Back 5

Vasopressin (AVP) or antidiuretic hormone
Oxytocin

Front 6

What regulates prolactin and where does it come from?

Back 6

Dopamine; comes from hypothalamus

Front 7

What stimulates Prolactin synthesis and secretion?

Back 7

reduced dopamine availability to the
lactotroph
thyrotropin‐releasing hormone (TRH)
estrogen
vasopressin
vasoactive intestinal polypeptide (VIP)
oxytocin
epidermal growth factor.

Front 8

What are the functions of prolactin?

Back 8

Breast differentiation
Duct proliferation and branching
Glandular tissue development
Milk protein and lactogenic enzyme synthesis

Front 9

What drugs can raise the prolactin levels?

Back 9

Metoclopramide and Risperidone
They are dopamine antagonists
Increase prolactin >200 ng/ml
Also could be estrogens, methyldopa, antipsychotics that block dopamine receptors
A prolactinoma has a concentration >250

Front 10

Mild to moderate hyperprolactinemia (25-100 ng) is typically d/t?

Back 10

Nonprolactin-secreting tumor with infundibular stalk compression and inhibition of dopamine transport to the lactograph

Front 11

What are the physiological causes of hyperProlactinemia?

Back 11

Pregnancy
Lactation

Front 12

Clinical presentation of Hyperprolactinemia

Back 12

young menstruating women present with menstrual irregularities, galactorrhea, and infertility
Men have decreased libido and ED (d/t inhibition of prolactin inhibiting FSH and LH)

Macro more common in Men then women (menstual sx show early)

Can have vision changes d/t optic chiasm compression

Front 13

Tx of Hyperprolactinemia

Back 13

Dopamine agonist-->Cabergoline (preferred) or Bromocriptine (patients undergoing fertility induction; requires more dosing)

Both reduce tumor size and restore gonadal function

Other Tx: resection, asymptomatic=no tx, Radiation therapy (unresectable; no dopamine)

Front 14

Somatostatin

Back 14

Major inhibitory factor for GH release

Front 15

GHRH

Back 15

Stimulates GH release

Front 16

What does GH stimulate? and function

Back 16

IGF-1 (insulin-like growth factor-1); is mostly bound to a protein called IGFBP-3; made in the liver

critical in determining longitudinal skeletal growth and skeletal maturation; carb, lipid and protein metabolis,; increase lypolysis and free fatty acid production; increase protein synthesis

Front 17

unrestrained hypersecretion of GH in adulthood

Back 17

Acromegaly
d/t a GH-secreting pituitary tumor (usually secrete prolactin too)

Front 18

Excessive GH secretion prior to closure of epiphyseal growth plate

Back 18

Gigantism
d/t a GH-secreting pituitary tumor (usually secrete prolactin too)

Front 19

Clinical presentation of Acromegaly

Back 19

Usually present for years; Enlargement of bones and soft tissues of hands and feet; mandible enlargement,, HTN, Viscermegaly, Menstrual abnormalities, hypogonadism, DM type 2, cardiomyopathy, Headache

Front 20

Diagnosis of Acromegaly

Back 20

Measure serum IGF-1 (usually in excess; has a longer 1/2 life than GH) False negs could include: estrogen ingestion, liver disease, uncontrolled DM, malnutrition

ORAL GLUCOSE tolerance test; usually glucose suppresses GH, but with acromegaly GH levels wont decrease substantially

Front 21

Tx of Acromegaly

Back 21

Transsphenoidal surgery (primary therapy)
Radiation (remission high; can cause Hypopituitarism; need to treat for 5-15 years)
Drug: Octreotide and Lanreotide (GH receptor antagonists; somatostatin; cause diarrhea and abd cramping); Pegvisomant (dopamine antagonist (can cause elevated LFTs and increase tumor size!)

Front 22

Deficiency of all anterior pituitary hormones

Back 22

Panhypopituitarism

Front 23

Manifestations of ACTH deficiency

maybe dont need to know

Back 23

Unintentional weight loss
Generalized weakness
Lethargy and fatigue
Nausea/vomiting/anorexia
Abdominal pain
Diffuse arthralgias and myalgias
Orthostatic hypotension
Hyponatremia
Hypoglycemia
Normal potassium and no hyperpigmentation with secondary adrenal insufficiency

Front 24

Manifestations of TSH deficiency
Same exact symptoms in secondary hypothyroidism

maybe dont need to know

Back 24

Weight gain
Generalized weakness
Fatigue and lethargy
Diffuse arthralgias and myalgias
Cold intolerance
Constipation
Dry skin and hair
Diffuse edema with periorbital edema
Bradycardia

Front 25

GH deficiency in adult manifestations

Back 25

Abnormal body composition with increased visceral fat and decreased lean muscle mass
Psychological impairment with reduced energy, social isolation, emotional lability, depressed
mood.
Reduced muscle strength and exercise performance
Reduced bone mineralization
Abnormal lipid profile with elevated LDL and TG and decreased HDL

Front 26

Gonadotropin deficiency or hypogonadotropichypogonadism manifestations
Males and females

maybe don't need to know

Back 26

Adult males: presents with decreased libido, sexual dysfunction, testicular atrophy, decreased
body or facial hair, decreased muscle mass, reduced bone mineralization
Adult females: amenorrhea is the hallmark of hypogonadotropichypogonadism in a
premenopausal woman, infertility, vaginal dryness, breast atrophy, reduced bone mineralization, decreased libido

Front 27

Lab levels in panhypopituitarism

Back 27

Low free T4 with low or inapp. normal TSH
ACTH or Insulin stim test to see if cortisol response is <18
Low Testosterone/estradiol with low or inapp. LH and FSH
Low IGF-1 (insulin tolerance test, GHRH-arginine stimulation test, glicagon stim test)

Front 28

Panhypopituitarism tx

Back 28

Hormone replacement
TSH-->LEVOTHYROXINE or T4
Estrogen and progesterone (female) also fertility drug Gonadotropin
Testosterone; fertility is HCG injections
GH is a subQ injection
Hydrocortisone in ACTH or Cortisol deficiency

Front 29

Neonate GH deficiency clinical signs

Back 29

Jaundice
Hypoglycemia
Microphallus
Traumatic delivery (contributing factor)

Front 30

GH deficiency clinical signs in the child

Back 30

Propensity for hypoglycemia
Increased fat
High‐pitched voice
Microphallus
Absent or delayed puberty in the adolescent
Weight less affected than height
central single tooth

Front 31

GH deficiency in children tx

Back 31

Recombinant human growth hormone; check IGF-1 to determine dose changes

Need smaller does of GH b/c they are more sensitive

Front 32

Histological feature of Pituitary adenoma

Back 32

Loss of mixture of cells seen in the normal anterior pituitary
Chromophobic staining
Supporting RETICULIN network is LOST

Front 33

What is the most common pituitary tumor?

Back 33

Prolactin cell adenoma
Chromophobic staining
More common in Women than men
Will have immunostaining against specific hormones

Front 34

Acidophilic staining

Back 34

Growth hormone adenoma

Front 35

Chromophobic staining

Back 35

Prolactin cell adenoma

Front 36

Basophilic Staining

Back 36

ACTH cell adenoma
Cushings disease

Front 37

Craniopharyngioma age peaks
and symptoms

Back 37

–Children (5 to 14yrs): usually adamantinomatous type
–Adults (65 to 74 yrs): usually papillary type

Visual abnormalities; hypopituitarism

Front 38

Microscopy of craniopharyngioma
Adamantinomatous and Papillary type

Back 38

Adamantinomatous-->Cystes filled with dark brown fluid (motor oil) and cholesterol crystals; PALISADING SQUAMOUS EPITHELIUM; ABUNDANT KERATIN

Papillary type-No Keratin formation

Front 39

Postpartum pituitary necrosis caused by ischemia of the pituitary gland

Back 39

Sheehan syndrome

Front 40

Cysts lined by ciliated cuboidal cells with scattered goblet cells and anterior pituitary cells

Back 40

Ranthke cleft cyst

Front 41

Hormones synthesized in hypothalamus and transported via axons

Back 41

Oxytocin and Antidiuretic hormone

Syndromes inclue SIADH and Diabetes insipidus

Front 42

What are the cell types in the parathyroid?

Back 42

Chief cells (main cell type)-secret PTH
oxyphilic cells (darker stained)
NORMAL parathyroid has a large amount of intervening stromal fat

Front 43

How is hormone secretion controlled in the parathyroid gland

Back 43

Calcium; related to bone disease-->osteitis fibrosia cystica; erosion of bone matrix by osteoclasts

Brown tumor-->reactive giant cells, hemorrhage (picture)

Front 44

Parathyroid adenoma histology

Back 44

Most common
solitary nodule in a SINGLE parathyroid gland
Loss of normal adipocytes
A rim of compressed normal parathyroid at periphery (on right in image)
Other glands may become atrophied

Front 45

Difference between parathyroid hyperplasia and adenoma

Back 45

Hyperplasia doesnt have a rim of normal gland at periphery and all 4 glands are involved

Front 46

Parathyroid carcinoma characteristics

Back 46

Firm (adenomas are soft); adheres to surrounding tissue d/t infiltration outside of the parathyroid capsule
Invade of surrounding tissue/metastasis
Look for mitotic activity, fibrous bands, and capsular/vascular invasion
Difficult to remove

Front 47

Cystic lesions within bone caused by bone resorption leading to thinned cortex and
marrow fibrosis with cystic degeneration

Back 47

Osteitisfibrosacystica
Bone lesion caused by hyperparathyroidism

Front 48

Brown tumors of hyperparathyroidism

Back 48

Aggregates of osteoclasts, reactive giant cells, and hemorrhagic debris form these
benign masses that can be mistaken for bone neoplasms

Front 49

Where is Ca mainly absorbed

Back 49

Duodenum and jejunum

Front 50

How is Calcium absorption regulated

Back 50

regulated by 1,25(OH)2D
Synthesis of 1,25(OH)2D is regulated by PTH

Front 51

Calcimimetic (cinacalcet) treats

Back 51

hyperparathyroidism' Will decrease PTH (neg feedback)

Front 52

Loss of CaSR function

Back 52

Familial hypocalciuric hypercalcemia (FHH)

Front 53

Gain of CaSR function

Back 53

Autosomal dominant hypocalcemia (ADH); excrete too much calcium; not enough Ca+2 in the blood

Front 54

Plant vit D

Back 54

D2

Front 55

PTH stimulates what reaction?

Back 55

1-hydroxylation of 25(OH)D in the kidney

Front 56

Symptoms of hypercalcemia

Back 56

Fatigue
Nausea, constipation
Anorexia
Polyuria, polydipsia
Memory impairment
Thinning of the bone cortex (can also cause Hyperparathyroid osteitis)

Can lead to a vicious cycle of hypercalcemia

Front 57

Primary Hyperparathyroidism can be d/t

Back 57

Sporadic (carcinoma, single gland disease)
Multiple endocrine neoplasias (MENs)
Hyperparathyroidism jaw tumor syndrome
FHH
Familial isolated hyperparathyroidism

Front 58

Familial Hypocalciuric Hypercalcemia

Back 58

Asymptomatic, modest LIFELONG (cant be aquired) hypercalcemia
Hypocalciuria
PTH not suppressed
Autosomal dominant
Surgery not indicated
THE KIDNEY IS GOING TO HOLD ONTO THE CALCIUM (receptors in the kidney too)

Front 59

Genetics of FHH

Back 59

– FHH1 Most families - CaSR (chromosome 3)
(~2/3)
• Codominant - neonatal severe
hyperparathyroidism

Not all FHH have CaSR mutations
Recent discovery of FHH2 and FHH3

Front 60

Causes of PTH-Independent Hypercalcemia

Back 60

Malignancy-->cone metastases, osteoclast activating factors, etc

Calcitriol mediated (inflammatory)

Hyperthyroidism
Milk/calcium-alkali syndrome
Immobilization

Front 61

Parathyroid-Hormone related peptide

Back 61

Humoral hypercalcemia of malignanc (breast, lung, kidney, squamous); Not measured on PTH assays

important in fetal development
found in high concentrations in milk

Front 62

Calcitriol (1,25[OH]2D)-Mediated Hypercalcemia
(Non-renal/unregulated expression of 1-hydroxylase)

Back 62

Sarcoid, Lymphoma

Front 63

Treatment of Hypercalcemia

Back 63

IV fluids
Loop diuretics-Furosemide (augment Ca+2 excretion; need to make sure that the pt is hydrated)
Calcitonin (Escape from the hormone)
Bisphosphophonates (inhibit osteoclastic bone resorption; preferred medication)

Front 64

Sx of Hypocalcemia

Back 64

Neuromuscular irritability (paresthesias, cramps, tetany)
Lowered seizure threshold
Mental status changes
Cardiac (prolonged QT, arrhythmias)
Basal ganglia calcification
Cataracts
Positive Chvostek's and Trousseau's sign

Front 65

Short stature
Round face
Short metacarpals (esp 4th)
Subq ossifications

Back 65

Albright's Hereditary Osteodystrophy (AHO)

Front 66

Hypoparathyroidism can be d/t

Back 66

• Genetic disorders
• Autoimmune
• Infiltrative
• Pseudohypoparathyroidism (PTH
resistance; GNAS mutation and Albright's)
– Type 1a has GNAS mutation and Albright’s
Hereditary Osteodystrophy (AHO)

Front 67

Tx of hypocalcemia

Back 67

Acute hypocalcemia is initially managed with IV calcium gluconate.
Chronic hypocalcemia due to hypoparathyroidism is treated
with calcium supplements and either vitamin D2 or D3 or calcitriol (calcitrol works better especially if they have primary hypoparathyroidism)

Front 68

FGF23

Back 68

made in bone cells
Increases Urinary Phosphate excretion
Decreases renal production of 1,25(OH)2D

kind of like the opposite to PTH

Front 69

Excess FGF23 causes

Back 69

hypophosphatemia and impaired bone mineralization

Front 70

Decreased FGF23

Back 70

Causes hyperphospatemia and tumoral calcinosis (very difficult to treat)

Occurs in many genetic forms of Rickets

Front 71

Causes of Hypophosphatemia

Back 71

Reduced renal tubular phosphate reabsorption
Excess FGF23 or other "phosphatonins"
Impaired intestinal phosphate absorption
• Shifts of extracellular phosphate into cells
Intravenous glucose
Insulin therapy for prolonged hyperglycemia or diabetic
ketoacidosis
Catecholamines (epinephrine, dopamine, albuterol)
Acute respiratory alkalosis
Rapid cellular proliferation
• Accelerated net bone formation
Intrinsic renal disease that causes phos wasting

Front 72

Causes of Hyperphosphatemia

Back 72

• Impaired renal phosphate excretion
Renal insufficiency
Hypoparathyroidism
Pseudohypoparathyroidism
Tumoral calcinosis
• Vitamin D intoxication
• Sarcoidosis, other granulomatous diseases
• Massive extracellular fluid phosphate loads
Rapid administration of exogenous phosphate
(intravenous, oral, rectal)
Extensive cellular injury or necrosis
• Transcellular phosphate shifts
Metabolic acidosis
Respiratory acidosis

Front 73

Macroadenoma

Back 73

Compression of infundibular stalk

Front 74

Presentation of Macroprolactinomas

Back 74

Headache, vision changes

Front 75

Dx of GH deficiency in Children

Back 75

Clonidine and Argining HCl tests

Front 76

Sheehan's Syndrome

Back 76

Postpartum ischemic necrosis of pituitary gland; Pituitary gland enlarges in pregnancy (d/t increased lactotrophs); obstetrical hemorrhage or shock

Sheets of dead areas in the pituitary

Front 77

Rathke Cleft Cyst Histology

Back 77

Columnar to cuboidal cells with cilia and occasionally mucin

Mass effect type lesion

Front 78

Large pituitary adenomas can cause

Back 78

bitemporal hemianopsia

Front 79

PTH effects

Back 79

Kidney: Ca++ reabsorption and convert 25(OH)D to 1,25(OH)2D

Intestine: Ca++ absorption

Bone: Ca++ resorption

Front 80

PTH and phosphate

Back 80

decreases phosphate absorption; carries large amounts of Ca in the urine

Front 81

Causes of PTH-independent Hypercalcemia

Back 81

Bone metastases, PTH-related protein, Unregulated Calcitriol production (1,25(OH)D), Hyperthyroidism (increases bone resorption), immobilization

Front 82

Create differential flow chart if patient has hypercalcemia

Back 82

Front 83

Create differential flow chart for Hypocalcemia with normal renal function

Back 83