Couga Endocrinology

Front 1

Peptide and Protein hormones
(a) solubility
(b) receptor location
(c) mechanism of action
(d) plasma protein binding
(e) synthesis

Back 1

(a) water soluble
(b) membrane surface
(c) 2nd messengers
(d) no (except somatomedins)
(e) RER

Front 2

Steroids and Thyroid Hormones
(a) solubility
(b) receptor location
(c) mechanism of action
(d) plasma protein binding
(e) synthesis

Back 2

(a) cytoplasm and/or nucleus
(b) mRNA transcription
(c) no (except thyroid as thyroglobulin)
(d) yes, acts as pool and prolongs effective half life
(e) smooth endoplasmic reticulum

Front 3

Name the steroid/thyroid hormones

Back 3

Progesterone
Estrogrogen
Testosterone
Cortisol
Aldoesterone
Thyrroxine and T3

Front 4

Result o f increased levels of sex hormone binding globulin in men

Back 4

Lower free testosterone (gynecomastia)

Front 5

Result of decreased sex hormone binding globuline in women

Back 5

High levels of free testosterone (hirsutism)

Front 6

Parathyroid hormone
(a) site produced
(b) stimuli to secretion or production
(c) effect on plasma free ca2+
(d) effect on plasma phosphate

Back 6

(a) site produced: parathyroid glands
(b) stimuli to secretion or production: low plasma Ca2+
(c) effect on plasma free ca2+: incr
(d) effect on plasma phosphate: decr

Front 7

1,25 OH VitD
(a) site produced
(b) stimuli to secretion or production
(c) effect on plasma free ca2+
(d) effect on plasma phosphate

Back 7

(a) skin to liver to kidney
(b) sunlight, PTH, dietary intake
(c) incr
(d) incr

Front 8

Calcitonin
(a) site produced
(b) stimuli to secretion or production
(c) effect on plasma free ca2+
(d) effect on plasma phosphate

Back 8

(a) site produced: parafollicular cells of thyroid
(b) stimuli to secretion or production: high plasma Ca2+
(c) effect on plasma free ca2+: decr
(d) effect on plasma phosphate: little to no effect

Front 9

Effect of PTH on
(a) kidney
(b) bone
(c) GI tract

Back 9

(a) incr Ca reabsorption; decr phosph reabs; incr production of 1,25(OH)2 vitD from precursor in liver
(b) receptors on osteoblasts ; rapid mobilization of Ca2+ from fluid; incr osteoclast activity via osteoblast mediators; cause bone resorption, release of Ca2+ and phosph
(c) indirectly stimulates Ca2+ and phosphate absorption via active vitD

Front 10

Effect of VitD (calcitriol) on
(a) kidney
(b) bone
(c) GI tract

Back 10

(a) decr Ca and phos excretion (incr reabsorption of both)
(b) incr resorption (w/PTH); release Ca2+ and phosphate into plasma (but normal growth and maintenance also requires both vitD and PTH)
(c) incr Ca2+ and phosphate absorption in intestine, incr both in plasma

Front 11

Effect of calcitonin on
(a) kidneys
(b) bone
(c) GI tract

Back 11

(a) incr phosphate excretion; decr Ca2+ excretion (minor)
(b) decr resorption; incr deposition; decr plasma Ca2+ (major effect)
(c) Incr Ca2+ and phos absorption in intestine (minor effect)

Front 12

Endocrine hormones that signal through cAMP

Back 12

FLAT CHAMP
FSH, LH, ACTH, TSH, CRH, hCG, ADH, MSH, PTH Calcitonin, glucagon

Front 13

Endocrine hormones that signal through cGMP

Back 13

ANP, EDRF, NO

Front 14

Endocrine hormones that signal through IP3

Back 14

GGOAT
GnRH, GHRH, Oxytocin, ADH (V1 receptor), TRH

Front 15

Endocrine hormones that signal through steroid receptors

Back 15

Glucocorticoid, Estrogen, Progesterone, Testosterone, Aldosterone, VitD, T3/T4

Front 16

Endocrine hormones that signal through tyrosine kinase

Back 16

Insulin, IGF-1, GFG, PDGF, Prolactin, GH

Front 17

prolactinoma
(a) epidemiology
(b) clinical presentation (males vs females)
(c) treatment

Back 17

(a) most common pituitary tumor
(b) Low libido/infertility
Males (galactorrhea and infertility)
Females (amenorrhea and galactorrhea)
(c) dopamine agonists (cabergoline, bromocryptine)

Front 18

Gigantism
(a) cause
(b) clinical presentation

Back 18

(a) excess GH secretion before fusion of growth plates
(b) excessive growth; eosinophilic granuloma

Front 19

Acromegaly
(a) cause
(b) clinical presentation
(c) diagnosis
(d) treatment

Back 19

(a) excess GH secretion after fusion of growth plates; circumferential deposition of bone in hands/feet
(b) large tongue w/deep furrows; large hands/feet; coarse facial featuresl deep voice; impaired glucose tolerance
(c) incr serum IGF-1; failure to suppress serum GH following oral glucose tolerance test
(d) pit adenoma resection followed by octreotide admin

Front 20

Dwarfism
(a) cause
(d) treatment

Back 20

(a) decr Gh or decr liver production of IGF (Laron syndrome) or defective GH receptors
(b) reversible w/GH treatment

Front 21

Large vs Small pituitary adenomas

Back 21

Large: can cause mass affect on optic chiasm (bitemporal hemianopia) and may invade surrounding structures
Small: usually secrete hormones so lesion is noticed when small due to hormonal effects

Front 22

Sheehan Syndrome
(a) cause
(b) clinical presentation

Back 22

Postpartum hypopituitarism
(a) enlargement of ant pit (incr lactotrophs) during pregnancy without incr blood supply incr risk of infarct following bleeding and hypoperfusion during delivery
(b) fatigue, anorexia, failure to lactate, loss of pubic and axillary hair

Front 23

Empty Sella Syndrome

Back 23

Atrophy of the pituitary; sella is enlarged on skull x ray and may mimic neoplasm

Front 24

Primary hypothyroidism
(a) T4
(b) TSH
(c) TRH
(d) gland mass (goiter?)

Back 24

(a) T4: low
(b) TSH: incr
(c) TRH: incr
(d) incr (goiter possible)

Front 25

Pituitary hypothyroidism
(a) T4
(b) TSH
(c) TRH
(d) gland mass (goiter?)

Back 25

(a) T4: low
(b) TSH: low
(c) TRH: high
(d) gland mass decr due to low TSH

Front 26

Hypothalamic hypothyroidism
(a) T4
(b) TSH
(c) TRH
(d) gland mass (goiter?)

Back 26

(a) T4 low
(b) TSH low
(c) TRH low
(d) gland mass decr due to low TSH

Front 27

Iodine deficiency (prolonged, severe)
(a) T4
(b) TSH
(c) TRH
(d) gland mass (goiter?)

Back 27

(a) T4 low
(b) TSH high
(c) TRH high
(d) increased gland mass and goiter likely

Front 28

Pituitary hyperthyroidism
(a) T4
(b) TSH
(c) TRH
(d) gland mass (goiter?)

Back 28

(a) T4 incr
(b) TSH incr
(c) TRH low
(d) increased gland mass, goiter possible

Front 29

Primary hyperthyroidism (tumor)
(a) T4
(b) TSH
(c) TRH
(d) gland mass (goiter?)

Back 29

(a) T4 incr
(b) TSH low
(c) TRH low
(d) decr due to low TSH

Front 30

Grave's disease
(a) T4
(b) TSH
(c) TRH
(d) gland mass (goiter?)

Back 30

(a) T4 high
(b) TSH low
(c) TRH low
(d) increased, goiter possible

Front 31

Hypothyroidism (adults)
(a) clinical findings
(b) Lab tests to order

Back 31

(a) cold intolerance, hypoactivity, wt gain, fatigue, lethargy, decr appetite, constipation, weakness, decr reflexes, myxedema (facial/periorbital), dry, cool skin, and coarse brittle hair
(b) Test TSH (high TSH sensitive for primary hypothyroidism); decr T4, Decr free T4, and decr T3 uptake

Front 32

Hypothyroidism (infants )clinical presentation

Back 32

Cretinism; protuberant abdomens, wide set eyes, dry rough skin, broad nose, delayed epiphyseal closure

Front 33

Hypothyroidism (older children) clinical presentation

Back 33

Short stature, retarded linear growth (GH deficiency caused by thyroid hormone deficiency), delayed onset of puberty

Front 34

Hyperthyroidism
(a) clinical findings
(b) lab tests to order

Back 34

(a) heat intolerance, hyperactivity, weight loss, chest pain/palpitations, arrhythmias, diarrhea, incr reflexes, warm, moist skin, and fine hair
(b) low TSH and elevated T4

Front 35

Graves disease
(a) epidemiology
(b) pathophys
(c) clinical presentation/complications
(d) pathology
(e) microscopic appearance

Back 35

(a)3rd and 4th decade peak; F>M; assoc w/other autoimmune dz
(b) Thyroid stimulating/TSH receptor antibodies.
(c) opthalmopathy (proptosis), pretibial myxedema, diffuse goiter;
Thyroid storm (stress induced catecholamine surge leading to death by arrhythmias)
(d) diffuse, moderate, symmetric gland enlargement
(e) hypercellular w/small follicles and little colloid

Front 36

Hashimoto's Thyroiditis
(a) pathophys
(b) epidemiology
(c) clinical presentation/complications
(d) microscopic appearance

Back 36

(a) autoimmune disorder resulting in hypothyroidism (antimicrosomal and antithyroglobulin Abs-against TSHR, T3, and T4)
(b) middle aged females; most common type of thyroiditis
(c) hypothyroidism; can have thyrotoxicosis during follicular rupture
Painless goiter, gland enlarged and firm
(d) lymphocytic and plasma cell infiltrate; Hurthe cells (eosinophilic granular cytoplasm in follicular cells)

Front 37

Diffuse Non Toxic Goiter
(a) pathophys
(b) clinical presentation

Back 37

(a) iodine deficiency
(b) diffuse enlargement of gland in euthyroid patients

Front 38

Subacute thyroiditis (deQuervan's)
(a) pathophys
(b) clinical presentation
(c) histology

Back 38

(a) self limited hypothyroidism often following flulike illness
(b) elevated ESR, jaw pain, early inflammation, very tender thyroid
NOTE: lymphocytic subacute thyroiditis is painless)
-may be hyperthyroid early in course
(c) granulomatous inflammation

Front 39

Reidel's thyroiditis
(a) pathophys
(b) clinical presentation

Back 39

(a) thyroid replaced by fibrous tissue (hypothyroid)
(b) presents with fixed, hard, painless goiter

Front 40

Toxic multinodular goiter

Back 40

Iodine deprivation followed by iodine restoration. Causes release of T3 and T4. Nodules are not malignant.

Front 41

Jod Basedow phenomenon

Back 41

Thrytoxicosis if patient w/iodine deficiency goiter is made iodine replete

Front 42

Cretinism
(a) cause (endemic vs sporadic)
(b) clinical presentation

Back 42

(a) endemic: lack of dietary iodine
Sporadic; caused by defect in T4 formation or developmental failure in thyroid formation
(b) pot bellied, pale, puffy faced child with protruding umbilicus and protuberant tongue; mental retardation

Front 43

Thyroid adenoma
(a) clinical presentation
(b) pathology

Back 43

(a) follicular adenoma most common; may cause pressure symptoms, pain, and rarely thyrotoxicosis
(b) small, well encapsulated solitary lesions

Front 44

Papillary carcinoma of the thyroid
(a) epidemiology
(b) histology
(c) metastasis/treatment/prognosis

Back 44

(a) most common; F>M; incr risk w/childhood radiation
(b) "ground glass" nuclei (orphan annie); psammoma bodies; nuclear grooves
(c) spread to local nodes common (hematogenous RARE); excellent prognosis (resection curative) usually

Front 45

Follicular carcinoma of the thyroid
(a) presentation
(b) histology
(c) metastasis/prognosis

Back 45

(a) dysphagia, dyspnea, hoarseness, cough
(b) uniform follicles; may be encapsulated w/penetration; sparse colloid
(c) hematogenous mets to lungs/bone common; good prognosis although more malignant than papillary

Front 46

Medullary carcinoma of the thyroid
(a) associations
(b) pathology

Back 46

(a) associated w/MEN 2A and 2B
(b) From parafollicular "C cells"; produces calcitonin, sheets of cells in amyloid stroma

Front 47

Undifferentiated/anaplastic thyroid carcinoma
(a) epidemiology
(b) pathology
(c) course/outcome

Back 47

(a) older patients
(b) rapid growing, bulky, invasive tumors w/undifferentiated anaplastic cells
(c) early, widespread mets and death w/in 2 yrs

Front 48

Diabetes Insipidus clinical presentation.
(a) clinical presentation
(b) diagnosis
(c) findings
(d) treatment

Back 48

(a) Intense thirst, polyuria w/inability to concentrate urine due to lack of ADH (central DI) or lack or renal response to ADH (nephrogenic D). Large volume of dilute urine (distinguises from dehydration).
(b) Water deprivation test: urine osmolality doesn't increase
(c) urine specific gravity ,1.006; serum osmolality >290
(d) adequate fluid intake
Central DI: intranasal desmopressin (ADH analogue)
Nephrogenic DI: hydrochlorothiazide, indomethacin, or amiloride

Front 49

How do you distinguish central vs nephrogenic diabetes insipidus?

Back 49

Test by response to ADH injection (nephrogenic will give no response; central will give response of increased concentration of urine)

Front 50

Causes of central diabetes insipidus

Back 50

Pituitary tumor, trauma, surgery, histiocytosis x

Front 51

Causes of nephrogenic diabetes insipidus

Back 51

Hereditary or secondary to hypercalcemia, lithium, demeclocycline [ADH antagonist]

Front 52

SIADH
(a) clinical presentation
(b) causes
(c) treatment

Back 52

(a) (1) excessive water retention (2) hyponatremia (3) urine osmolarity>serum osmolarity (small amnt of concentrated urine)
(b) (1) ectopic ADH (small cell lung cancer)(2) CNS disorders/head trauma (3) pulmonary disease (4) drugs (e.g. cyclophosphamide)
(c) demeclocycline or H20 restriction

Front 53

Primary polydypsia

Back 53

Hypervolemia, hyponatremia, large volume of dilute urine

Front 54

Findings in Cushing's syndrome

Back 54

Cortisol excess
HTN, wt gain, moon face, truncal obesity, buffalo hump, hyperglycemia (insulin resistance), skin changes (thinning, striae), osteoporosis, amenorrhea, and immune suppression

Front 55

Primary (adrenal) cortisol excess
(a) plasma cortisol
(b) plasma CRH
(c) plasma ACTH
(d) hyperpigmentation

Back 55

(a) plasma cortisol: high
(b) plasma CRH: low
(c) plasma ACTH: low
(d) hyperpigmentation: no

Front 56

Primary deficiency of cortisol
(a) plasma cortisol
(b) plasma CRH
(c) plasma ACTH
(d) hyperpigmentation

Back 56

(a) plasma cortisol: low
(b) plasma CRH: high
(c) plasma ACTH: high
(d) hyperpigmentation: yes

Front 57

Secondary (pituitary) excess
(a) plasma cortisol
(b) plasma CRH
(c) plasma ACTH
(d) hyperpigmentation

Back 57

(a) plasma cortisol: high
(b) plasma CRH: low
(c) plasma ACTH: high
(d) hyperpigmentation: yes

Front 58

Secondary deficiency of cortisol (pituitary)
(a) plasma cortisol
(b) plasma CRH
(c) plasma ACTH
(d) hyperpigmentation

Back 58

(a) plasma cortisol: low
(b) plasma CRH: high
(c) plasma ACTH: low
(d) hyperpigmentation: no

Front 59

Corticosteroid administration
(a) plasma cortisol
(b) plasma CRH
(c) plasma ACTH
(d) hyperpigmentation

Back 59

(a) plasma cortisol: low (but symptoms of excess)
(b) plasma CRH low
(c) plasma ACTH low
(d) hyperpigmentation no

Front 60

Results of dexamethasone suppression test (low and high dose)
(1) Healthy
(2) ACTH pituitary tumor
(3) ectopic ACTH
(4) cortisol producing tumor

Back 60

(1) healthy: decreased cortisol after low dose
(2) ACTH pituitary tumor: still high cortisol after low dose; decreased cortisol after high dose
(3) Ectopic ACTH producing tumor: high cortisol before low and high dose
(4) cortisol producing tumor: high cortisol before and after high dose

Front 61

Conn's disease
(a) cause
(b) clinical presentation
(c) lab values
(d) pathology
(e) treatment

Back 61

(a) increased aldosterone secretion (primary hyperaldosteronism); usually adrenal adenoma
(b) diastolic HTN, weakness, fatigue, polyuria, polydypsia, HA, no edema
(c) hypokalemia, low renin, metabolic alkalosis, hypernatremia, failure to suppress aldo w/salt loading
(d) single, well circumscribed adenoma (lipid laden clear cells)
(e) spironolactone (aldosterone antagonist)

Front 62

Secondary hyperaldosteronism
(a) etiologies
(b) clinical presentation
(c) lab values
(d) treatment

Back 62

(a) CHF, renal artery stenosis, chronic renal failure, nephrotic syndrome (kidney perception of low IVV results in overactive RAAS)
(b) same as for primary but edema may be present
(c) high renin, hypernatremia, hyokalemia
(d) spironolactone

Front 63

Addison's disease
(a) cause/description
(b) clinical presentation
(c) lab values
(d) pathology

Back 63

(a) primary deficiency of aldosterone and cortisol due to adrenal atrophy or destruction by disease (TB, infx, mets, hemorrhage)
(b) hypotension, skin pigmentation (MSH is a byproduct of ACTH production from POMC)
(c) ACTH high, cortisol and aldo levels low; hyponatremia; hyperkalemia
(d) bilateral atrophied adrenal glands

Front 64

Waterhouse-Friderichsen syndrome

Back 64

Acute adrenocortical insufficiency due to adrenal hemorrhage associated with meningococcal septicemia

Front 65

Secondary (pituitary) adrenocortical insufficiency
(a) etiology
(b) distinguished from primary how?

Back 65

(a) decreased pituitary secretion of ACTH; from mets, irradiation, infx, infarction affecting the HPA axis
(b) No skin hyperpigmentation or hyperkalemia

Front 66

Hypoaldosteronism
(a) presentation
(b) primary hypoaldosteronism lab values
(c) secondary hypoaldosteronism lab values

Back 66

(a) hyponatremia, hypovolemia, hypotension, metabolic acidosis, hyperkalemia
(b) primary; decr aldo, incr rening and AII
(c) secondary; decr aldo, decr renin and AII, dec total periphreal resistance

Front 67

Adrenal adenomas vs adrenal carcinomas (symptoms and gross appearance)

Back 67

Adenomas are usually asymptomatic and don't produce steroids (can cause Conn, Cushing, or virilization). Small, unilateral, yellow, poorly encapsulated
Carcinomas are rare and usually very malignant; 90% are steroid producing (large, yellow w/areas of hemorrhage and necrosis)

Front 68

Pheochromocytoma
(a) embryonic derivation
(b) tumor products
(c) clinical presentation
(d) lab values
(e) associations
(f) treatment

Back 68

(a) neural crest derived
(b) most produce epi, NE, and dopamine
(c) Pressure (elevated); Pain (HA); Perspiration; Palpitations (tachycardia); Pallor
(d) elevated catecholamines, urinary homovanillic acid and vanillylmandelic acid (breakdown products of NE)
(e) MEN 2A and 2B
(f) alpha antagonists, esp phenoxybenzamine (non selective irreversible alpha blocker)

Front 69

Rule of 10's for pheochromocytoma

Back 69

10% extraadrenal
10% bilateral
10% malignant
10% affect children
10% familial

Front 70

Neuroblastoma
(a) epidemiology
(b) gene association
(c) clinical
(d) pathology
(e) microscopic appearance

Back 70

(a) most common malignant extracranial solid tumor of childhood
(b) N-myc oncogene
(c) rapidly growing tumor, anywhere along sympathetic chain; mets esp to bone; less likely to develop HTN
(d) lobulated w/necrosis, hemorrhage, and calcification
(e) rosette pattern

Front 71

MEN 1 (Werner's syndrome)

Back 71

Parathyroid tumors
Pituitary tumors (prolactin or GH)
Pancreatic endocrine tumors (ZE syndrome, insulinomas, VIPomas, glucagonomas-rare)

Front 72

MEN 2A (Sipple's Syndrome)

Back 72

Medullary thyroid carcinoma (secretes calcitonin)
Pheochromocytoma
Parathyroid tumors

Front 73

MEN 2B

Back 73

Medullary thyroid carcinoma
Pheochromocytoma
Oral/intestinal ganglioneuromatosis (assoc w/maranoid habitus)

Front 74

MEN syndrome inheritence pattern

Back 74

All are autosomal dominant

Front 75

Which Men syndromes are assoc w/ret gen?

Back 75

MEN 2A and 2B

Front 76

Common characteristic of all congenital adrenal hyperplasias

Back 76

Bilateral adrenal hyperplasia with enlargement of adrenal glands and increased ACTH (due to decr levels of cortisol)

Front 77

Name the 3 most common enzymes deficient in congenital bilateral adrenal hyperplasia

Back 77

17 alpha hydroxylase
21 alpha hydroxylase
11beta hydroxylase

Front 78

17 alpha hydroxylase deficiency (congenital bilateral adrenal hyperplasia):
(a) glucocorticoids
(b) mineralcorticoids
(c) androgens
(d) Signs/sx

Back 78

(a) glucocorticoids : decr
(b) mineralcorticoids: incr
(c) androgens: decr
(d) Signs/sx: HTN, hypokalemia
Males: pseudohermaphrodism
Females: lack secondary sex characteristics

Front 79

21alpha hydroxylase deficiency
(congenital bilateral adrenal hyperplasia):
(a) glucocorticoids
(b) mineralcorticoids
(c) androgens
(d) Signs/sx

Back 79

Most common
(congenital bilateral adrenal hyperplasia):
(a) glucocorticoids : decr
(b) mineralcorticoids: decr
(c) androgens: incr
(d) Signs/sx: masculinization, female pseudohermaphrodism, hypotension, hyperkalemia, high renin, volume depletion

Front 80

11beta hydroxylase deficiency
(congenital bilateral adrenal hyperplasia):
(a) glucocorticoids
(b) mineralcorticoids
(c) androgens
(d) Signs/sx

Back 80

(congenital bilateral adrenal hyperplasia):
(a) glucocorticoids : decreased
(b) mineralcorticoids: decr aldo and corticosterone but incr 11deoxycorticosterone
(c) androgens: increased
(d) Signs/sx: masculinization, HTN (due to 11 deoxycorticosterone acting as a mineralcorticoid)

Front 81

20, 22 desmolase
(congenital bilateral adrenal hyperplasia):
(a) glucocorticoids
(b) mineralcorticoids
(c) androgens
(d) Signs/sx

Back 81

(congenital bilateral adrenal hyperplasia):
(a) glucocorticoids : low
(b) mineralcorticoids: low
(c) androgens: low
(d) Signs/sx: lethal if complete

Front 82

17,20 L
(congenital bilateral adrenal hyperplasia):
(a) glucocorticoids
(b) mineralcorticoids
(c) androgens
(d) Signs/sx

Back 82

(congenital bilateral adrenal hyperplasia):
(a) glucocorticoids : normal
(b) mineralcorticoids: normal
(c) androgens: decr
(d) Signs/sx: absent secondary sex characteristics of both sexes; amenorrhea

Front 83

Glucose counter regulation hormones

Back 83

Glucagon
Cortisol
Epinephrine
Growth hormone
Thyroid hormone

Front 84

Glucagon
Glucose counter regulation:
(a) stimulus
(b) actions

Back 84

(a) fasting, hypoglycemia, stress
(b) inhibits insulin response (mainly in liver), and promotes catabolism, gluconeogenesis, glycogenolysis

Front 85

Cortisol
Glucose counter regulation:
(a) stimulus
(b) actions

Back 85

(a) stress, fasting, hypoglycemia
(b) inhibits response to insulin, reduces cellular glucose uptake, permissive for lipolysis, increases gluconeogenesis and protein catabolism

Front 86

Epinephrine
Glucose counter regulation:
(a) stimulus
(b) actions

Back 86

(a) stress, severe hypoglycemia
(b) increases glycogenolysis and lipolysis

Front 87

Growth hormone
Glucose counter regulation:
(a) stimulus
(b) actions

Back 87

(a) fasting, sleep, stress
(b) inhibits cellular uptake of glucose, and stimulates lipolysis

Front 88

Thyroid hormone
Glucose counter regulation:
(a) stimulus
(b) actions

Back 88

(a) cold, stress
(b) permissive for epinephrines effects; required for production of GH

Front 89

Type I diabetes (juvenile onset, IDDM)
(a) primary defect
(b) insuline necessary treatment
(c) age (exceptions commonly occur)
(d) association with obesity
(e) genetic predisposition
(f) associations w/HLA system
(g) glucose intolerance
(h) ketoacidosis
(i) beta cell numbers in the islets
(j) serum insulin level
(k) classic symptoms of polyuria polydipsia thirst, wt loss
(l) insulin levels

Back 89

(a) primary defect: viral or immune destruction of beta cells
(b) insulin necessary treatment: always
(c) age (exceptions commonly occur): <30
(d) association with obesity: no
(e) genetic predisposition: weak/polygenic
(f) associations w/HLA system: HLA DR3, 4
(g) glucose intolerance: severe
(h) ketoacidosis: common
(i) beta cell numbers in the islets: decr
(j) serum insulin level: decr
(k) classic symptoms of polyuria polydipsia thirst, wt loss: common
(l) low serum insulin levels

Front 90

Type II diabetes (adult onset, NIDDM)
(a) primary defect
(b) insuline necessary treatment
(c) age (exceptions commonly occur)
(d) association with obesity
(e) genetic predisposition
(f) associations w/HLA system
(g) glucose intolerance
(h) ketoacidosis
(i) beta cell numbers in the islets
(j) serum insulin level
(k) classic symptoms of polyuria polydipsia thirst, wt loss
(l) insulin levels

Back 90

(a) primary defect: incr resistance to insulin
(b) insuline necessary treatment: sometimes
(c) age (exceptions commonly occur): >40
(d) association with obesity: Yes
(e) genetic predisposition: strong, polygenic
(f) associations w/HLA system: No
(g) glucose intolerance: mild to moderate
(h) ketoacidosis: rare
(i) beta cell numbers in the islets: variable (w/ amyloid deposits)
(j) serum insulin level (variable)
(k) classic symptoms of polyuria polydipsia thirst, wt loss: no
(l) high serum insulin levels

Front 91

Cause of diabetic ketoacidosis

Back 91

One of the most important complications in IDDM usually due to incr insulin requirements from incr stress. (infx). Excess fat breakdown and incr ketogenesis from FFA's are made into ketone bodies (betahydroxybutyrate>acetoacetate)

Front 92

Diabetic ketoacidosis
(a) signs
(b) labs
(c) treatment

Back 92

(a) Kussmaul respiration, n/v, abdominal pain, delirium, dehydration, fruity breath (acetone)
(b) hyperglycemia, incr H+, decr HCO3 (anion gap), incr ketones, leukocytosis. Hyperkalemia but depleted K+ due to K+ shift out of cells from decr insulin
(c) fluids, insulin, K+; glucose if necessary to prevent hypoglycemia

Front 93

Complications of DKA

Back 93

Life threatening mucomycosis, Rhizopus inx, cerebral edema, cardiac arrythmia, heart failure

Front 94

Hyperosmlar nonketotic coma

Back 94

In patients w/TIIDM
Blood glucose can be elevated. Treatment similar to DKA

Front 95

Patients w/DM are at high risk for what type of infections (over normal)

Back 95

Klebsiella
Sinus mucormycosis
Malignant otitis externa

Front 96

Beta cell tumors
(a) pathogenesis
(b) clinical features
(c) pathology

Back 96

(a) beta cell tumors produce hyperinsulinemia leading to hypoglycemia
(b) nausea, tremor, coma, disorientation, dizziness, etc relieved by glucose intake
(c) most are well differentiated adenomas; 10% are malignant

Front 97

Zollinger Ellison Syndrome
(a) cause
(b) associations
(c) clinical
(d) pathology

Back 97

(a) gastrinoma
(b) assoc w/MEN type I
(c) intractable peptic ulcer disease w/severe diarrhea
(d) 60% malignant, most tumors located in pancreas

Front 98

Carcinoid tumors
(a) clinical presentaiton
(b) cause
(c) treatment

Back 98

(a) diarrhea, cutaneous flushing, asthamatic wheezing, right sided valvular disease
(b) carcinoid tumors (neuroendocrine cells) esp metastatic small bowel tumors that secrete high serotonin levels. Not seen if tumor limited to GI (first pass metabolism in liver)
(c) octreotide

Front 99

Rule of 1/3's concerning carcinoid syndrome

Back 99

1/3 metastasize
1/3 present with second malignancy
1/3 multiple

Front 100

Type 2 diabetes
(a) glucose
(b) insulin
(c) C peptide
(d) ketoacidosis
(e) other features

Back 100

(a) glucose: incr
(b) insulin: high or normal
(c) C peptide: normal or incr
(d) ketoacidosis: uncommon
(e) other features: familial, often obese

Front 101

Type I DM
(a) glucose
(b) insulin
(c) C peptide
(d) ketoacidosis
(e) other features

Back 101

(a) glucose: incr
(b) insulin: decr
(c) C peptide: decr
(d) ketoacidosis: yes
(e) other features: often islet antibodies

Front 102

Insulinoma
(a) glucose
(b) insulin
(c) C peptide
(d) ketoacidosis
(e) other features

Back 102

(a) glucose: decr
(b) insulin: incr
(c) C peptide: incr
(d) ketoacidosis: no
(e) other features: tachycardia (epinephrine)

Front 103

Insulin overdose
(a) glucose
(b) insulin
(c) C peptide
(d) ketoacidosis
(e) other features

Back 103

(a) glucose: low
(b) insulin: high
(c) C peptide: low
(d) ketoacidosis: no
(e) other features: tachycardia (epinephrine)

Front 104

Fasting hypoglycemia
(a) glucose
(b) insulin
(c) C peptide
(d) ketoacidosis
(e) other features

Back 104

(a) glucose: decr
(b) insulin: incr
(c) C peptide: incr
(d) ketoacidosis: no
(e) other features: insulin remains at posprandial level in fasting

Front 105

Primary hyperparathyroidism
(a) plasma Ca
(b) plasma phos
(c) effects on bone

Back 105

(a) plasma Ca: incr
(b) plasma phos: decr
(c) effects on bone: demineralization and osteopenia

Front 106

Primary hypoparathyroidism
(a) plasma Ca
(b) plasma phos
(c) effects on bone

Back 106

(a) plasma Ca: decr
(b) plasma phos: incr
(c) effects on bone: malformation

Front 107

Deficient vitD
(a) plasma Ca
(b) plasma phos
(c) effects on bone

Back 107

(a) plasma Ca: decr
(b) plasma phos: decr
(c) effects on bone: osteonalacia in adults
Rickets in children

Front 108

Excess vitD (secondary hypoparathyroidism)
(a) plasma Ca
(b) plasma phos
(c) effects on bone

Back 108

(a) plasma Ca: incr
(b) plasma phos: incr
(c) effects on bone: osteoporosis

Front 109

Renal failure w/high plasma phosphate
(a) plasma Ca
(b) plasma phos
(c) effects on bone

Back 109

(a) plasma Ca: decr (precipitation)
(b) plasma phos: incr
(c) effects on bone: osteomalacia and osteosclerosis

Front 110

Primary hyperparathyroidism
(a) cause
(b) clinical presentation
(c) lab values

Back 110

(a) parathyroid adenoma usually cause
(b)often asymptomatic; can cause stones,bones, and groans
(c) elevated Ca; hypophosphatemia, incr PTH, incr alkP, incrcAMP in urine, inc

Front 111

Osteitis fibrosa cystica
(a) cause
(b) description

Back 111

(a) occurs in chronic primary hyperparathyroidism
(b) cystic changes in bone due to resorption; fibrous replacement may lead to "brown tumor"

Front 112

Renal osteodystrophy

Back 112

Bone lesions due to secondary hyperparathyroidism due in turn to renal disease

Front 113

Secondary hyperparathyroidism
(a) cause
(b) signs/symptoms
(c) lab values

Back 113

(a) most often chronic renal failure (causes hypovitaminosis D and decr Ca absorption); also vitD and malabsorption can cause
(b) may show soft tissue calcification and osteosclerosis
(c) incr PTH and alkP, hypocalcemia, hyperphosphatemia

Front 114

Hypoparathyroidism
(a) common causes
(b) clinical signs
(c) lab values

Back 114

(a) accidental surgical excision (thyroid surgery), autoimmune destruction, DiGearge syndrome
(b) tetany, irritability, ansiety, lens calcifications; Chvostek's sgn (tapping of facial nerve leads to facial muscle contraction); Trousseau's sign (occlusion of brachial artery w/BP cuff leading to carpal spasm)
(c) hypocalcemia, hyperphosphatemia

Front 115

Pseudohypoparathyroidism
(a) cause
(b) clinical signs

Back 115

(a) AR disorder resulting in kidney unresponsive to circulating PTH
(b) skeletal abnormalities, short stature, shortened 4th and 5th carpals and metacarpals

Front 116

Hypercalcemia
(a) common causes
(b) clinical presentation

Back 116

(a) CHIMPANZEES (calcium ingestion-milk alkali syndrome, Hyperparathyroid, Hyperthyroid, Iatrogenic-thiazides, multiple myeloma, Paget's disease, Addison's disease, Neoplasms, Zollinger Ellison, Excess vitD, Excess vitA, Sarcoidosis

Front 117

Somatropin/Somatrem
(a) mechanism
(b) indications

Back 117

(a) recombinant forms of GH; stimulates linear/skeletal growth for pediatric patients
(b) growth failure, Turner's, cachexia, somatotropin deficiency

Front 118

Octreotide
(a) mechanism
(b) indications

Back 118

(a) long acting octapeptide that mimics somatostatin; inhibits release of GH, glucagon, gastrin, thyrotropin, insulin
(b) acromegaly, carcinoid, glucagonoma, gastrinoma, other endocrine tumors

Front 119

Thioamides
(a) examples
(b) indications
(c) mechanism
(d) side effects

Back 119

(a) PTU, methimazole
(b) long term hyperthyroid tx
(c) inhibit synth against thyroid hormones (do NOT inactivate existing T4, T3); PTU can inhibit peripheral conversion of T4 to T3
(d) skin rash (common); hematologic effects (rare)

Front 120

Iodides
(a) examples
(b) indications
(c) mechanism

Back 120

(a) Lugol's solution, potassium iodide alone
(b) prep for thyroid surgery; treat thyrotoxic crisis and thyroid blocking in radiation emergency
(c) inhibit release of T4 and T4 (primary); also inhibit biosynth of T4, T3 and decrease size and vascularity of thyroid gland

Front 121

Beta blockers in thyroid treatment
(a) examples
(b) indication
(c) mechanism

Back 121

(a) nadolol, propranolol
(b) nonselective beta blockers used for palpitation, anxiety, tremor and heat intolerance; partially inhibit conversion of T4

Front 122

Radioactive iodine
(a) indications
(b) mechanism

Back 122

(a) 1st line therapy for Grave's; treatment of choice for thyrotoxicosis in adults/elderly
(b) ablation of thyroid gland

Front 123

Glucocorticoids
(a) example
(b) indications
(c) mechanism

Back 123

(a) hydrocortisone
(b) adrenocortical insufficiency (Addison disease, acute adrenal insufficiency from other causes)
(c) replacement therapy

Front 124

Mineralcorticoids
(a) example
(b) indications
(c) mechanism

Back 124

(a) gludrocortisone
(b) chronic treatment of Addison's disease in patients requiring mineralcorticoids
(c) replacement therapy

Front 125

Glucocorticoid synthesis inhibitors
(a) examples
(b) indications

Back 125

(a) aminoglutethimide, metyrapone, ketoconazole
(b) suppress adrenocortical steroid roduction (Cushing's, Cushingoid states, congenital adrenal hyperplasia)

Front 126

Bisphosphonates
(a) examples
(b) indications
(c) mechanism
(d) side effects

Back 126

(a) alendronate, etidronate, pamidronate, risedronate
(b) osteoporosis, Paget disease
(c) decr bone resorption
(d) esophageal ulceration may occur

Front 127

Reactive hypoglycemia
(a) glucose
(b) insulin
(c) C peptide
(d) ketoacidosis
(e) other features

Back 127

(a) glucose: decr
(b) insulin: incr
(c) C peptide: incr
(d) ketoacidosis: no
(e) other features: excessive secretion w/oral glucose tolerance test

Front 128

Give examples
(a) short acting
(b) rapid acting
(c) intermediate acting
(d long acting
(e) ultralong acting

Back 128

(a) short acting: lispro, aspart
(b) rapid acting: regular
(c) intermediate acting: NPH, Lente
(d long acting: ultralente
(e) ultralong acting: glargine, detemir

Front 129

Insulin
(a) action
(b) clinical use
(c) toxicity

Back 129

(a) Bind insulin receptor (tyrosine kinase activity)
Liver: incr glucose (stored as glycogen)
Muscle: incr glycogen and protein synth; K+ uptake
Fat: aids TG storage
(b) TI and TIIDM; also life threatening hyperkalemia and stress induced hyperglycemia
(c) hypoglycemia, hypersensitivity (rare)

Front 130

Name 1st generation sulfonylureas

Back 130

Tolbutamide
Chlopropamide

Front 131

Name 2nd generation sulfonylyreas

Back 131

Glyburide
Glimepiride
Glipizide

Front 132

Sulfonylureas
(a) action
(b) clinical use
(c) toxicities

Back 132

(a) close K+ channel in beta cell membrane so cell depolarizes, triggerig insulin release via increased Ca++ influx
(b) stimulates release of endogenous insulin in type II DM. Require some islet fct so not used in TIDM
(c) first generation: disulfiram like effects
Second gen: hypoglycemia

Front 133

Biguanides
(a) examples
(b) mechanism of action
(c) clinical use
(d) toxicities

Back 133

(a) metformin
(b) possibly decr gluconeogenesis, incr glycolysis, decr serum glucose levels (acts as an insulin sensitizer)
(c) oral hypoglycemic; used in patients without islet fct
(d) can cause lactic acidosis

Front 134

Glitazones/Thiazolidinediones
(a) examples
(b) mechanism of action
(c) clinical use
(d) toxicities

Back 134

(a)rosiglitazone, pioglitazone
(b) bind PPARgamma receptor to incr target tissue sensitivity to insulin, inhibits hepatic glucose output, incr glucose uptake
(c) used as monotherapy in TIIDM or combined with other agents
(d) wt gain, edema, hepatotoxicity, CV toxicity

Front 135

Alpha glucosidase inhibitors
(a) examples
(b) mechanism of action
(c) clinical use
(d) toxicities

Back 135

(a) acarbose, miglitol
(b) inhibit intestinal brush border alpha glucosidase to delay sugar hydrolysis, glucose absorption (leads to decreased posprandial hyperglycemia)
(c) used as monotherapy in TIIDM or in combo with other agnets
(d) Gi disturbances (flatulence and diarrhea)

Front 136

Pramlintide
(a) mechanism of action
(b) clinical use
(c) toxicity

Back 136

(a) mimetic; decreases glucagon
(b) type IIDM
(c) hypoglycemia, nausea, diarrhea

Front 137

GLP-1 mimics
(a) examples
(b) mechanism of action
(c) toxicity

Back 137

(a) exenatide
(b) increase insulin, decrease glucagon release
(c) type IIDM
(d) nausea, vomiting;

Front 138

Orlistat
(a) mechanism
(b) clinical use
(c) toxicity

Back 138

(a) inhibits pancreatic lipase
(b) long term obesity management (in conjunction w/diet)
(c) steatorrhea, GI discomfort, reduced absorption of fat soluble vits, HA

Front 139

Sibutramine
(a) mechanism
(b) clinical use
(c) toxicity

Back 139

(a) sympathomimetic serotonin and norep reuptake inhibitor
(b) short and long term obesity management
(c) HTn and tachycardia

Front 140

PTY, methimazole
(a) mechanism
(b) clinical use
(c) toxicity

Back 140

(a) inhibit organification and coupling of TH synthesis; PTU also decr converstin of T4 to T3
(b) hyperthyroidism
(c) skin rash, agranulocytosis (rare), aplastic anemia

Front 141

Hypothalamic/pituitary drugs clinical uses
(a) GH
(b) somatostatin (octreotide)
(c) oxytocin
(d) ADH (desmopressin)

Back 141

(a) GH: GH deficiency, Turner's
(b) somatostatin (octreotide): acromegaly, carcinoid, gastrinoma, glucagonoma
(c) oxytocin: stimulates labor, uterine contractions, mil let down; controls uterine hemorrhage
(d) ADH (desmopressin): pituitary diabetes insipidus

Front 142

Levothyroxine, triidiothyronine
(a) mechanism
(b) clinical use
(c) toxicity

Back 142

(a) thyroxine replacement
(b) hypothyroidism, myxedema
(c) tachycardia, heat intolerance, tremors, arrhythmias

Front 143

Glucocorticoids
(a) examples
(b) mechanism
(c) clinical use
(d) toxicity

Back 143

(a) hydrocortisone, prednisone, triamcinolone, dexamethasone, becomethasone
(b) decr the production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and expression of COX2
(c) addison's disease, inflammation, immune suppression, asthma
(d) Iatrogenic cushings;osteoporosis, adrenocorticocal atrophy, peptic ulcers, diabetes (if chronic)

Front 144

Demeclocycline
(a) mechanism
(b) clinical use
(c) toxicity

Back 144

(a) ADH antagonist (member of tetracycline family)
(b) Diabetes Insipidus, SIADH
(c) photosensitivity, abnormalities of bone/teeth