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Step 1 Subjects > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Congenital hypothyroidism

A

Decreased T4 levels

  • Endemic Cretinism= insufficient iodine in utero
  • Sporadic= defect in T4 formation in utero, developmental thyroid formation failure

Symptoms:
- Lethargy, poor feeding
- Jaundice, macroglossia
- Constipation, umbilical hernia, myxedema
- Muscle hypotonia, hoarse cry
- ASD, VSD
Pot bellied, Pale, Puffy-faced child with Protruding umbilicus, protuberant tongue

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2
Q

Somatomedin C

A

AKA IGF-1= insulin-like growth factor 1

  • GH Secreted by pituitary–> liver produces IGF-1
  • induces chondrocytes to proliferate along epiphyseal plate (long bone growth!)
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3
Q

Fetal adrenal gland

A

Outer zone= adult zone

  • No function until late in gestation: begins secreting cortisol
  • Controlled by ACTH and CRH from fetal pituitary and placenta
  • Cortisol–> fetal lung maturation and surfactant secretion

Inner zone= Active fetal zone

  • Produces androgens with placenta
  • Lacks 3-beta-hydroxysteroid to convert pregnolone–> progesterone
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4
Q

Anterior pituitary

A

Secretes FSH, LH, ACTH, TSH, prolactin, GH, MSH

  • Derived from oral ectoderm (Rathke’s pouch–> craniopharyngioma) vs posterior pituitary= neuroectoderm
  • Alpha subunit= TSH, LH, FSH, hCG common subunit
  • Beta subunit= hormone-specific
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5
Q

GLUT-1 receptors

A

Insulin INDEPENDENT

- RBCs, Brain

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6
Q

GLUT-2 receptors

A

Bidirectional

  • Beta-islet cells
  • Liver, kidney, small intestine (insulin-independent uptake)
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7
Q

GLUT-4 receptors

A

Insulin DEPENDENT

  • Adipose tissue
  • Skeletal muscle
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8
Q

Insulin release

A

Beta cells in pancreas: center of islet

  1. GLUT-2 transporter brings in glucose
  2. Glycolysis in Beta cell–> ATP/ADP ratio increase
  3. ATP binds and closes K+ channels
  4. Membrane depolarizes
  5. Ca+2 influx into beta cell
  6. Exocytosis of insulin granules
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9
Q

Glucagon release

A

Alpha-cells in pancreas: periphery of islet

Secreted in response to:

  • Hypoglycemia
  • Increased serum [amino acids]
  • Adrenergic stimulation (epi–> alpha2 receptors)
  • CCK
  • Ach

Inhibited by:

  • Insulin
  • Hyperglycemia
  • Somatostatin
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10
Q

17-alpha-hydroxylase deficiency

A

Hypertension, hypokalemia

Males: decreased DHT–> pseudohermaphroditism (ambiguous genitalia, undescended testes

Females: internally and externally phenotypic female lacking secondary sex characteristics

**Enlarged adrenal glands d/t increased ACTH

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11
Q

21-hydroxylase deficiency

A

HYPOtension, hyperkalemia, increased renin activity, volume depletion

Females: masculinization; pseudohermaphroditism

**Enlarged adrenal glands d/t increased ACTH

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12
Q

11-beta-hydroxylase deficiency

A

HYPERtension:

  • increased 11-deoxycorticosterone= mineralocorticoid, secreted in excess (HTN)
  • Decreased aldosterone

Females: Masculinization

**Enlarged adrenal glands d/t increased ACTH

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13
Q

Growth Hormone

A

Anterior pituitary

Stimulates linear growth:
- increases liver IGF-1/somatomedin C secretion–> - induces chondrocytes to proliferate along epiphyseal plate (long bone growth)

Increased secretion in exercise, sleep
- Inhibited by glucose, somatostatin

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14
Q

Cortisol

A

Adrenal zona fasciculata, bound to corticosteroid-binding globulin (CBG)

  • Maintains BP (upregulates alpha1 receptors on arterioles–> increased sensitivity to NE, epi
  • Decreases bone formation
  • Anti-inflammatory/immune suppressive (blocks IL-2, etc)
  • Increased insulin resistance
  • Increased gluconeogenesis, lipolysis, proteolysis
  • Inhibits fibroblasts–> striae
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15
Q

PTH

A

Secreted by chief cells in parathyroid

Regulated by:

  • depleted Ca+2–> increased PTH
  • Decreased Mg+2–> increased PTH
  • Absent Mg+2–> decreased PTH (needs Mg+2 for manufacuring in chief cells); can be caused by diarrhea, aminoglycosides, diuretics, alcohol abuse

MOA:

  • Stimulates cAMP–> increased osteoblastic RANK-L + M-CSF expression–> increased osteoclast activity
  • Decreases osteoprotegerin release (OPG= inhibitor at RANK-L)
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16
Q

cAMP signaling hormones (Gs/Gi)

A 
Releasing hormones:
FSH
LH--> leydig (testosterone)/ Corpus luteum (progesterone)
SCT
TSH
CRH
hCG
ADH (V2 receptor)
MSH
PTH
Calcitonin
GHRH
Glucagon
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17
Q

cGMP signaling hormones

A

Vasodilators:

ANP
NO (endothelial derived relaxing factor)
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18
Q

IP3 signaling hormones (Gq)

A 
GnRH
GHRH
Oxytocin
ADH
TRH
Histamine (H1)
Angiotensin II
Gastrin
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19
Q

Steroid receptor

A 
Vitamin D
Estrogen
Testosterone
T3/T4
Cortisol
Aldosterone
Progesterone
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20
Q

Intrinsic tyrosine kinase

A

Growth factors:

Insulin
IGF-1
FGF
PDGF
EGF
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21
Q

Receptor-associated tyrosine kinase (JAK/STAT)

A

Prolactin
Immunomodulators (cytokines, IL-2,6,8, IFN)
GH

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22
Q

Sex hormone binding globulin (SHBG)

A

Binds sex hormones:

Men: increased SHBG–> decreased free T–> gynecomastia

Women: decreased SHBG–> increased free T–> hirsutism
- SHBG increased in pregnancy

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23
Q

Thyroid hormone function

A
  1. bone growth (synergism with GH)
  2. CNS maturation
  3. increases B1 receptors in heart
  4. increases BMR (basal metabolic rate)
  5. increases glycogenolysis, gluconeogenesis, lipolysis
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24
Q

Thyroid hormone production

A
  1. Iodine (I-) uptaken from blood by follicular cell
  2. TPO (Thyroid Peroxidase) oxidizes I- –> I2
  3. Follicular cell secretes I2, thyroglobulin into lumen (colloid)–> MIT/DIT
  4. Peroxidase (TPO) in lumen couples MIT/DIT–> T3/T4
  5. T3/T4 re-imported into follicular cell–> proteolysis–> released into blood (bound to TBG= thyroid binding globulin)
    - TBG increased by estrogen, decreased by liver failure
    - T4= major product; converted by 5’-deiodinase in periphery to active T3
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25
Q

Wolff-Chaikoff effect

A

Excess iodine temporarily inhibits TPO
(thyroid peroxidase)
–> decreased iodine organification
–> Decreased T3/T4 production

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26
Q

Propylthiouracil

A

PTU
MOA:
- blocks TPO formation of T3/T4
- Blocks 5’deiodinase conversion of T4–> T3

Tox: skin rash, agranulocytosis, aplastic anemia, hepatotoxicity

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27
Q

Methimazole

A

MMI
MOA; blocks TPO formation of T3/T4

Tox: skin rash, agranulocytosis, aplastic anemia, teratogen?

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28
Q

Dexamethasone suppression test

A

Normal function: cortisol suppressed by low dexamethasone

ACTH-pituitary tumor (Cushing’s): suppressed by high dexamethasone

  • Also can take venous sample of petrosal sinus
  • 24 hour urine collection: free cortisol 3x upper limit of normal

Ectopic ACTH-producing tumor (SCLC, bronchial carcinoids)/ Cortisol-producing tumor (adrenal adenoma): remains elevated with high dose dexamethasone

29
Q

Conn’s syndrome

A

Aldosterone-secreting adrenal adenoma

  • Hypertension, Hypokalemia (like 17-alpha-hydroxylase deficiency)
  • Metabolic alkalosis
  • low plasma renin

Symptoms:

  • HTN
  • Weakness, paresthesias (hypoklemia)

Bilateral or unilateral

Treatment:

  • Surgery to remove tumor
  • Spironolactone (aldosterone antagonist)
30
Q

Secondary hyperaldosteronism

A

Low perfusion in kidney (d/t renal artery stenosis, chronic renal failure, CHF, cirrhosis, nephrotic syndrome)
–> increased renin production

Treatment:
- Spironolactone

31
Q

Addison’s disease

A

Chronic primary adrenal insufficiency
- Adrenal atrophy/destruction of adrenals (autoimmune- increased risk with T1DM, TB, metastasis)

Deficiency of aldosterone, cortisol

  • Hypotension (hyponatremic volume contraction)
  • Hyperkalemia
  • Acidosis
  • Skin hyperpigmentation (MSH: increased ACTH–> MSH increase from POMC)

Treatment: Corticosteroids

32
Q

Secondary adrenal insufficiency

A

Decreased pituitary ACTH

  • No skin hyperpigmentation
  • no hyperkalemia

Tx: responds to ACTH

33
Q

Pheochromocytoma

A

Tumor of adrenal medulla in ADULTS
- Chromaffin cell (neural crest)

Secretes epi, NE, DA–> episodic HTN

Labs:

  • Increased urinary VMA (breakdown product of NE, epi)
  • Increased plasma catecholamines

Associated with:

  • NF-1
  • MEN 2A, 2B

Treatment:

  • Alpha-antagonist (irreversible): pheoxybenzamine (avoid hypertensive crisis)
  • Beta blocker: slow HR
  • Surgical removal

rule of 10s (10%): malignant, bilateral, extra-adrenal, calcify, kids

34
Q

Neuroblastoma

A

MOST Common Tumor of adrenal medulla in children

Presentation:

  • Opsoclonus-myoclonus syndrome= non-rhythmic conjugate eye movements + myoclonus
  • Retroperitoneal mass, anorexia, weight loss
  • Less likely to see HTN
  • elevated HVA in urine (catecholamines)

Histo:

  • Solid sheets of small blue round cells
  • Can occur anywhere along sympathetic chain

**Overexpression of N-myc–> rapid tumor progression (transcription factor)

35
Q

Hashimoto’s thyroiditis

A

anti-TPO, antithyroglobulin antibodies

  • HLA-DR5
  • Increased risk of non-Hodgkin’s lymphoma
  • Normal ESR
  • Chronic, progressive

Histo:

  • Hurthle cells
  • Lymphocytic infiltrate with germinal centers
  • Enlarged, nontender thyroid
36
Q

Subacute thyroiditis (de Quervain’s)

A

Self-limited hypothyroidism after flu-like illness

Histo: granulomatous inflammation

  • Neutrophils: lymphocytes, histiocytes, multi-nucleated giant cells (granuloma)
  • disrupted follicles around collioid

Findings:

  • Increased ESR, jaw pain, early inflammation, tender thyroid
  • Thyrotoxic–> hypothyroid–> euthyroid

Tx: NSAIDs for pain

37
Q

Riedel’s thyroiditis

A

Thyroid replaced by fibrous tissue (hypothyroid)

Findings:

  • Fixed, hard (rock-like) painless goiter
  • May extend into surrounding tissue
    • Manifestation of IgG4-related systemic disease (autoimmune pancreatitis)
38
Q

Hypothyroid myopathy

A

Pale muscle fibers with:

  • decreased striation
  • deposition of mucinous material
  • atrophy of Type II mucle fibers

Symptoms:

  • Weakness
  • Fatiguability
  • Muscle pain, cramping
39
Q

Toxic multinodular goiter

A

Focal patches of hyperfunctioning follicular cells

  • Work independently of TSH (mutation in TSH receptor)
  • Increased release of T3, T4

Jod-Basedow phenomenon= thyrotoxicosis after repletion of iodine deficency

40
Q

Grave’s disease

A

Diffusely enlarged goiter secreting TSI (thyroid-stimulating immunoglobulins)–> autoimmune hyperthyroidism

  • Proptosis (opthalmopathy, EOM swelling)
  • Pretibial myxedema
  • Increase in connective tissue deposition

Stress-induced (Childbirth)

41
Q

Thyroid Storm

A

Thyrotoxicosis:

  • Stress-induced catecholamine surge–> death by arrhythmia
  • Serious complication of Grave’s, hyperthyroid disorders

Increased ALP d/t increased bone turnover

Tx:

  • Glucocorticoids for exopthalmos
  • Beta-blockers for relief of sympathetic activation
  • Block iodine organification (Iodide salts, Propylthiouracil, Methimazole)
  • Radioactive iodine (ablate thyroid with I-131)
42
Q

Primary hyperparathyroidism

A

Adenoma–> Hypercalcemia

  • Hypercaluria, hypophosphatemia
  • Increased PTH, alk phos, cAMP in urine
  • Weakness, constipation

Osteitis fibrosa cystica= cystic bone spaces with brown fibrous tissue (bone pain)

43
Q

Secondary hyperparathyroidism

A

Decreased gut Ca+2 absorption, increased phosphate
- Chronic renal disease (hypovitaminosis D–> decreased Ca+2 absorption)

Hypocalcemia, hyperphosphatemia in chronic renal failure (decreased phosphate in other causes)
- Increased alk phos, PTH

Renal osteodystrophy= bone lesions d/t secondary/tertiary hyperpara

44
Q

Tertiary hyperparathyroidism

A

Refractory (autonomous) hyperparathyroidism d/t chronic renal disease

VERY elevated PTH, elevated Ca+2

45
Q

Albright’s hereditary osteodystrophy

A

AD: kidney unresponsive to PTH

  • -> hypocalcemia,
  • shortened 4th/5th digits
  • short stature
  • Resistance to TSH, LH, FSH (all stimulate Gs alpha pathway)
46
Q

Acromegaly

A

Pituitary adenoma–> excess GH

  • Large tongue, deep furrows
  • Deep voice
  • Large hands, feet, coarse faces
  • Impaired glucose tolerance

Diagnosis:

  • Increased serum IGF-1
  • fail to suppress serum GH after oral glucose tolerance test

Tx: resect adenoma, somatostatin analog if not cured

47
Q

Causes of diabetes insipidus

A 
Central: lack ADH
- Pituitary tumor
- Trauma
- Surgery
- Langerhans cell Histiocytosis
Treatment: intranasal Desmopressin

Nephrogenic= kidney doesn’t respond to ADH
- hereditary
- secondary to hypercalcemia
- Lithium
- Demeclocyline (ADH antagonist)
Treatment: HCTZ, indomethacin (NSAID), amiloride

48
Q

SIADH

A

Causes:

  • Ectopic ADH (SCLC)
  • CNS/head trauma
  • Pulmonary disease
  • Drugs (cyclophosphamide)
Treatments:
Fluid restriction
IV saline
Conivaptan
Tolvaptan
Demeclocycline
49
Q

Maternal diabetes

A

Insulin must be given to control blood glucose (insulin does not cross placenta)

Poor control

  • Hypoglycemia of newborn (beta islet cell hyperplasia due to excess glucose exposure in utero)
  • Caudal regression syndrome (sacral agenesis–> lower extremity paralysis, urinary incontinence)
  • Transposition of the great vessels
50
Q

Glucagonoma

A

Pancreatic tumor (rare)

Presentation:

  • Migratory erythema
  • Hyperglycemia (diabetes)
  • Stomatitis, chelosis
  • Abdominal pain
51
Q

VIPoma

A

Pancreatic tumor

Presentation:

  • Diarrhea
  • Metabolic acidosis
  • Hypokalemia
52
Q

Somatostatinoma

A

Pancreatic delta cell tumor

Presentation:

  • Abdominal pain
  • Gallstones
  • Constipation
  • Steatorrhea

Labs:

  • Decreased insulin, glucagon, CCK, secretins
  • Decreased gastric motility
53
Q

Carcinoid syndrome

A

Carcinoid tumor= neuroendocrine cells

  • Metastatic small bowel tumor secreting 5-HT (most common tumor of appendix)
  • Only seen if tumor metastasizes from bowel (5-HT digested in liver)

Symptoms:

  • Recurrent diarrhea
  • Cutaneous flushing
  • Asthmatic wheezing
  • Right-sided valvular disease
  • Increased serotonin in urine
  • Niacin deficiency

Treatment: Somatostatin analog (octreotide)

54
Q

MEN 1

A

Werner’s syndrome: Autosomal Dominant
DIAMOND; 3Ps

  • Pituitary tumor
  • Parathyroid tumors
  • Pancreatic endocrine tumors (Zollinger-Ellison, insulinoma, VIPoma, glucagonoma)

Presentation: kidney stones, stomach ulcers

55
Q

MEN 2A

A

Sipple’s syndrome: Autosomal Dominant
SQUARE: 2 Ps

  • Parathyroid tumors: 3rd/4th pharyngeal pouch
  • Pheochromocytoma
  • Medullary thyroid carcinoma (calcitonin): 4th/5th pharyngeal pouch

** ret gene mutation (tyrosine kinase)

56
Q

MEN 2B

A

Autosomal dominant
TRIANGLE: 1 P

  • Oral/intestinal ganglioneuromatosis (marfanoid habitus)
  • Medullary thyroid carcinoma (calcitonin)
  • Pheochromocytoma

** ret gene mutation (tyrosine kinase)

57
Q

Metformin

A

Biguanide
MOA: unknown;
- decreases gluconeogensis
- increases glycolysis, peripheral glucos uptake

Oral: 1st line in T2DM

Tox:

  • GI upset
  • Lactic acidosis (contraindicated in renal failure)
58
Q

Tolbutamide, chlorpropamide

A

Sulfonylureas (1st generation)
MOA: close K+ channel in Beta cell membrane (like ATP)–> cell depolarizes–> Ca+2 influx–> insulin release

Only for T2DM

Tox: Disulfiram-like effects

59
Q

Glyburide
Glimepiride
Glipizide

A

Sulfonylureas (2nd generation)
MOA: close K+ channel in Beta cell membrane (like ATP)–> cell depolarizes–> Ca+2 influx–> insulin release

Only for T2DM

Tos: hypoglycemia

60
Q

Pioglitazone, Rosglitazone

A

Glitazones/thiazolidinediones
MOA: Binds PPAR-gamma nuclear transcription regulator–> increased insulin-responsive genes–> increased insulin sensitivity in peripheral tissue

Mono or combo in T2DM

Tox:
- Weight gain, edema, hepatotoxic, heart failure

61
Q

Acarbose, miglitol

A

Alpha-glucosidase inhibitors

MOA: inhibit intestinal brush-border alpha-glucosidases–> delayed sugar hydrolysis, glucose absorption

Mono or combo in T2DM

Tox: GI disturbances

62
Q

Pramlintide

A

Amylin analog

MOA: decreases glucagon

T1 and T2DM

TOx: hypoglycemia, nausea, diarrhea

63
Q

Exenatide, Liraglutide

A

GLP-1 analogs

MOA: increased insulin, decreased glucagon release

T2DM

Tox: N/V, pancreatitis

64
Q

Linagliptin
Saxagliptin
Sitagliptin

A

DPP-4 inhibitors

MOA: increased insulin, decreased glucagon release

T2DM

Tox: urinary, respiratory infections

65
Q

Somatostatin

A

Octreotide

Use: acromegaly, carcinoid tumor
gastrinoma, glucagonoma, esophageal varices

66
Q

Demeclocyline

A

Tetracycline, ADH antagonist

Use: SIADH

Tox:

  • Nephrogenic DI
  • Photosensitivity
  • Abnormalities of bone, teeth
67
Q

Basal insulin types

A

NPH (2 times/day)

Glargine, Detemir (1x/day)

68
Q

Post-prandial insulin

A

Regular: peaks 2-4 hours after administration
- use IV in DKA

Lispro, aspart, glulisine: peak 45 minutes after administration
- Use to prevent post-meal hyperglycemia

69
Q

T2 Mature onset diabetes of the young (MODY)

A

Defect in Glucokinase enzyme (specific to liver, pancreatic beta-cells)- has high Km
- Can also have defect in transcription factors for insulin

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