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Endocrine Flashcards

0
Q

What does the thyroglossal duct become?

What if it persists?

A

Normally thyroglossal duct –> foramen cecum

If it persists –> thyroglossal duct cyst
midline mass that moves with swallowing

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1
Q

What is the most common site of ectopic thyroid tissue?

A

The tongue

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2
Q

What adenohypophyseal hormones share a common subunit?

A

These all share the same alpha subunit (beta determines spec.)

TSH
LH
FSH
hCG

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3
Q

What do the basophil cells secrete in the anterior pituitary?

A

B-FLAT

Basophils:
FSH
LH
ACTH
TSH
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4
Q

What endocrine cell types are found in the pancreas?

A

Beta - Insulin
Alpha - Glucagon
Delta - Somatostatin
PP - Pancreatic polypeptide

This is the order of abundance

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5
Q

What tissues can take up glucose regardless of insulin status?

A

BRICK L

Brain
RBC's
Intestine
Cornea
Kidney
Liver
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6
Q

What are the glucose transporters and their locations?

A

GLUT1 (insulin-independent) –> RBC’s & brain

GLUT2 (bidirectional) –> Beta cells, liver, kidney, small intestine

GLUT4 (insulin-dependent) –> Adipose tissue, skeletal muscle

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7
Q

What is insulin’s effect on renal tubules?

A

Causes sodium retention

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8
Q

What 3 things cause release of insulin?

What 3 things inhibit it?

A

Release:
Hyperglycemia
GH (causes insulin resistance –> increased release)
Beta2 agonists

Inhibit:
Hypoglycemia
Somatostatin
Alpha2 agonists

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9
Q

What are the steps within beta cells leading to insulin release?

A 
Glucose enters via GLUT2
Glycolysis --> ^ATP
ATP-sensitive K+ channels close --> Depolarization
Voltage-gated Ca2+ channels open
Exocytosis of insulin granules
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10
Q

What pathways are responsible for the intracellular effects of insulin?

A

Phosphoinositide-3 kinase pathway –> GLUT4 inserted into membrane & synthesis of glycogen, lipids, proteins

RAS/MAP kinase pathway –> Cell growth, DNA synthesis

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11
Q

What changes occur within target tissues that cause insulin resistance?

A

Serine kinase phosphorylation of signaling molecules. This causes inhibition of the Phosphoinositide-3 kinase pathway so that GLUT4 cannot be inserted into the membrane.

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12
Q

What is the regulation of prolactin?

A

TRH –> +Prolactin

Dopamine –> -Prolactin

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13
Q

What does CRH stimulate release of?

A

ACTH
Melanocyte-Stimulating Hormone (MSH)
Beta-endorphin

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14
Q

What is Somatostatin’s effect in the pituitary?

A

Decreases GH & TSH release

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15
Q

What are the effects of growth hormone?

A

Stimulates linear growth & muscle mass (IGF-1 mediated)

Insulin resistance

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16
Q

What can stimulate GH secretion?

Inhibit?

A

Stimulated by:
Pulsatile GHRH
Sleep
Exercise

Inhibited by:
Glucose
Somatostatin

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17
Q

How does 17-alpha-hydroxylase deficiency present?

A

Cortisol & androgens cannot be produced:
Hypertension
Males - pseudohermaphroditism (ambiguous genitalia)
Females - normal anatomy, no secondary sex characteristics

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18
Q

How does 21-alpha hydroxylase deficiency present?

A

Most common form of congenital adrenal hyperplasia
^Androgens, deficient cortisol & mineralocorticoids

Hypotension
Hyperkalemia
Masculinization in females –> pseudohermaphroditism

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19
Q

How does 11-beta-hydroxylase deficiency present?

A

^Androgens, ^mineralocorticoids, deficient cortisol

Hypertension (11-deoxycorticosterone)
Hypokalemia
Masculinization of females

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20
Q

What is seen with congenital aromatase deficiency?

A

Increased Testosterone and decreased Estrogen levels
Maternal hirsutism while pregnant w/ affected fetus
Female pseudohermaphroditism

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21
Q

What are the actions of cortisol?

A

BBIIG:
Bones/BP
Immunosuppression/Insulin resistance
Glucose production

Decreases bone formation
Upregulates alpha1 receptors on arterioles (sensitizes)
Anti-inflammatory
Diabetogenic
Gluconeogenesis, lipolysis, proteolysis, inhibits fibroblasts

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22
Q

How can one differentiate primary adrenal insufficiency vs HPA axis dysregulation?

A

Metyrapone test

Metyapone inhibits 11-beta-hydroxylase –> should see compensatory rise in ACTH –> Increased cortisol precursors (urinary 17-hydroxy-corticosteroids or 11-deoxycortisol)

If ACTH^ but not the precursors –> adrenal problem
If no ACTH^ –> HP axis problem

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23
Q

How does cortisol affect blood pressure?

A

1) It upregulates Alpha1 adrenergic receptors on arterioles –> sensitizes them to catecholamines
2) It increases transcription of phenylethanolamine-N-Methyltransferase (NE–>EPI)

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24
Q

How does PTH stimulate osteoclastic activity?

A

Increases production of M-CSF & RANK-L in osteoBLASTS

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25
Q

How is PTH secretion regulated?

A

Decreased serum Ca2+ –> ^PTH
Decreased serum Mg2+ –> PTH
Very low serum Mg2+ –> Decreased PTH

Thus, if magnesium levels are very low, a patient may not respond well to Calcium supplementation (need Mg2+ as well).

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26
Q

What can cause hypomagnesemia?

A

Diarrhea
Aminoglycosides
Diuretics
Alcohol abuse

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27
Q

What form of Vit. D is active?

What forms are inactive?

A 
Active = 1,25-Cholecalciferol = Calcitriol
Inactive = 25-OH-D3 & 24,25-OH-D3
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28
Q

How is Vit. D acquired?

Where is Vit. D activated?

A

D2 is dietary, D3 is synthesized in skin

Converted to 25-OH-D3 in liver
Converted to 1,25-OH-D3 in kidney PCT

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29
Q

What are the effects of Calcitriol?

A

^Bone resorption of calcium & phosphate

^GI absorption of calcium & phosphate

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30
Q

What hormones function through cAMP?

A

FLAT ChAMP

FSH
LH
ACTH
TSH
CRH
hCG
ADH (V2)
MSH
PTH
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31
Q

What hormones function through cGMP pathways?

A

The vasodilators:
NO (EDRF)
ANP

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32
Q

What hormones function through tyrosine kinase –> MAPK?

A 
Growth factors:
Insulin
IGF-1
FGF
PDGF
EGF
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33
Q

What hormones function through a steroid receptor?

A

VETT CAP

Vit. D
Estrogen
Testosterone
T3/T4
Cortisol
Aldosterone
Progesterone
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34
Q

What hormones function through tyrosine kinase –> JAK/STAT?

A

Acidophiles & cytokines:
Prolactin
GH
IL-2,IL-6,IL-8,IFN

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35
Q

What are the steroid hormones bound to in the circulation?

A

Testosterone/Estrogen - Sex Hormone Binding Globulin (SHBG)
Corticosteroids - Transcortin (CBG)
T3/T4 - Thyroxine Binding Globulin (TBG)
Aldosterone/Progesterone - Albumin, CBG

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36
Q

What is the function of T3?

A 
4 B's:
Brain maturation
Bone growth
Beta-adrenergic effects
Basal metabolic rate

^Beta1 receptors in the heart –> ^CO,HR,SV,Contractility
^Na+/K+ ATPase activity –> ^BMR,RR,Temperature
^Glycogenolysis, gluconeogenesis, lipolysis

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37
Q

What maintains the high testosterone levels seen in the testes?

A

Androgen Binding Protein (ABP) secreted by Sertoli cells

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38
Q

What can change the levels of Thyroxine Binding Globulin (TBG)?

A

Liver failure –> decreased TBG

Pregnancy/OCP’s –> Increased TBG

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39
Q

What type of thyroid hormone is most active?

A

T3 is most active
T4 is the majority produced in thyroid
rT3 is not active at all

T4–>T3 in periphery via 5-deiodinase

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40
Q

What is the Wolff-Choikoff effect?

A

Excess iodine inhibits Thyroid Peroxidase (TPO) temporarily –> decreased organification of iodine –> decreased T3/T4

Can be used if radioactive iodide is accidentally ingested to make sure that it is not incorporated into T3/T4.

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41
Q

How do corticosteroids inhibit inflammation?

A

1) Inhibition of phospholipase A2 –> no arachidonic acid (LT/PG)
2) Inhibition of IL-2
3) Prevents release of histamine

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42
Q

What are the causes of Cushing’s syndrome?

A

Exogenous corticosteroids!!
Cushing’s disease (pituitary adenoma)
Ectopic ACTH (small cell lung carcinoma
Adrenal adenoma/carcinoma/nodular hyperplasia

Can distinguish somewhat using ACTH levels.

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43
Q

What is seen in Cushing’s syndrome?

A 
Hypertension
Moon facies, thin limbs, truncal obesity, buffalo hump
Hyperglycemia
Purple abdominal striae
Osteoporosis
Immune suppression
Amenorrhea
44
Q

What is seen with a normal Dex test?
Cushing’s disease?
Ectopic ACTH production?

A

Normal - cortisol levels inhibited by low dose
Pituitary adenoma - cortisol levels inhibited by high dose only
Ectopic - cortisol levels not affected by high dose

45
Q

What is the treatment for Hyperaldosteronism?

A

Primary (Conn syndrome) - Surgical resection or Spironolactone

Secondary (CHF, etc.) - Spironolactone

46
Q

What can cause secondary hyperaldosteronism?

A 
CHF
Renal artery stenosis
Chronic renal failure
Cirrhosis
Nephrotic syndrome
Reninoma
47
Q

What hormones are affected in primary renal insufficiency?

Secondary?

A

Primary = all cortical hormones (Aldosterone, Cortisol, Sex)

Secondary = Cortisol & sex hormones (aldosterone controlled more by RAA axis)

48
Q

How can primary and secondary adrenal insufficiency be distinguished?

A

Primary - Skin pigmentation & hyperkalemia

Secondary - no compensatory ^ in ACTH & no hypoaldosteronism

49
Q

What can cause Addison’s disease?

A

Addison’s = chronic primary adrenal insufficiency

Autoimmune destruction
TB dissemination
Metastatic cancer (LUNG CANCER)
50
Q

What are the adrenal medullae derived from?

A

Chromaffin cells of neural crest

51
Q

What is seen with pheochromocytoma?

A

^serum Metanephrine & urinary VMA

Episodic:
Headache
^Blood pressure
Sweating
Palpitations
Pallor
52
Q

What are the breakdown products of Dopamine?
NE?
EPI?

A

Dopamine –> HVA
NE –> Normetanephrine, VMA
EPI –> Metanephrine, VMA

53
Q

What is the treatment for pheochromocytoma?

A

1) Alpha blockade (Phenoxybenzamine)
2) Beta blockade
3) Surgery

Alpha blockade must be given first to prevent hypertensive crisis (just like cocaine).

54
Q

What is the most common adrenal tumor in children?

What is seen?

A

Neuroblastoma

Can be located anywhere along sympathetic chain
Small blue cell tumor
^HVA (dopamine metabolite) in urine
N-myc mutation

55
Q

What is the 10% tumor?

A

Pheochromocytoma

10% malignant
10% bilateral
10% familial
10% extra-adrenal
10% calcify
56
Q

What is seen in Hashimoto’s thyroiditis?

A

Transient hyperthyroid –> hypothyroid
Enlarged nontender thyroid
Anti-thyroglobulin Ab’s, Anti-TPO Ab’s (do not mediate dz)

57
Q

What causes Hashimoto’s Thyroiditis?

What is seen on histology?

A

Autoimmune destruction of thyroid (HLA-DR5)
Hurthle cells
Germinal centers –> ^ risk of lymphoma

58
Q

What is seen with cretinism?

A

“TAUS are retards”

Tongue enlargement
Abdominal distension
Umbilical hernia
Skeletal abnormalities (short stature, craniofacial abn)
Retardation

also jaundice, myxedema, hypotonia

59
Q

What causes cretinism?

A

Severe fetal hypothyroidism

Maternal iodine deficiency (developing countries)
Defective T4 formation
Thyroid developmental failure

60
Q

What is seen with subacute DeQuervain’s granulomatous thyroiditis?

A

Transient hyperthyroidism –> self-limited hypothyroidism
Follows a viral infection
TENDER THYROID
Granulomatous inflammation

61
Q

What is seen with Riedel’s thyroiditis?

A

Hypothyroidism
Thyroid is replaced by fibrous tissue
Hard, rock/wood-like, painless goiter
Can involve local structures

Classically seen in younger patients (vs. anaplastic carcinoma which is older patients & can also involve surrounding structures)

62
Q

What is the Jod-Basedow phenomenon?

A

Thyrotoxicosis seen when an iodine-deficient patient is given iodine. Seen in patients with multinodular goiter.

63
Q

What is seen in Graves’ disease?

Histologically?

A

Hyperthyroidism
Exophthalmos & Pretibial myxedema (glycosaminoglycans)
Diffuse goiter

Histo: Large follicles with scalloped borders

64
Q

What is seen in thyroid storm?

A

Underlying thyrotoxicosis + Stress (infection, surgery, etc.) –> T3/T4 & catecholamine surge –> Arrhythmia –> death

^Alkaline phosphatase may be seen

65
Q

What are the types of thyroid cancer?

A

Papillary carcinoma (80%)
Follicular carcinoma
Medullary carcinoma
Anaplastic carcinoms

66
Q

What is seen on with papillary carcinoma of the thyroid on histology?

A

Orphan Annie eyed nuclei
PSaMMoma bodies
Nuclear grooves

^risk with childhood irradiation

67
Q

What is seen on with medullary carcinoma of the thyroid on histology?

A

Sheets of cells in an amyloid stroma

Amyloid is calcitonin

Associated with MEN2A & MEN2B

68
Q

What causes primary hyperparathyroidism?

What is seen?

A

Parathyroid adenoma is most common cause

Hypercalcemia & “Stones, Bones, Groans, Psychic Moans”
Renal stones
Osteitis fibrosa cystica (cystic bone spaces, brown fibrous tissue)
Constipation
Depression, confusion

69
Q

What is seen in the serum/urine with primary hyperparathyroidism?

A 
Hypercalcemia
Hypophasphatemia
^PTH
^Alkaline phosphatase
^cAMP in urine
70
Q

What causes secondary hyperparathyroidism?

A

Chronic renal failure (high phosphate)

Most other causes of secondary hyperparathyroidism show low phosphate (^spilling at the PCT)

72
Q

What is seen in Addison’s disease?

A

Addison’s = chronic primary adrenal insufficiency

Hypotension
Hyperkalemia
Metabolic acidosis
Skin hyperpigmentation (secondary ^^POMC–>ACTH/MSH)

86
Q

What ketoacids are seen in DKA?

A

beta-hydroxybutyrate > acetoacetate

87
Q

What is seen on labs in DKA?

A

Hyperglycemia
Anion gap metabolic acidosis
Ketones
Leukocytosis
Hyperkalemia (shifted from inside cells, actually low total body K+)
Hyponatremia (dilutional - serum osmolarity pulls H2O out of cells)

88
Q

What is seen with carcinoid syndrome?

What is the treatment?

A 
Most common tumor of the appendix, small bowel most common
Diarhhea
Flushing
Asthmatic wheezing
Right-sided valvular disease
^5-HIAA in urine
Niacin deficiency

Tx: Octreotide (the tumors contain somatostatin receptors –> decreases 5-HT release)

89
Q

What is seen in Zollinger-Ellison syndrome?

A 
Gastrin-secreting tumor
Found in pancreas or duodenum
Recurrent ulcers
Ulcers in jejunum
Associated w/ MEN1
90
Q

What is seen with MEN1?

A

Commonly presents with kidney stones & GI ulcers

Pituitary
Parathyroid
Pancreas (ZES, Insulinoma, VIPoma, Glucagonoma)

91
Q

What is seen in MEN2A?

A

Parathyroid HYPERPLASIA
Medullary thyroid carcinoma
Pheochromocytoma

92
Q

What is seen in MEN2B?

A

Marfanoid habitus
Oral ganglioneuromas
Medullary thyroid carcinoma
Pheochromocytoma

93
Q

What mutation is seen in MEN?

A

MEN2A & MEN2B = ret mutation

94
Q

What are the short acting insulins?

Long acting?

A

Short = Lispro & Aspart

Long = Glargine & Detmir

95
Q

What is the mechanism of Metformin?

A

Decreases hepatic gluconeogenesis (primary)
Increases glycolysis
Increases peripheral insulin sensitivity

96
Q

What is the mechanism of Sulfonylureas?

What are their toxicities?

A

Close K+ channel on beta cells –> ^insulin release
Requires some islet function so T2DM only

Toxicities:
Tolbutamide/Chlorpopamide - Disulfiram reaction
Glipizide/Glyburide/Glimepiride - Hypoglycemia

97
Q

What is the mechanism of Thiazolidinediones?

What are their toxicities?

A

Pioglitazone & Rosiglitazone

Bind PPAR-gamma nuclear transcription factor –> ^insulin sens.

Toxicities:
Weight gain
Edema
Hepatotoxicity
Heart failure

“Ross is all Glitzed up for the PPARty, hope no one breaks his Heart”

98
Q

What are the alpha-glucosidase inhibitors?

A

Acarbose & Miglitol

They inhibit intestinal brush-border glucosidases to delay glucose absorption –> decreased postprandial hyperglycemia

Can cause GI upset

99
Q

What is the mechanism of Pramlintide?

A

Amylin analog –> decreased glucagon

Used to treat T1DM & T2DM

100
Q

What are Exenatide & Liraglutide?

What toxicities are seen?

A

They are GLP-1 analogs used to treat T2DM. They cause ^insulin release and decreased glucagon release.

Toxicities:
N/V
Pancreatitis

101
Q

What are the -gliptin drugs used for?

What are their toxicities?

A

Linagliptin, Saxagliptin, Sitagliptin
They are DPP-4 inhibitors used for T2DM

Toxicities:
Urinary or respiratory infections

102
Q

What drugs are used for hyperthyroidism?

What are their side effects?

A

Methimazole, Propylthiouracil (PTU)

They are thyroid peroxidase inhibitors. PTU also blocks 5’-deiodinase to prevent T4–>T3 in peripheral tissues.

Toxicities:
Agranulocytosis
Aplastic anemia
Hepatotoxicity (PTU)
Methimazole is a teratogen
103
Q

What conditions does octreotide treat?

A 
Acromegaly
Carcinoid syndrome
Gastrinoma
Glucagonoma
Esophageal varices
104
Q

What is exogenous oxytocin used for?

A

Induction of labor
Uterine contractions
Milk let-down
Control of uterine hemorrhage

105
Q

What is Demecycline used for?

What toxicities are seen?

A

ADH-antagonist used for SIADH
(-vaptan drugs are also ADH antagonists)

Toxicities:
Nephrogenic diabetes insipidus
Photosensitivity
Bone/Tooth abnormalities

121
Q

What clinical signs can test for hypercalcemia?

A

Chvostek’s sign - tapping facial nerve causes twitch

Trousseau’s sign - Inflation of BP cuff causes carpal spasm

122
Q

What is seen with Lymphocytis hypophysitis?

A

Occurs during late pregnancy/early postpartum
Autoimmune destruction of pituitary

Acute headache
Bitemporal hemianopsia
Adrenal insufficiency

123
Q

What is seen with a prolactinoma?

What is the treatment?

A

Most common type of pituitary adenoma

Bitemporal hemianopsia
Women - amenorrhea, galactorrhea
Men - low libido, infertility

Tx: Bromocryptine (dopamine agonist)

124
Q

How is acromegaly diagnosed?

What is the treatment?

A

^serum IGF-1
serum GH not suppressed following oral glucose tolerance test
Pituitary mass on MRI

Tx: Surgical excision and/or Octreotide (somatostatin)

125
Q

What can cause diabetes insipidus?

A

Central - pituitary tumor, trauma, surgery, histiocytosis x

Nephrogenic - hereditary, hypercalcemia, lithium

126
Q

What lab findings are seen with diabetes insipidus?

What tests are done?

A

Urine specific gravity < 1.006
Serum osmolarity > 290 mOsm/L

Water deprivation test:
Urine osmolarity doesn’t ^
Response to desmopressin differentiates central/nephrogenic

127
Q

What is the treatment for diabetes insipidus?

A

Central - Intranasal desmopressin (ADH)

Nephrogenic - Hydrochlorothiazide

128
Q

What can cause SIADH?

A

Ectopic ADH secretion (small cell lung carcinoma)
CNS tumors/head trauma
COPD
Cyclophosphamide

129
Q

What is seen in SIADH?

A

^ADH secretion –> secondary hypoaldosteronism –> hyponatremia w/ near-normal volume status

Seizures can be seen with severe hyponatremia

130
Q

What is the treatment for SIADH?

A 
Fluid restriction
IV saline (to correct hyponatremia)
-vaptan drugs (ADH antagonists)
131
Q

What can cause hypopituitarism?

A

Nonsecreting pituitary adenoma/Craniopharyngeoma

Sheehan’s syndrome:
intrapartum blood loss –> failure to lactate & loss of pubic hair

Empty sella syndrome:
atrophy or compression, seen in obese women

Brain injury/hemorrhage

Radiation

132
Q

What is seen with an insulinoma?

A

Episodic hypoglycemia w/ mental status changes
Low glucose
High insulin
High C-peptide (vs. exogenous insulin administration)

133
Q

What is seen with a somatostatinoma?

A

Achlorhydria (inhibition of gastrin)

Cholelithiasis & steatorrhea (inhibition of CCK –> no GB contraction)

134
Q

What aspects of diabetes cause the chronic effects seen?

A

Nonezymatic glycosylation (large & small vessel disease)

Osmotic damage (Schwann cells, cataracts)
Preferentially occurs in cells with aldose reductase & insufficient aldose dehydrogenase
135
Q

What is seen on pancreatic histology in T1DM?

T2DM?

A

T1DM - WBC infiltrate (Type IV hypersensitivity)

T2DM - Amyloid deposition (Amylin = Islet Amyloid Polypeptide)

136
Q

What type of diabetes is strongly correlated to genetics?

A

T2DM is more genetically influenced

Both T1DM & T2DM are polygenic

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