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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
How does PTH stimulate osteoclastic activity?
Increases production of M-CSF & RANK-L in osteoBLASTS
25
How is PTH secretion regulated?
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).
26
What can cause hypomagnesemia?
Diarrhea Aminoglycosides Diuretics Alcohol abuse
27
What form of Vit. D is active? | What forms are inactive?
``` Active = 1,25-Cholecalciferol = Calcitriol Inactive = 25-OH-D3 & 24,25-OH-D3 ```
28
How is Vit. D acquired? | Where is Vit. D activated?
D2 is dietary, D3 is synthesized in skin Converted to 25-OH-D3 in liver Converted to 1,25-OH-D3 in kidney PCT
29
What are the effects of Calcitriol?
^Bone resorption of calcium & phosphate | ^GI absorption of calcium & phosphate
30
What hormones function through cAMP?
FLAT ChAMP ``` FSH LH ACTH TSH CRH hCG ADH (V2) MSH PTH ```
31
What hormones function through cGMP pathways?
The vasodilators: NO (EDRF) ANP
32
What hormones function through tyrosine kinase --> MAPK?
``` Growth factors: Insulin IGF-1 FGF PDGF EGF ```
33
What hormones function through a steroid receptor?
VETT CAP ``` Vit. D Estrogen Testosterone T3/T4 Cortisol Aldosterone Progesterone ```
34
What hormones function through tyrosine kinase --> JAK/STAT?
Acidophiles & cytokines: Prolactin GH IL-2,IL-6,IL-8,IFN
35
What are the steroid hormones bound to in the circulation?
Testosterone/Estrogen - Sex Hormone Binding Globulin (SHBG) Corticosteroids - Transcortin (CBG) T3/T4 - Thyroxine Binding Globulin (TBG) Aldosterone/Progesterone - Albumin, CBG
36
What is the function of T3?
``` 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
37
What maintains the high testosterone levels seen in the testes?
Androgen Binding Protein (ABP) secreted by Sertoli cells
38
What can change the levels of Thyroxine Binding Globulin (TBG)?
Liver failure --> decreased TBG Pregnancy/OCP's --> Increased TBG
39
What type of thyroid hormone is most active?
T3 is most active T4 is the majority produced in thyroid rT3 is not active at all T4-->T3 in periphery via 5-deiodinase
40
What is the Wolff-Choikoff effect?
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.
41
How do corticosteroids inhibit inflammation?
1) Inhibition of phospholipase A2 --> no arachidonic acid (LT/PG) 2) Inhibition of IL-2 3) Prevents release of histamine
42
What are the causes of Cushing's syndrome?
Exogenous corticosteroids!! Cushing's disease (pituitary adenoma) Ectopic ACTH (small cell lung carcinoma Adrenal adenoma/carcinoma/nodular hyperplasia Can distinguish somewhat using ACTH levels.
43
What is seen in Cushing's syndrome?
``` Hypertension Moon facies, thin limbs, truncal obesity, buffalo hump Hyperglycemia Purple abdominal striae Osteoporosis Immune suppression Amenorrhea ```
44
What is seen with a normal Dex test? Cushing's disease? Ectopic ACTH production?
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
What is the treatment for Hyperaldosteronism?
Primary (Conn syndrome) - Surgical resection or Spironolactone Secondary (CHF, etc.) - Spironolactone
46
What can cause secondary hyperaldosteronism?
``` CHF Renal artery stenosis Chronic renal failure Cirrhosis Nephrotic syndrome Reninoma ```
47
What hormones are affected in primary renal insufficiency? | Secondary?
Primary = all cortical hormones (Aldosterone, Cortisol, Sex) Secondary = Cortisol & sex hormones (aldosterone controlled more by RAA axis)
48
How can primary and secondary adrenal insufficiency be distinguished?
Primary - Skin pigmentation & hyperkalemia Secondary - no compensatory ^ in ACTH & no hypoaldosteronism
49
What can cause Addison's disease?
Addison's = chronic primary adrenal insufficiency ``` Autoimmune destruction TB dissemination Metastatic cancer (LUNG CANCER) ```
50
What are the adrenal medullae derived from?
Chromaffin cells of neural crest
51
What is seen with pheochromocytoma?
^serum Metanephrine & urinary VMA ``` Episodic: Headache ^Blood pressure Sweating Palpitations Pallor ```
52
What are the breakdown products of Dopamine? NE? EPI?
Dopamine --> HVA NE --> Normetanephrine, VMA EPI --> Metanephrine, VMA
53
What is the treatment for pheochromocytoma?
1) Alpha blockade (Phenoxybenzamine) 2) Beta blockade 3) Surgery Alpha blockade must be given first to prevent hypertensive crisis (just like cocaine).
54
What is the most common adrenal tumor in children? | What is seen?
Neuroblastoma Can be located anywhere along sympathetic chain Small blue cell tumor ^HVA (dopamine metabolite) in urine N-myc mutation
55
What is the 10% tumor?
Pheochromocytoma ``` 10% malignant 10% bilateral 10% familial 10% extra-adrenal 10% calcify ```
56
What is seen in Hashimoto's thyroiditis?
Transient hyperthyroid --> hypothyroid Enlarged nontender thyroid Anti-thyroglobulin Ab's, Anti-TPO Ab's (do not mediate dz)
57
What causes Hashimoto's Thyroiditis? | What is seen on histology?
Autoimmune destruction of thyroid (HLA-DR5) Hurthle cells Germinal centers --> ^ risk of lymphoma
58
What is seen with cretinism?
"TAUS are retards" ``` Tongue enlargement Abdominal distension Umbilical hernia Skeletal abnormalities (short stature, craniofacial abn) Retardation ``` also jaundice, myxedema, hypotonia
59
What causes cretinism?
Severe fetal hypothyroidism Maternal iodine deficiency (developing countries) Defective T4 formation Thyroid developmental failure
60
What is seen with subacute DeQuervain's granulomatous thyroiditis?
Transient hyperthyroidism --> self-limited hypothyroidism Follows a viral infection TENDER THYROID Granulomatous inflammation
61
What is seen with Riedel's thyroiditis?
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
What is the Jod-Basedow phenomenon?
Thyrotoxicosis seen when an iodine-deficient patient is given iodine. Seen in patients with multinodular goiter.
63
What is seen in Graves' disease? | Histologically?
Hyperthyroidism Exophthalmos & Pretibial myxedema (glycosaminoglycans) Diffuse goiter Histo: Large follicles with scalloped borders
64
What is seen in thyroid storm?
Underlying thyrotoxicosis + Stress (infection, surgery, etc.) --> T3/T4 & catecholamine surge --> Arrhythmia --> death ^Alkaline phosphatase may be seen
65
What are the types of thyroid cancer?
Papillary carcinoma (80%) Follicular carcinoma Medullary carcinoma Anaplastic carcinoms
66
What is seen on with papillary carcinoma of the thyroid on histology?
Orphan Annie eyed nuclei PSaMMoma bodies Nuclear grooves ^risk with childhood irradiation
67
What is seen on with medullary carcinoma of the thyroid on histology?
Sheets of cells in an amyloid stroma Amyloid is calcitonin Associated with MEN2A & MEN2B
68
What causes primary hyperparathyroidism? | What is seen?
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
What is seen in the serum/urine with primary hyperparathyroidism?
``` Hypercalcemia Hypophasphatemia ^PTH ^Alkaline phosphatase ^cAMP in urine ```
70
What causes secondary hyperparathyroidism?
Chronic renal failure (high phosphate) Most other causes of secondary hyperparathyroidism show low phosphate (^spilling at the PCT)
72
What is seen in Addison's disease?
Addison's = chronic primary adrenal insufficiency Hypotension Hyperkalemia Metabolic acidosis Skin hyperpigmentation (secondary ^^POMC-->ACTH/MSH)
86
What ketoacids are seen in DKA?
beta-hydroxybutyrate > acetoacetate
87
What is seen on labs in DKA?
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
What is seen with carcinoid syndrome? | What is the treatment?
``` 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
What is seen in Zollinger-Ellison syndrome?
``` Gastrin-secreting tumor Found in pancreas or duodenum Recurrent ulcers Ulcers in jejunum Associated w/ MEN1 ```
90
What is seen with MEN1?
Commonly presents with kidney stones & GI ulcers Pituitary Parathyroid Pancreas (ZES, Insulinoma, VIPoma, Glucagonoma)
91
What is seen in MEN2A?
Parathyroid HYPERPLASIA Medullary thyroid carcinoma Pheochromocytoma
92
What is seen in MEN2B?
Marfanoid habitus Oral ganglioneuromas Medullary thyroid carcinoma Pheochromocytoma
93
What mutation is seen in MEN?
MEN2A & MEN2B = ret mutation
94
What are the short acting insulins? | Long acting?
Short = Lispro & Aspart Long = Glargine & Detmir
95
What is the mechanism of Metformin?
Decreases hepatic gluconeogenesis (primary) Increases glycolysis Increases peripheral insulin sensitivity
96
What is the mechanism of Sulfonylureas? | What are their toxicities?
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
What is the mechanism of Thiazolidinediones? | What are their toxicities?
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
What are the alpha-glucosidase inhibitors?
Acarbose & Miglitol They inhibit intestinal brush-border glucosidases to delay glucose absorption --> decreased postprandial hyperglycemia Can cause GI upset
99
What is the mechanism of Pramlintide?
Amylin analog --> decreased glucagon Used to treat T1DM & T2DM
100
What are Exenatide & Liraglutide? | What toxicities are seen?
They are GLP-1 analogs used to treat T2DM. They cause ^insulin release and decreased glucagon release. Toxicities: N/V Pancreatitis
101
What are the -gliptin drugs used for? | What are their toxicities?
Linagliptin, Saxagliptin, Sitagliptin They are DPP-4 inhibitors used for T2DM Toxicities: Urinary or respiratory infections
102
What drugs are used for hyperthyroidism? | What are their side effects?
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
What conditions does octreotide treat?
``` Acromegaly Carcinoid syndrome Gastrinoma Glucagonoma Esophageal varices ```
104
What is exogenous oxytocin used for?
Induction of labor Uterine contractions Milk let-down Control of uterine hemorrhage
105
What is Demecycline used for? | What toxicities are seen?
ADH-antagonist used for SIADH (-vaptan drugs are also ADH antagonists) Toxicities: Nephrogenic diabetes insipidus Photosensitivity Bone/Tooth abnormalities
121
What clinical signs can test for hypercalcemia?
Chvostek's sign - tapping facial nerve causes twitch Trousseau's sign - Inflation of BP cuff causes carpal spasm
122
What is seen with Lymphocytis hypophysitis?
Occurs during late pregnancy/early postpartum Autoimmune destruction of pituitary Acute headache Bitemporal hemianopsia Adrenal insufficiency
123
What is seen with a prolactinoma? | What is the treatment?
Most common type of pituitary adenoma Bitemporal hemianopsia Women - amenorrhea, galactorrhea Men - low libido, infertility Tx: Bromocryptine (dopamine agonist)
124
How is acromegaly diagnosed? | What is the treatment?
^serum IGF-1 serum GH not suppressed following oral glucose tolerance test Pituitary mass on MRI Tx: Surgical excision and/or Octreotide (somatostatin)
125
What can cause diabetes insipidus?
Central - pituitary tumor, trauma, surgery, histiocytosis x Nephrogenic - hereditary, hypercalcemia, lithium
126
What lab findings are seen with diabetes insipidus? | What tests are done?
Urine specific gravity < 1.006 Serum osmolarity > 290 mOsm/L Water deprivation test: Urine osmolarity doesn't ^ Response to desmopressin differentiates central/nephrogenic
127
What is the treatment for diabetes insipidus?
Central - Intranasal desmopressin (ADH) Nephrogenic - Hydrochlorothiazide
128
What can cause SIADH?
Ectopic ADH secretion (small cell lung carcinoma) CNS tumors/head trauma COPD Cyclophosphamide
129
What is seen in SIADH?
^ADH secretion --> secondary hypoaldosteronism --> hyponatremia w/ near-normal volume status Seizures can be seen with severe hyponatremia
130
What is the treatment for SIADH?
``` Fluid restriction IV saline (to correct hyponatremia) -vaptan drugs (ADH antagonists) ```
131
What can cause hypopituitarism?
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
What is seen with an insulinoma?
Episodic hypoglycemia w/ mental status changes Low glucose High insulin High C-peptide (vs. exogenous insulin administration)
133
What is seen with a somatostatinoma?
Achlorhydria (inhibition of gastrin) | Cholelithiasis & steatorrhea (inhibition of CCK --> no GB contraction)
134
What aspects of diabetes cause the chronic effects seen?
Nonezymatic glycosylation (large & small vessel disease) ``` Osmotic damage (Schwann cells, cataracts) Preferentially occurs in cells with aldose reductase & insufficient aldose dehydrogenase ```
135
What is seen on pancreatic histology in T1DM? | T2DM?
T1DM - WBC infiltrate (Type IV hypersensitivity) T2DM - Amyloid deposition (Amylin = Islet Amyloid Polypeptide)
136
What type of diabetes is strongly correlated to genetics?
T2DM is more genetically influenced Both T1DM & T2DM are polygenic

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