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*First Aid in Brainscape* > Steve Hawking's Electronic Endocrine Enigma > Flashcards

Steve Hawking's Electronic Endocrine Enigma Flashcards

1
Q

Thyroid development

A

Thyroid diverticulum arises from floor of primitive pharynx, and descends into neck. Connected to tongue by thyroglossal duct (may persist as pyramidal lobe of thyroid);
Foramen cecum is normal remnant of thyroglossal duct. Most common ectopic thyroid tissue site is the tongue.

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2
Q

How does a thyroglossal duct cyst present

A

Presents as an anterior midline neck mass that moves with swallowing or protrusion of the tongue (vs. persistent cervical sinus leading to branchial cleft cyst in lateral neck)

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3
Q

Adrenal medulla and cortex are derived from what embryonic structures

A

Adrenal cortex: mesoderm

Adrenal medulla: neural crest

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4
Q

Zona Glomerulosa

A

outer most layer of the aderenal cortex; regulated by renin-angiotensin; secretes Aldosterone

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5
Q

Zona Fasiculata

A

Middle layer of the adrenal cortex (thickest of the 3); regulated by ACTH and CRH; secretes Cortisol, sex hormones

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6
Q

Zona Reticularis

A

Inner most layer of the adrenal cortex; regulated by ACTH and Sympathetic fibers; releases sex hormones like androgens

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7
Q

Adrenal Medulla

A

made up of chromaffin cells; derived from neural crest cells; regulated by preganglionic sympathetic fibers; releases catecholamines (norepi, epi)

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8
Q

Adrenal Gland drainage

A

Left adrenal gland into the left adrenal vein into the left renal vein into the IVC; or Right adrenal gland into the right adrenal vein into the IVC (Same as left right gonadal vein)

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9
Q

Posterior Pituitary

A

Neyrohypophysis; secretes vasopressin (ADH), and oxytocin, made in hypothalamus, and shipped to posterior pituitary via neurophysins (carrier proteins); Derived from neuroectoderm (diencephalon)

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10
Q

Anterior Pituitary

A

Adenohypophysis; secretes FSH, LH, ACTH, TSH, prolactin, GH, melanotropin (MSH); derived from oral ectoderm (rathke pouch); Alpha subunit- Hormone subunit common to TSH, LH, FSH, hCG; Beta subunit- determines hormone specificity

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11
Q

Acidophils in anterior pituitary release what

A

GH, prolaction

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12
Q

Basophils in Anterior pituitary release what

A

B-FLAT; Basophils- FSH, LH, ACTH, TSH

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13
Q

Endocrine pancreas cell types

A

Islets of langerhans are collections of alpha and beta and Delta endocrine cells. Islets arise from pancreatic buds. alpha=glucagon (peripheral), beta=insulin (Central); delta=somatostatin (interspersed).

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14
Q

Synthesis of insulin

A

Preproinsulin (synthesized in RER) gets cleaved of “presignal” making proinsulin (stored in secretory granules) then cleavage of proinsulin then you get exocytosis of insulin and C-peptide equally. Insulin and C-peptide and increase in insulinoma, whereas exogenous insulin lacks C-peptide.

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15
Q

Effects of insulin

A

Anabolic effects of insulin: increase glucose transport in skeletal and adipose tissue; increase glycogen synthesis and storage, increase triglyceride synthesis and storage, increase triglyceride synthesis, increase Na retention (kidneys), increases protein synthesis (muscles), increase cellular uptake of K and amino acids, decrease glucagon release.

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16
Q

Insulin dependent glucose transporter

A

GLUT-4: in adipose and skeletal muscle

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17
Q

Insulin independent glucose transporters

A

GLUT-1: RBCs, Brain, Cornea;
GLUT-2 (bidirectional): beta islet cells, liver, kidney, small intestine;
GLUT-5 (Fructose): Spermatocytes and GI tract

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18
Q

What does the brain use for its energy source

A

Fed state: glucose;

Starvation: ketone bodies

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19
Q

What do RBCs use for energy

A

Always use glucose; they lack mitochondria

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20
Q

Regulation of insulin release

A

Glucose enters the cell via glut-2; Glucose goes through glycolysis and increase ATP/ADP; ATP closes ATP sensitive K channels; this leads to depolarization; voltage gated Ca channels open; intracellular Ca increases; Exocytosis of insulin granules

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21
Q

Glucagon

A

Made from alpha cells of pancreas; Catabolic effects include: Glycogenolysis, gluconeogenesis, lipolysis and ketone production; Regulation: secreted in response to hypoglycemia, inhibited by insulin, hyperglycemia, and somatostatin

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22
Q

What is this hormones function: CRH

A

increased ACTH, MSH, beta endorphin; decrease in chronic exogenous steroid use

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23
Q

What is this hormones function: Dopamine

A

Decreases prolactin; Dopamine antagonists (like antipsychotics) can cause galactorrhea

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24
Q

What is this hormones function: GnRH

A

Increases FSH, LH; Regulated by prolactin, Tonic GnRH suppresses HPA axis, Pulsatile GnRH leads to puberty, fertility

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25
Q

What is this hormones function: Prolactin

A

Decreases GnRH; Pituitary prolactinoma can lead to amenorrhea, osteoporosis

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26
Q

What is this hormones function: Somatostatin

A

Decreases GH, TSH; Analogs used to treat acromegaly

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27
Q

What is this hormones function: TRH

A

increases TSH, prolactin

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28
Q

Prolactin: secreted from

A

Secreted from anterior pituitary

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29
Q

Prolactin: function

A

Stimulates milk production in breast; inhibits ovulation in females and spermatogenesis in males by inhibiting GnRH synthesis and release; Excessive amounts of Prolactin can lead to decreased libido

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30
Q

Prolactin: Regulation

A

Prolactin secretion from anterior pituitary is tonically inhibited by dopamine from hypothalamus. Prolactin in turn inhibits its own secretion by increasing dopamine synthesis and secretion from hypothalamus. TRH increases prolactin secretion.

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31
Q

What does Dopamine do to Prolactin

A 
Dopamine agonists (bromocriptine) inhibit prolactin secretion and can be used in treatment of prolactinoma. 
Dopamine antagonists (most antipsychotics) and estrogens (OCPs, pregnancy) stimulate prolactin secretion.
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32
Q

Growth Hormone (somatotropin): Source

A

Secreted mainly by anterior pituitary

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33
Q

Growth Hormone (somatotropin): Function

A

Stimulates linear growth and muscle mass through IGF-1/somatomedin secretion. Increased insulin resistance (diabetogenic).

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34
Q

Growth Hormone (somatotropin): Regulation

A

Released in pulses in response to growth hormone-releasing hormone (GHRH). Secretion increases during exercise and sleep. Secretion inhibited by glucose and somatostatin.
Excess secretion of GH (pituitary adenoma) may cause acromegaly (adults) or gigantism (children).

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35
Q

Antidiuretic hormone: Source

A

Synthesized in hypothalamus (supraoptic nuclei), release by posterior pituitary.

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36
Q

Antidiuretic hormone: Function

A

Regulates serum osmolarity (V2 receptor) and blood pressure (V1 receptor). Primary function is serum osmolarity regulation (ADH decreased serum osmolarity, increased urine osmolarity) via regulation of aquaporin channel transcription in principal cells of renal collecting duct.

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37
Q

Antidiuretic hormone: diabetes insipidus

A

decreased ADH in central; normal or increased in nephrogenic DI or primary polydipsia. Nephrogenic DI can be caused by mutation in V2 receptor.
Desmopressin (ADH analog) = treatment for central DI

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38
Q

Antidiuretic hormone: How is it regulated

A

Osmoreceptors in hypothalamus (primary); hypovolemia (secondary)

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39
Q

17 alpha hydroxylase deficiency

A

Increase in Mineralcorticoids, decreased cortisol and sex hormones; Labs would show HTN, Hypokalemia, decreased DHT; Presents two main ways: XY presentation would be pseudohermaphroditism (ambigous genitalia, undescended testes). XX lack secondary sexual development.

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40
Q

21 hydroxylase deficiency

A

decreased mineralcorticoids and cortisol; increased sex hormones; labs show hypotension, hyperkalemia, increased renin activity, increased 17-hydroxy-progesterone; most commonly presents in infancy (salt wasting) or childhood (precocious puberty, XX would be virilization

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41
Q

11beta hydroxylase deficiency

A

decreased aldosterone but increased 11-deoxycorticosterone (aldosterone intermediate), decreased cortisol, increased sex hormones; HTN with low renin; XX presents with virilization

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42
Q

Cortisol: source

A

adrenal zona fasiculata; bound to corticosteroid-binding globulin,

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43
Q

Cortisol: function

A

increased blood pressure (upregulates alpha 1 receptors on arterioles causing increased sensitivity to Epi, NE), Increased insulin resistance (diabetogenic) increased gluconeogenesis lipolysis proteolysis, decreased fibroblasts activity (causes striae), decreased inflammatory responses (inhibits production of leukotrienes and prostaglandins, inhibits leukocyte adhesion leading to neutrophilia, blocks histamine release from mast cells, reduces eosinophils, blocks IL-2 production; decreased born formation (Decreased osteoblast activity); Cortisol is a BIG FIB, exogenous corticosteroids can reactivate TB and candidiasis (blocked IL-2 production)

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44
Q

Cortisol: regulation

A

CRH (from hypothalamis) stimulates ACTH release (pituitary), causing cortisol production in adrenal zona fascilulata, excess cortisol decreases CRH, ACTH and cortisol. Chronic stress induces prolonged secretion

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45
Q

PTH: source

A

Chief cells of parathyroid gland

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46
Q

PTH: Function

A

Increased bone resorption, increased kidney reabsorption of Ca in distal convoluted tubule, decreased reabsorption of PO4 in proximal convoluted tubule, Increased 1,25 (OH)2 D3 (calcitrol) production by stimulating kidney 1alpha-hydroxylase. PTH increases serum Ca, decreases serum phosphate, uncreased urine phosphate. Increased production of macrophage colony-stimulating facotr and RANK-1 (activator of NF-kappaB ligand), RNAK-L binds RANK on osteoblast causing osteoclast stimulation and increased Ca.

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47
Q

PTH related peptide

A

PTHrP functions like PTH and is commonly increased in malignancies (e.g. paraneoplastic syndrome)

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48
Q

PTH: regulation

A

Decreased serum Ca leads to increased PTH secretion;
Decreased serum Mg leads to increased PTH secretion;
Massively decreased MG leads to decreased PTH secretion;
Common causes of decreased mg include diarrhea, aminoglycosides, diuretics, and alcohol abuse.

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49
Q

Calcium homeostasis

A

Plasma Ca exists in three forms: ionized (~45%), Bound to albumin (~40%), Bound to anions (~15%); Increase in pH causing increased affinity of albumin (negative charge) to bind Ca causing clinical manifestations of hypocalcemia of hypocalcemia (cramps, pain, paresthesias, carpopedal spasm).

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50
Q

Vitamin D (cholecalciferol): Source

A

D3 from sun exposure in skin. D3 ingested from plants. Both converted to 25-OH in liver and to 1,25 (OH)2 (active form) in kidney. 24,25-(OH)2 D3 is an inactive form of vitamin D. Vit D absorbed in ilium.

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51
Q

Vitamin D (cholecalciferol): Deficiency

A

Causes rickets in kids and osteomalacia in adults. Cause by malabsorption, decreased sunlight, poor diet, chronic kidney failure.

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52
Q

Vitamin D (cholecalciferol): Function

A

Increased absorption of dietary Ca and PO; increased bone resorption causing increased Ca and PO; PTH leads to increased Ca reabsoprtion and decreased PO4 reabsorption in the kidney whereas 1,25 OH leads to increased absorption of both Ca and PO in the gut.

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53
Q

Vitamin D (cholecalciferol): Regulation

A

Increased PTH, decreased Ca, decreased PO3 all causine increasd 1,25 (OH)2 production. 1,25 (OH)2 feedback inhibits its own production

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54
Q

Calcitonin: Source

A

Parafollicular cells (C cells) of thyroid

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55
Q

Calcitonin: function

A

decreased bone resorption of Ca; calcitonin opposes action of PTH. Not important in normal Ca homeostasis.

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56
Q

Calcitonin: regulation

A

Increased serum Ca causes calcitonin secretion

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57
Q

What hormones work through cAMP pathway

A

FLAT ChAMP: FSH, LH, ACTH, TSH, CRH, hCG, ADH (v2 receptor, MSH, PTH, calcitonin, GHRH, glucagon

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58
Q

What hormones work through the cGMP pathway

A

ANP, NO (EDRF); think vasodilators

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59
Q

What hormones work through the IP3 pathway

A

IP 3 GOAT HAGs: GnRH, Oxytocin, ADH (V1 receptor), TRH, Histamine (H1 receptor), Angiotensin II, Gastrin

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60
Q

What hormones work through Steroid receptor

A

VETTT CAP: Vit D, Estrogen, Testosterone, T3/T4, Cortisol, Aldosterone, Progesterone

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61
Q

What hormones work through the intrinsic tyrosine kinase pathway

A

MAP kinase pathway, think growth factors: Insulin, IGF-1, FGF, PDGF, EGF

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62
Q

What hormones work through the receptor associated tyrosine kinase

A

JAK/STAT pathway, think acidophiles and cytokines: PIG; Prolactin, Immunomodulators (cytokines, IL2, IL6, IL8, IFN), GH

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63
Q

Signal pathway of steroid: how do they travel through the blood

A

Are lipophilic and therefore must circulate bound to specific binding globulins, which increase their solubility

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64
Q

Signaling pathway of steroids: In men, what happens when you increases SHBG

A

Increased sex hormone-binding globulin (SHBG) lowers free testosterone leading to gynecomastia

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65
Q

Signaling pathway of steroids: In women, what happens when you decrease SHBG

A

Decreased sex hormone-binding globulin (SHBG) raises free testosterone levels leading to hirsutism

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66
Q

Signaling pathway of steroids: In pregnancy, what happens to SHBG and free estrogen

A

Pregnancy increases SHBG but free estrogen levels remain the same

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67
Q

What are thyroid hormones

A

T3 and T4;
Iodine containing hormones that control the body’s metabolic rate;
T3 is the major active one, T4 is converted to T3, but there is more T4 in the body

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68
Q

Thyroid hormones: functions

A 
Bone growth (synergistic with GH), CNS maturation; increased beta 1 receptors on the heart= increased CO, HR, SV, contractility; Increased metabolic rate via increased Na/K atpase activity= increased O2 consumption, RR, body temperature; 
Increased glycogenolysis, gluconeogenesis, lipolysis
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69
Q

Thyroid function: Regulation

A

TRH from hypothalamus, stimulates TSH in pituitary, which stimulates follicular cells. Negative feedback from T3/T4 to anterior pituitary decreases sensitivity to TRH.

70
Q

Wolff-Chaikoff effect

A

Excess iodine temporarily inhibits thyroid peroxidase causing decrease iodine organification causing decreased T3/T4 production.

71
Q

T4 is converted to T3 by

A

5’-deoidinase; located in the peripheral tisuue

72
Q

Thyroxine binding globulin: what is it, what effects it

A

TBG binds T3 and T4 in the blood (makes them inactive), Get decreased TBG in hepatic failure, Increased estrogen (OCPs or pregnancy) increases TBG

73
Q

Thyroid hormone and peroxidase

A

Peroxidase is an enzyme responsible for the oxidation and organification of monoiodotyrosine (MIT) and diiodotyrosine (DIT); 2 DIT on a thyroglobulin is a T4, One MIT and one DIT on a thyroglobulin make T3

74
Q

Etiology of Cushing Syndrome

A

Increased cortisol due to a variety of causes:
Exogenous corticosteroid-#1 cause, results in decreased ACTH, bilateral adrenal atrophy;
Primary Adrenal adenoma, hyperplasia, or carcinoma-Results in decreased ACTH, atrophy of uninvolved adrenal gland, can also present as primary aldosteronism (Conn syndrome);
ACTH-secreting Pituitary adenoma (AKA cushing disease), paraneoplastic ACTH secretion (like small cell lung cancer, bronchial carcinoids)-results in increased ACTH, bilateral adrenal hyperplasia. Cushing disease is responsible for the majority of endogenous cases of Cushing syndrome

75
Q

Findings in Cushing Syndrome

A

HTN, weight gain, moon facies, truncal obesity, buffalo hump, hyperglycemia (insulin resistance), skin changes (thinning and striae), osteoporosis, amenorrhea, and immune suppression.

76
Q

Diagnosis of Cushing syndrome

A

Screening tests: increased free cortisol on 24 urinalysis, midnight salivary cortisol, and overnight low dose dexamethasone suppression test (measure serum ACTH. if decreased, suspect adrenal tumor. If increased, distinguish between Cushing disease and ectopic ACTH secretion with a high dose (8mg) dexamethasone suppression test and CRH stimulation test. Ectopic secretion will not decreases with dexa because it doesn’t respond to negative feedback. Ectopic secretion will not increase with CRH because pituitary ACTH is suppressed.

77
Q

Primary hyperaldosteronism

A

Caused by adrenal hyperplasia or an aldosterone secreting adrenal adenoma (Conn syndrome), resulting in HTN, Hypokalemia, metabolic alkalosis (alpha intercalated secrete H+ when aldosterone hits it), and low plasma renin (kidneys be like NOOOO). Normal sodium and no edema. May be bilateral or unilateral

78
Q

Secondary hyperaldosteronism

A

Renal perception of low intravascular volume leads to overactive Renin-Angiotensin system (think renal artery stenosis, CHF, cirrhosis, or nephrotic syndrome. Associated with high plasma renin.

79
Q

Addison disease

A

Chronic primary adrenal insufficiency; due to adrenal atrophy or destruction by disease (like autoimmune, TB, metastasis). Deficiency of aldosterone and cortisol, causing hypotension (hyponatremic volume contraction), hyperkalemia, acidosis, and skin and mucosal hyperpigmentation (due to MSH, a by product of increased ACTH) from pro-opiomelanocortin (POMC). Characterized by adrenal atrophy and absence of hormone insufficiency (decreased pituitary ACTH production), which has no skin/mucosal hyperpigmentation and no hyperkalemia.

80
Q

Waterhouse-Friderichsen Syndrome

A

Acute primary adrenal insufficiency due to adrenal hemorrhage associated with Neisseria meningitidis septicemia, DIC, and endotoxic shock

81
Q

Neuroblastoma

A

The common tumor of the adrenal medulla in children, usually

82
Q

Pheochromocytoma: etiology

A

Most common tumor of the adrenal medulla in adults. Derived from chromaffin cells (arise from neural crest); Rule of 10s: 10% malignant, 10% bilateral, 10% extra-adrenal, 10% calcify, 10% kids

83
Q

Pheochromocytoma: symptoms

A

Most tumors secrete Epi, NE, and dopamine, which can cause episodic HTN. Associated with Von-Hippel-Lindau disease, MEN 2A and 2B. Symptoms occur in spells that relapse and remit;
Episodic hyperadrenergic symptoms (5 p’s): Pressure (increased BP), Pain (headache), Perspiration, Palpatation (tachycardia), Pallor

84
Q

Pheochromocytoma: treatment

A

Irreversible alpha antagonists (phenoxybenzamine) and beta blockers followed by tumor resection. Alpha blockade must be achieved before giving beta blocker to avoid HTN crisis. Alpha blockers must be given during surgery because surgeon might squeeze out some Epi, NE, and dopamine when he cuts it out.

85
Q

Signs and symptoms of Hypothyroidism

A

Cold intolerance (decreased heat production), Weight gain, decreased appetite, Hypoactivity, Lethargy, fatigue, weakness, constipation, decreased reflexes, myxedema (facial/periorbital), Dry cool skin, brittle hair, Bradycardia, dyspnea on exertion.

86
Q

Lab findings in hypothyroidism

A

increased TSH (sensitive test for primary hypothyroidism), decreased free T3 and T4, Hypercholesterolemia (due to decreased LDL receptor expression)

87
Q

Symptoms of Hyperthyroidism

A

Heat intolerance (increased heat production), weight loss, increased appetite, hyperactivity, Diarrhea, increased reflexes, pretibial myxedema (graves disease), periorbital edema, warm moist skin, fine hair, Chest pain, palpatations, arrhythmias, increased number and sensitivity of beta receptors

88
Q

Lab findings in hyperthyroidism

A

Decreased TSH (if primary), increased free or total T3 and T4, Hypocholesterolemia (due to increased LDL receptor expression)

89
Q

Hashimoto thyroiditis

A

Most common cause of hypothyroidism in iodine-sufficient regions; an autoimmune disorder (anti-thyroid peroxidase, anti-thyroglobulin antibodies). Associated with HLA-DR5. Increased risk of non-Hodgkin B cell lymphoma. May be hyperthyroid early in course due to thyrotoxicosis during follicular rupture. Histology shows: Hurthle cells, lymphoid aggregate with germinal centers. Findings: moderately enlarged, nontender thyroid.

90
Q

Congenital hypothyroidism (cretinism)

A

Severe fetal hypothyroidism due to maternal hypothyroidism, thyroid agenesis, thyroid dysgenesis (most common cause in the US), iodine deficiency, dyshormonogenic goiter.
Findings: Pot-bellied, Pale, Puffy-face child, with protruding umbilicus, protuberant tongue, and poor brain development: the 6 P’s;
At birth baby can be normal due to placental transfer of T4 from mom;
can get secondary decrease in Growth Hormone

91
Q

Subacute granulomatous thyroiditis (de Quervain)

A

Self-limited hypothyroidism often following a flu-like illness;
May be hyperthyroid early in course.
Histology shows granulomatous inflammation.
Findings: increased ESR, jaw pain, early inflammation, very tender thyroid!!!! The tender thyroid with granulomatous inflammation is a give away!

92
Q

Riedel Thyroiditis

A

Thyroid replaced by fibrous tissue (hypothyroid). Fibrosis may extend to local structures (e.g. airways), mimicking anaplastic carcinoma. Considered a manifestation of IgG4 related systemic disease.
Findings: fixed, hard, rock like, and painless goiter.

93
Q

Toxic multinodular goiter

A

Causes hyperthyroidism. Focal patches of hyperfunctioning follicular cells working independently of TSH due to mutation in TSH receptor. Increase release of T3 and T4. Hot nodules are rarely malignant.

94
Q

Jod-Basedow phenomenon

A

Thyrotoxicosis if a patient with iodine deficiency goiter is made iodine replete

95
Q

Graves disease

A

Most common cause of hyperthyroidism. IgG autoantibodies stimulate TSH receptors on thyroid (hyperghyroidism, diffuse goiter), retro-orbital fibroblasts (exophthalmos: proposis, extraocular muscle swelling), and dermal fibroblasts (periorbital myxedema). Often presents during stress (e.g. childbirth)

96
Q

Thyroid storm

A

Stress-induced catecholamine surge seen as a serious complication of Graves disease and other hyperthyroid disorders. Presents with agitation, delirium, fever, diarrhea, coma, and tachyarrhythmia (Cause of death). May see increased ALP due to Increased bone turnover. Treat with the 3 P’s: Propanolol (beta blocker), Propylthiouracil, Prednisolone (corticosteroids).

97
Q

Thyroid cancer

A

Thyroidectomy is treatment option for thyroid cancers and hyperthyroidism. Complications of surgery include hoarseness (recurrent laryngeal nerve damage), hypocalcemia (Due to removal of parathyroid glands), and transection of inferior thyroid artery.

98
Q

Papillary carcinoma

A

Most common, excellent prognosis. Empty-appearing nuclei (orphan annie eyes), Psammoma bodies (concentric calcifications), nuclear grooves, increased risk with RET and BRAF mutations, childhood irradiation.
Described as “fibrous stroma, microscopic blood vessels, with cell clusters. A cancer of thyroid epithelial cells”

99
Q

Follicular carcinoma

A

Good prognosis, invades thyroid capsule (unlike follicular adenoma), uniform follicles, If you do Fine Needle biopsy you may not be able to tell if disease if follicular (may not see invasion).

100
Q

Medullary carcinoma

A

From parafollicular “C Cells”; Produces calcitonin, sheets of cells in an amyloid stroma. Associated with MEN 2A and 2B (RET mutations).

101
Q

Undifferentiated/Anaplastic carcinoma

A

Older patients; invades local structure like lungs, very poor prognosis

102
Q

Thyroid cancer: Lymphoma is associated with

A

Associated with Hashimoto thyroiditis

103
Q

Primary hyperparathyroidism

A

Usually an adenoma; Hypercalcemia, hypercalciuria (Renal stones), hypophosphatemia, increased PTH ALP cAMP in urine; Can be asymptomatic, My present as weakness and constipation (Groans), abdominal/flank pain (kidney stones or acute pancreatitis), depression (psychiatric overtones); Get Osteitis fibrosa cystica- Cystic bone spaces filled with brown fibrous tissues (bone pain).
“Stones, Bones, Groans, and Psychiatric Overtones”

104
Q

Secondary Hyperparathyroidism

A

Secondary hyperplasia due to decreased gut Ca absorption and increased PO4, most often in chronic renal disease (Causes hypovitaminosis D causing decreased Ca absorption). Hypocalcemia, hyperphosphatemia in chronic renal failure vs hypophosphatemia with most other causes, increased ALP, increased PTH

105
Q

Renal osteodystrophy

A

Due to Secondary or Tertiary hyperparathyroidism. Bone lesions in kidneys, due in turn to renal disease.

106
Q

Tertiary Hyperparathyroidism

A

Refractory (autonomous) hyperparathyroidism resulting from chronic renal disease. Massively increased PTH and increased Ca

107
Q

Cortisol’s effect on glycogenolysis

A

It decreases glycogenolysis and increases glycogen synthesis, via increasing cAMP

108
Q

Hyperparathyroidism

A

Due to accidental surgical excision, autoimmune destruction, or DiGeorge syndrome;
Findings- Hypocalcemia, tetany, Chvostek sign (tapping of facial nerve and the facial muscles contract), Trosusseau sign (occulsion of brachial artery with BP cuff leads to carpal spasms)

109
Q

Psuedohypoparathyroidism

A

AKA albright hereditary osteodystrophy; autosomal dominant; unresponsiveness PTH receptors to PTH. Get Hypocalcemia, shortened 4th and 5th digits, short stature. You won’t see urinary cAMP increase after giving PTH (remember that PTH works through Gs)

110
Q

Pituitary adenoma

A

Most commonly a prolactinoma (benign). Can be functional (makes hormone) or nonfunctional (silent). Can get mass effect (bitemporal hemianopia, hypopituitarism, headache).

111
Q

Treatment for prolactinoma

A

Dopamine agonists like bromocriptine or cabergoline

112
Q

Findings in Acromegaly

A

Large tongue with deep furrows, deep voice, large hands and feet, coarse facial features, impaired glucose tolerance (insulin resistance).

113
Q

How to diagnose acromegaly

A

Uncreased serum IGF-1; failure to suppress serum GH following oral glucose tolerance test; pituitary mass seen on brain MRI

114
Q

Treatment for acromegaly

A

Pituitary adenoma resection (most common cause). If not cured, treat with octreotide (somatostatin analog) or pegvisomant (growth hormone receptor antagonist)

115
Q

Increased GH in children leads to

A

Gigantism; increased linear bone growth; cardiac failure most common cause of death.

116
Q

Symptoms of Diabetes insipidus

A

Characterized by intense thirst and polyuria with inability to concentrate urine due to lack of ADH function.

117
Q

Central Diabetes insipidus

A

Etiology: Pituitary tumor, autoimmune, trauma, surgery, ischemic encephalopathy, idiopathic;
Findings: Decreased ADH, urine specific gravity 290, Hyperosmotic volume contraction;
Diagnosis: Water restriction test shows >50% increase in urine osmolarity
Treatment: intranasal DDAVP, hydration

118
Q

Nephrogenic Diabetes Insipidus

A

Etiology: Hereditary, secondary to hypercalcemia/lithium/demeclocycline (ADH antagonist);
Findings: normal ADH levels, Urine specific gravity 290, Hyperosmotic volume contraction;
Diagnosis: Water restriction test leads to no change in urine osmolarity;
Treatment: HCTZ, indomethacin, amiloride, Hydration

119
Q

SIADH

A

Syndrome of inappropriate antidiuretic hormone secretion: Excessive water retention, Hyponatremia with continued Na urine excretion, Urine osmolarity > Serum osmolarity;
Body responds to water retention with decreased aldosterone (causing hyponatremia) to maintain near normal volume status. Very low serum Na levels can lead to cerebral edema, seizures. Corrects slowly to prevent central pontine myelinolysis.

120
Q

Causes of SIADH

A

Ectopic ADH (small cell lung cancer); CNS disorders/head trauma, Pulmonary disease, Drugs (like cyclophosphamide)

121
Q

Treatment for SIADH

A

Fluid restriction; IV hypertonic saline, conivaptan, tolvaptan, demeclocycline.

122
Q

Hypopituitarism

A

Undersecretion of pituitary hormones due to: Nonsecreting pituitary adenoma, craniopharyngioma, Sheehan syndrome, Empty Sella Syndrome (common in obese women), Brain injury, hemorrhage (pituitary apoplexy), radiation;
Treatment: Hormone replacement therapy

123
Q

Acute manifestations of Diabetes

A

Polydipsia, polyuria, polyphagia, weight loss, DKA (type 1), Hyperosmolar coma (type 2); rarely can be caused by unopposed secretion of GH and Epi

124
Q

Chronic manifestations of Diabetes

A 
Nonenzymatic glycosylation: Small vessel disease (defuse thickening of the basement membrane) causing retinpathy, glaucoma, nephropathy;
Large Vessel Atherosclerosis, CAD, peripheral vascular disease, and gangrene causing limb loss, cerebrovascular disease. MI most common cause of death. 
Osmotic damage (sorbitol accumulation in organs with aldose reductase and decreased or absent sorbital dehydrogenase): nephropathy, Cataracts;
125
Q

When is an A1C test inaccurate

A

When you have a condition that is extending the life of RBCs; like b12/folate deficiency, iron deficiency (increased life of RBC leads to increased A1C)

126
Q

Genetic predisposition of type 1 and type 2 diabetes

A

Type 1: weak (50% concordance in identical twins), polygenic

Type 2: Relatively strong (90% concordance in identical twins, polygenic)

127
Q

Type 1 diabetes is associated with what HLA

A

HLA-DR3 and 4

128
Q

Histology of pancreas in type 1 and type 2 diabetes

A

Type 1: Islet leukocytic infiltrate

Type 2: Islet amyloid polypeptide (IAPP) deposits

129
Q

Diabetic Ketoacidosis: signs/symptoms

A

Kussmaul respirations (rapid/deep breathing), nausea/vomiting, abdominal pain, psychosis/delirium, dehydration, fruity odor (due to exhaled acetone).

130
Q

Diabetic Ketoacidosis: labs

A

Hyperglycemia, Increased H+, decreased HCO3- (anion gap metabolic acidosis), increased blood ketone levels, leukocytosis, hyperkalemia, but depleted intracellular K+ due to transcellular shift from decreased insulin.

131
Q

Diabetic Ketoacidosis: Complications

A

Life-threatening mucormycosis (usually called by Rhizopus infection), cerebral edema, cardiac arrhythmias, heart failure.

132
Q

Diabetic Ketoacidosis: Treatment

A

IV fluids, IV insulin, and K+ (to replete intracellular stores); glucose if necessary to prevent hypoglycemia.

133
Q

Insulinoma

A

Tumor of Beta cells of pancreas leads to overproduction of insulin leading to hypoglycemia. Whipple triad of episodic CNS symptoms: lethargy, syncope, and diplopia/ Symptomatic patients have decreased blood glucose and increase C-peptide levels (vs. exogenous insulin use). Treatment: surgical resection

134
Q

Carcinoid syndrome

A

Rare syndrome caused by carcinoid tumors (neuroendocrine cells), especially metastatic small bowel tumors, which secrete high levels of serotonin (5-HT), not seen if tumor is limited to GI tract (5-HT degraded by liver), Results in recurrent diarrhea, cutaneous flushing, asthmatic wheezing, and right sided valvular disease (lungs degrade 5-HT). Increased 5-HIAA in urine, niacin deficiency. Treat: resection, somatostatin analog (octreotide). Rule of 1/3: 1.3 metastasize, 1/3 Present with 2nd malignancy, 1/3 are multiple.

135
Q

Zollinger Ellison syndrome

A

Gastrin secreting tumor in pancreas or duodenum. Acid hypersecretion causes recurrent ulcers in distal duodenum and jejunum. Presents with abdominal pain (Peptic Ulcer Disease, distal ulcers), diarrhea (malabsorption). May be associated with MEN 1.

136
Q

MEN 1 (Wermer Syndrome): Where do you get tumors

A

Remember the diamond;
Parathyroid, Pituitary (prolactin or GH), Pancreatic Tumors (Zollinger-Ellison syndrome, insulinomas, VIPomas, glucagonomas are rare);
Commonly presents with kidney stones and stomach ulcers

137
Q

MEN 2A (Sipple Syndrome): where do you get problems

A

Remember the Box;

Parathyroid hyperplasia, Pheochromocytoma, Medullary thyroid carcinoma (secretes calcitonin)

138
Q

MEN 2B: where do you get problems

A

Medullary Thyroid cacinoma (secretes calcitonin), Pheochromocytoma; Oral/intestinal ganglioneuromatosis (mucosal neuromas), Associated with marfanoid habitus (tall, thin, hyper-extendable joints, long fingers)

139
Q

Inheritance of MEN (multiple Endocrine Neoplasias

A

Autosomal dominant

140
Q

Diabetes drugs: treatment strategies

A

For DM1: low-sugar diet, insulin replacement;
For DM2: Dietary modification and exercise for weight loss, oral agents, non-insulin injectables, insulin replacement;
Gestational DM: dietary modifications, exercise, insulin replacement if lifestyle modification fails

141
Q

Rapid acting insulin drugs

A

Lispro, Aspart, Glulisine;
Bind insulin receptor (tyrosine kinase);
Liver: increased glycogen
Muscle: increased glycogen and protein synthesis, Increased K+ uptake
Fat: increased TG stores
For postprandial glucose control of all DM types

142
Q

Short Acting Insulin drugs

A

Regular;
Bind insulin receptor (tyrosine kinase);
Liver: increased glycogen
Muscle: increased glycogen and protein synthesis, Increased K+ uptake
Fat: increased TG stores
For all DM types and DKA, and hyperkalemia

143
Q

Intermediate acting insulin drugs

A 
NPH
Bind insulin receptor (tyrosine kinase);
Liver: increased glycogen
Muscle: increased glycogen and protein synthesis, Increased K+ uptake
Fat: increased TG stores
For all DM types
144
Q

Long Acting Insulin Drugs

A 
Glargine, Determir
Bind insulin receptor (tyrosine kinase);
Liver: increased glycogen
Muscle: increased glycogen and protein synthesis, Increased K+ uptake
Fat: increased TG stores
For basal control of all DM types
145
Q

Biguanides

A

Metformin;
Exact mechanism is unknown. decreased gluconeogenesis, increased glycolysis, Increased peripheral glucose uptake (insulin sensitivity);
Oral, first line therapy of DM2, can be used in patients without islet function;
Get GI upset, can get lactic acidosis so contraindicated in renal failure

146
Q

Sulfonylureas: first generation drug names

A

Tolbutamide, Chlorpropamide

147
Q

Sulfonylureas: Second generation drug names

A

Glyburide, Glimerpiride, glipizide (sulfa drug)

148
Q

Sulfonylureas: mechanism, uses, side effects

A

Closes K+ channels on Beta cells leading to depolarization then calcium comes in and releases insulin vesicles.
Need islet function so only useful in DM2;
Hypoglycemia in renal failure, 1st gens cause disulfiram like effects, 2nd gens cause hypoglycemia

149
Q

Glitazones and thiazolidinediones

A

Pioglitazone, Rosiglitazone;
increases insulin sensitivity in peripheral tissue. Binds to PPAR gamma nuclear transcription factor.
Used in DM2, can cause GI problems, DO NOT USE IN HEART FAILURE

150
Q

Alpha glucosidase inhibitors

A

Acarbose, Miglitol;
inhibits intestinal brush border alpha glucosidases; Delay sugar hydrolysis and glucose absorption leading to decreased postprandial hyperglycemia.
Uses: DM2;
Can cause GI problems

151
Q

Amylin analogs

A

Pramlintide;
Action: decreases gastric emptying, decreases glucagon;
Uses: DM 1 and 2
Toxicities: Hypoglycemia, nausea, diarrhea

152
Q

GLP-1 Analogs

A

Exenatide, Liraglutide
increase insulin, decrease glucagon release’
For DM 2;
Can get Nausea, vomiting, pancreatitis;

153
Q

DPP-4 inhibitors

A

Linagliptin, Saxagliptin, Sitagliptin;
Work to increase insulin, decreased glucagon release;
Used in DM2;
Can get mild urinary or respiratory infections

154
Q

Propylthiouracil and Methimazole: Mechanism

A

Block thyroid peroxidase, inhibiting the oxidation of iodide and the organification of Iodine causing inhibition of thyroid synthesis. Propylthiouracil also block 5’-deiodinase blocking the conversion of T4 to T3 in the periphery.

155
Q

Propylthiouracil and Methimazole: Clinical use

A

Hyperparathyroidism; PTU blocks Peripheral conversion, used in Pregnancy

156
Q

Propylthiouracil and Methimazole: Toxicity

A

Skin rash, agranulocytosis, aplastic anemia, hepatotoxicity, methimazole is a possible teratogen (aplastic crisis)

157
Q

Levothyroxine, Triiodothyronine:

A

Thyroxine replacement;
Used for hypothyroidism, myxedema;
Can cause tachycardia, heat intolerance, tremors, arrhythmias

158
Q

Hypothalamic/pituitary drugs: GH

A

Used for GH deficiency and Turner’s Syndrome

159
Q

Octreotide

A

Somatostatin analog;

Used for Acromegaly, Carcinoid, Gastrinoma, Glucagonoma, Esophageal varices.

160
Q

Hypothalamic/pituitary drugs: Oxytocin

A

Stimulates labor, uterine contractions, milk let-down, controls uterine hemorrhage

161
Q

Hypothalamic/pituitary drugs: ADH

A

Also called DDAVP;

Used to treat Central DI

162
Q

Demeclocycline

A

Mechanism: ADH antagonist (member of the tetracycline family);
Clinical Use: SIADH;
Toxicity: Nephrogenic DI, photosensitivity, abnormalities of teeth and bone

163
Q

Glucocorticoids: Name them

A

Hydrocortisone, Prednisone, Triamcinolone, Dexamethason, Beclomethasone, Fludrocortisone (has gluco and mineralcorticoid activity)

164
Q

Glucocorticoids: Mechanism

A

Metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as FN-kappaB.

165
Q

Glucocorticoids: Uses

A

Addison disease, inflammation, immune suppression, asthma

166
Q

Glucocorticoids: Toxicity

A

Iatrogenic cushing syndrome- Buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis (treat with bisphosphonates), adrenocortical atrophy, peptic ulcers, diabetes if chronic. Adrenal insufficiency when stopped abruptly after chronic use

167
Q

Patient on propylthiouracil or methimazole reports arthralgias fever and sore throat, what do you do

A

This is their awful side effect, they have agranunulocytosis and you need to give them a med to increase granulocyte colony stimulation.

168
Q

3 P’s of MEN1

A

Pancreatic, Pituitary, Parathyroid tumors

169
Q

renal failure and parathyroid

A

You will get secondary parathyroidism due to the inability to excrete Phosphate.

170
Q

Alcoholics with Trousseau’s sign

A

They will have low magnesium which leads to short term increase in PTH, but chronically low magnesium actually decreases PTH so you get decrease in Serum Calcium.
Treat by giving magnesium (and get the drunkard to stop drinking)

171
Q

What hormones does somatostatin inhibit

A

GH and TSH (octreotide, a somatostatin analog will inhibit both as well)

172
Q

If you get a patient with Type 1 diabetes in your office really early on in the disease process, what antibodies can you find in their blood?

A

Glutamic acid decarboxylase (GAD65) antibodies;

This is a Beta cell enzyme

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