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STEP 1 > High Yield Topics-Endocrine > Flashcards

High Yield Topics-Endocrine Flashcards

1
Q

The type of vitamin D that is obtained from exposure of skin to sun or through ingestion from dairy products

A

vitamin D3 (aka. Cholecalciferol)

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2
Q

The type of vitamin D that is obtained from ingestion of plants, fungi, and yeasts

A

vitamin D2 (Ergocalciferol)

  • STUDY AID: think of ERGOsterol in FUNGAL cell membrane
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3
Q

Both cholecalciferol and ergocalciferol convert into what storage and active forms?

A
  • 25-OH D3 (storage form)

- 1,25-(OH)2D3 (active form; calcitriol)

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4
Q

cholecalciferol and ergocalciferol convert into storage form in what organ?

A

liver

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5
Q

cholecalciferol and ergocalciferol convert into active form (calcitriol) in what organ?

A

kidney (PCT)

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6
Q

Why is vitamin D required to increase serum Ca+2 level?

A

Active Vitamin D increases intestinal absorption of Ca+2 (and PO43- also)

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7
Q

Enzyme that converts inactive/storage form (25-hydroxyvitamin D) to active form (1,25-dihydroxyvitamin D)

A

1α-hydroxylase

  • mainly in the kidneys
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8
Q

A disorder causing ↑ β-adrenergic receptor expression, leading to ↑ catecholamine effects; presents with SYSTOLIC hypertension, sweating, hot intolerance, diarrhea, warm/moist skin, palpitations/tachycardia, weight loss, hyperreflexia, and can mimic anxiety disorder

A

Hyperthyroidism

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9
Q

An autoimmune disordercaused by thyroid-“stimulating” antibody that binds and stimulates TSH receptors on thyroid; presents with hyperthyroid symptoms

A

Graves Disease

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10
Q

Caused by orbital fibroblasts
and T-Cells activation by thyrotropin (aka. TSH) receptor antibodies –> cytokine release (TNF-a, IFN-Y) –> glycosaminoglycan (GAG) deposition in eyes –> expansion/inflammation of extraocular muscles –> exophthalmos (protruding eyes)

A

Graves Ophthalmopathy

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11
Q

Lab findings of Hyperthyroidism

TSH, T4, T3, TBG

A

TSH:↓
T4: ↑
T3: ↑
TBG: normal

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12
Q

Improve Graves ophthalmopathy by decreasing the severity of inflammation and reducing the excess extraocular volume

A

Glucocorticoids

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13
Q

Caused by accumulation of GAGs in leg skin due to activation of dermal fibroblasts by thyroid-stimulating antibodies

A

Pretibial myxedema

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14
Q

The adrenergic receptor symptoms (systolic hypertension, sweating, hot intolerance, palpitations/tachycardia, hyperreflexia) can be relieved by what drug?

A

β blockers

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15
Q

Drugs that ↓ the formation of TSH (thyrotropin) via inhibition of thyroid peroxidase, the enzyme responsible for both iodine organification and coupling of iodotyrosines

A

Thioamides

  • methimazole
  • PTU
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16
Q

Which Thioamide also decreases the peripheral conversion of T4 to T3?

A

PTU

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17
Q

A serious complication of Thioamides that results in granulocyte destruction and consequent neutropenia; initially presents with fever, sore throat, and oral ulcerations

A

Agranulocytosis

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18
Q

If drug-induced agranulocytosis is suspected, what should be done?

A

Discontinue the drug and obtain CBC w/ diff to confirm diagnosis

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19
Q

A condition characterized by ↑ free T4, suppressed TSH, and low/undetectable TG; occurs with surreptitious levothyroxine abuse, use of animal-sourced thyroid supplements, and erroneous dosing of thyroid replacement therapy

A

Exogenous Hyperthyroidism

aka. Thyrotoxicosis

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20
Q

The lack of TSH stimulation continued by Exogenous Hyperthyroidism (levothyroxine) can lead to

A

ATROPHIC thyroid follicles

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21
Q

The main regulator of lipid metabolism by stimulating the mobilization and degradation of lipids (TG)

A

Thyroid hormone

  • TH ↓TG
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22
Q

HLA (Human MHC) associated with Graves disease (2)

A
  1. HLA-DR3

2. HLA-B8

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23
Q

Caused by hyperfunctioning follicular cells (hot nodules) due to TSH receptor mutations and not due to increased TSH; ↑ release of T3 and T4

A

Toxic Multinodular Goiter

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24
Q

(Hot/cold) nodules produce excess thyroid hormone, show up on the scan because they take up more of the isotope than normal thyroid tissue, and almost always are NONcancerous

A

Hot nodules

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25
Q

(Hot/cold) nodules take up less of the isotope and ARE cancerous

A

Cold nodules

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26
Q

Occurs when hyperthyroidism is left untreated and gets worse during stress (surgery, infection); presents with fever, diarrhea, delirium, and tachyarrhythmia

A

Thyroid Storm

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27
Q

The condition that occurs when large amount of excess iodide (counterintuitive) is given as a tx for thyroid storm or thyrotoxicosis –> inhibits thyroid hormone synthesis

A

Wolff-Chaikoff Effect

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28
Q

What is hyperthyroidism that occurs following administration of iodine in a patient with iodine deficiency or autonomous nodule (nodule that autonomously produce thyroid hormone)?

  • Opposite of Wolff-Chaikoff Effect
A

Jod-Basedow Effect

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29
Q

Autoimmune disorders (Graves , Hashimoto’s) and iodine deficiency cause (smooth or diffuse/nodular) goiter

A

smooth or diffuse

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30
Q

Toxic multinodular goiter and thyroid adenoma/cancer/cyst cause (smooth or diffuse/nodular) goiter

A

nodular

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31
Q

Benign solitary growth of thyroid that are nonfunctional (cold)

A

Thyroid adenoma

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32
Q

Histological finding of thyroid adenoma

A

Follicular (follicle-like)

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33
Q

Primarily produced by conversion from T4 in PERIPHERAL tissues; has a short ½ life

A

T3

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34
Q

Hypothyroidism causes ↓ expression of ____ receptors in the liver, leading to ↓ clearance of ____ and ↑ blood ____ levels

  • ____ is all same
A

LDL

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35
Q

Hypothyroidism causes ↑ level of _____ , which ↑ the risk of coronary atherosclerosis

A

TG

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36
Q

The thyroid releases ___ and ____ in response to ____ from the pituitary, which is regulated by _____ from the hypothalamus

A
  • T4 & T3
  • TSH
  • TRH
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37
Q

The most sensitive test for thyroid function; first to be outside the normal range in thyroid dysfunction

A

Serum TSH level

low TSH, low T3, low T4

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38
Q

Presents with myalgias, proximal muscle weakness, delayed relaxation of deep tendon reflexes, and “↑ CK” (creatine kinase) level due to hypothyroidism; diagnosis made by ↑ TSH

A

HYPOthyroid Myopathy

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39
Q

Inactive form of Triiodothyronine

A

rT3 (reverse T3)

  • T3 is the active form
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40
Q

Ischemic necrosis of the pituitary gland (esp. anterior) that is typically caused by systemic hypotension during DELIVERY; may present with hypothyroidism and deficiency of other pituitary hormones

A

Sheehan Syndrome

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41
Q

_______ increase serum T4-binding globulin (TBG), thereby increasing serum total T4 concentrations; serum FREE (biologically active) T4 concentration remain normal via negative feedback

A

estrogen (pregnancy)

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42
Q

Biologically active T4 (thyroxine) is (bound/free)

A

free

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43
Q

An autoimmune disorder caused by antibodies against thyroid peroxidase (TPO) and thyroglobulin (substrate needed to make thyroid hormone); present as hyperthyroid early in course due to follicular rupture causing ↑ thyroid hormone release

A

Chronic Lymphocytic Thyroiditis

aka. Hashimoto

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44
Q

Histologically presents with lymphocytic infiltrate with germinal centers

A

Chronic Lymphocytic Thyroiditis

aka. Hashimoto

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45
Q

Large, pink-staining cells filled with granular cytoplasm seen in Hashimoto’s

A

Hürthle cells

  • STUDY AID: “H”urthle cells for “H”ashimoto’s
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46
Q

HLA (Human MHC) associated with Hashimoto’s (2)

A

HLA-DR3

HLA-DR5

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47
Q

Hashimoto’s increase the risk of what lymphoma?

A

non-Hodgkin lymphoma

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48
Q

Fetal hypothyroidism caused by maternal hypothyroidism, thyroid dysgenesis, or iodine deficiency; presents with pot-bellied, puffy face, macroglossia (big tongue), big umbilicus, and poor feeding

A

Congenital hypothyroidism

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49
Q

Congenital hypothyroidism is aka.

A

Cretinism

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50
Q

A self-limiting condition following a viral illness like flu; presents with ↑ ESR and PAINFUL thyroid enlargement

A

Subacute Granulomatous Thyroiditis

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51
Q

Subacute Granulomatous Thyroiditis is aka.

A

(de Quervain)

  • STUDY AID: Quer”vain” for “pain”
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52
Q

Histological finding of Subacute GRANULOMATOUS Thyroiditis (de Quervain)

A

Granulomatous Inflammation (resembles granulomas)

  • Inflammatory infiltrate w/ macrophages and multinucleated giant cells
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53
Q

A self-limiting condition that can arise up to 1 year AFTER delivery and present as transient HYPERthyroidism –> HYPOthyroidism or vice versa; majority become euthyroid after resolution

A

Postpartum Thyroiditis

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54
Q

A condition when thyroid is replaced by FIBROUS tissue and inflammatory infiltrate due to IgG-related systemic disease; presents with a hard, PAINLESS goiter

A

Riedel Thyroiditis

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55
Q

The most common cause of goiter (enlarged thyroid) worldwide, not in US

A

Iodine deficiency

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56
Q

Drugs that interfere with the normal function of the thyroid gland (can cause both hypo- and hyperthyroidism) and can cause goiter by stimulating TSH

A

Goitrogens

  • Amiodarone
  • Lithium
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57
Q

The most common cause of hypoparathyroidism with resultant hypocalcemia

A

Complication of thyroidectomy due to inadvertent injury or removal of the parathyroid glands.

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58
Q

Post-operation hypocalcemia can be treated using

A

Ca+2 and vitamin D supplements

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59
Q

Spasm/contraction of facial muscles upon tapping of facial nerve of cheek due to hypocalcemia

A

Chvostek sign

*STUDY AID: Chvostek for “Cheek”

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60
Q

Carpal spasms when brachial artery (triceps) is occluded with BP cuff

A

Trousseau sign (백조 손모양)

  • STUDY AID: Trousseau sign for “Triceps”
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61
Q

Lab findings of hypocalcemia and hyperphosphatemia due to low parathyroid hormone

A

Primary Hypoparathryodism

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62
Q

Thymic and parathyroid hypoplasia in DiGeorge syndrome results from maldevelopment of ___ and ____ pharyngeal/branchial pouches

A
  • 3rd (inferior PT and thymus)

- 4th (superior PT)

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63
Q

Hypocalcemia can cause

  1. (Hypertension/Hypotension)
  2. neuromuscular (hyperexcitability/hypoexcitability)
A
  1. Hypotension
  2. hyperexcitability
  • STUDY AID:
    1. think about ca+2 blockers
    2. muscle spasm (chevostek sign))
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64
Q

A hereditary condition with hypocalcemia due to kidneys and bones NOT responding to the actions of PTH; presents with short stature, round face, developmental delay

A

Pseudohypoparathyroidism (type 1 A)

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65
Q

Bone abnormality seen in Pseudohypoparathyroidism; aka. Albright Hereditary Osteodystrophy

A

shortened 4th/5th fingers

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66
Q

Lab findings of Pseudohypoparathyroidism

PTH, Ca+2, Phosphate

A

↑ PTH
↓ calcium
↑ phosphate

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67
Q

Mutation of what gene is responsible for causing Pseudohypoparathyroidism?

A

GNAS gene

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68
Q

A hereditary condition that has same physical findings as in Pseudohypoparathyroidism but has COMPLETELY NORMAL lab findings; caused by GNAS gene mutation WITHOUT end-organ resistance to PTH

A

Pseudopseudohypoparathyroidism

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69
Q

Lab findings of Pseudopseudohypoparathyroidism

PTH, Ca+2, Phosphate

A

ALL NORMAL!

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70
Q

Lab findings of hypercalcemia, hypercalciuria, hypophosphatemia, and high parathyroid hormone; usually due to parathyroid adenoma or hyperplasia

A

Primary Hyperparathyroidism

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71
Q

↑ bone resorption in Primary Hyperparathyroidism increases the risk of what bone disorder?

A

Osteoporosis

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72
Q

PULSATILE administration of _______ induces a greater ↑ in osteoblast activity in proportion to osteoclast activity and a net ↑ in bone formation; used as a tx for osteoporosis

A

Recombinant PTH analog (Teriparatide)

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73
Q

Clinical features/signs of hypercalcemia due to primary hyperparathyroidism

*STUDY AID: “stones, thrones, bones, groans, and psychiatric overtones”

A
  • Stones: renal stones due to hypercalciuria
  • Thrones: polyuria
  • Bones: bone pain
  • Groans: constipation
  • Psychiatric Overtones: confusion, depression, memory loss, etc.
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74
Q

Cystic bone spaces filled with BROWN fibrous tissue causing bone pain in primary hyperparthyrodism due to increased bone turnover

A

Osteitis Fibrosa Cystica

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75
Q

Osteitis Fibrosa Cystica consists of osteoclasts and deposition of

A

hemosiderin (a protein that stores iron)

  • why it looks brown
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76
Q

A disorder caused by defective Ca-sensing receptors in the parathyroid gland and kidneys which leads to excessive renal Ca+2 reabsorption –> Hypercalcemia, HYPOcalciuria, and normal/↑ PTH

A

Familial Hypocalciuric Hypercalcemia

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77
Q

Why is PTH level normal or ↑ in Familial Hypocalciuric Hypercalcemia?

A

Because it requires HIGHER than normal calcium level to suppress PTH

  • body increases PTH thinking Ca+2 is not enough until it can finally sense with higher than normal Ca+2 level
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78
Q

Diuretic drug that can cause hypercalcaemia by ↑ the DCT reabsorption of Ca2+; lab findings include hypercalcemia and low PTH

A

Thiazides

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79
Q

↑ PTH due to ↓ Ca+2 absorption and/or ↑ phosphate level; most often caused by “chronic kidney disease” (can’t activate vitamin D, can’t reabsorb Ca+2 in kidney, and can’t excrete phosphate in kidney)

A

Secondary Hyperparathyroidism

  • look for signs of CKD (↑ serum creatine or ↑ ALP)
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80
Q

Lab findings of Secondary Hyperparathyroidism

PTH, Ca+2, Phosphate

A

↑ PTH
↓ calcium
↑ phosphate

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81
Q

Autonomous overproduction of PTH due to chronic kidney disease (end-stage), leading to ↑Ca+2

A

Tertiary Hyperparathyroidism

82
Q

Lab findings of Tertiary Hyperparathyroidism

PTH, Ca+2

A

↑↑ PTH

↑ calcium

83
Q

What enzyme converts T4 into T3 (active) and rT3 (inactive) forms?

A

5’-Deiodinase

84
Q

Shortened relaxation of deep tendon reflexes will be seen in (hypo/hyperthyroidism)

A

Hyperthyroidism

*STUDY AID: high thyroid hormone level –> increase BMR –> shortened reflex

85
Q

Delayed relaxation of deep tendon reflexes will be seen in (hypo/hyperthyroidism)

A

Hypothyroidism

*STUDY AID: low thyroid hormone level –> decrease BMR –> delayed reflex

86
Q

The thyroid-stimulating antibody of Graves disease is what kind of immunoglobuin?

A

IgG

87
Q

Poor weight gain and stridor (due to compressive goiter) are serious neonatal manifestations of (hypothyroidsm/hyperthyroidism) seen in untreated maternal disease

A

Hyperthyroidism

  • Neonatal Thyrotoxicosis due to untreated maternal Graves disease/hyperthyrodism
88
Q

T4 and T3 are (steroid/peptide) hormones

A

Steroid

  • can cross the placenta
89
Q

TSH is a (steroid/peptide) hormone

A

peptide

90
Q

ECG abnormality most likely seen in hypocalcemia

A

Prolonged QT

91
Q

How does CKD affect vitamin D, Ca+2, and phosphate levels?

A
  1. Vitamin D: decreased active form –> ↓Ca+2 absorption from gut –> Hypocalcemia
  2. ↓ Ca+2 reabsorption in kidney –> Hypocalcemia
  3. ↓ Phosphate excretion in kidney –> Hyperphosphatemia
92
Q

The site of PTH production and secretion

A

Parathyroid CHIEF cells

93
Q

Tx that uses iodine-131, a radioactive element that emits beta rays, to destroy thyroid tissue.; used for Graves disease

A

RADIOACTIVE iodine ablation

94
Q

Tx used for the IMMEDIATE control of symptoms in patients with hyperthyroidism/thyroid storm

A

Non-selective beta blocker (propranolol)

95
Q

The transmembrane carrier/receptor that transports both iodine (both radioactive iodine or natural iodine) and Na+ into thyroid tissue

A

NIS (sodium/iodide symporter)

96
Q

Elevated serum _____ indicates increased bone turnover in hyperparathyroidism

A

ALK (alkaline phosphatase)

97
Q

Cytokine secreted by osteoblast when induced by PTH to activate osteoclasts –> increase serum calcium

A

IL-1

98
Q

Enzyme that assists the chemical reaction that adds iodine to a protein called thyroglobulin, a critical step in GENERATING thyroid hormones

A

Thyroid Peroxidase (TPO)

99
Q

The sites (2) of hypothalamus that produce ADH and oxytocin

A

Supraoptic nucleus (SON) & Paraventricular nucleus (PVN) of hypothalamus

100
Q

Carrier proteins that carry Oxytocin and ADH from hypothalamus to posterior pituitary

A

Neurophysins

101
Q

Characterized by low serum Na+ and osmolality, inappropriately concentrated urine, and clinically normal volume status (euvolemic hyponatremia)

A

SIADH

102
Q

Characterized by intense thirst and polyuria with inability to concentrate urine due to LACK of ADH; caused by injury to hypothalamus (permanent) or posterior pituitary (transient)

A

Central Diabetes Insipidus

103
Q

Tx for Central DI

A

Desmopressin

  • urine osmolality will increase to normal level for central DI
104
Q

Characterized by intense thirst and polyuria with inability to concentrate urine due to failure of response to ADH; caused by ADH receptor mutation or medications (lithium)

A

Nephrogenic Diabetes Insipidus

105
Q

Tx for nephrogenic DI

A

Thiazide

*diuretic but produces a paradoxical antidiuretic effect in nephrogenic DI

106
Q

Characterized by excessive intake of water, leading to hyponatraemia and polyuria; water restriction concentrates urine osmolality

A

1° (Psychogenic) polydipsia

107
Q

The most common hormone produced by pituitary adenomas; causes hypogonadism in males & amenorrhea and galactorrhoea in females

A

Prolactin

  • prolactinoma
108
Q

Ocular defect due to compression of optic chiasm by pituitary adenoma; decreased peripheral vision

A

Bitemporal Hemianopsia

109
Q

Prolactin (increases/suppresses) GnRH, leading to ____ LH & FSH

A

suppresses; decreased

110
Q

Prolactin can cause ↓ GnRH, leading to ↓_____ production —> ↑ risk of osteoporosis and vaginal dryness & atrophy

A

Estrogen

111
Q

Tx for prolactinoma

A

DA agonists

  • Bromocriptine
  • Cabergoline
112
Q

Hypercortisolism caused by ACTH-secreting pituitary adenoma, ectopic ACTH production, or exogenous corticosteroids; presents with stretch marks and central obesity

A

Cushing syndrome

113
Q

A Cushing syndrome caused by ACTH-secreting pituitary adenoma

A

Cushing disease

114
Q

How do you distinguish Cushing syndrome caused by Cushing disease (pituitary adenoma) vs. ectopic ACTH secretion (SCLC)

A

ACTH and cortisol levels will be suppressed with HIGH-dose dexamethasone in Cushing Disease

  • ACTH and cortisol will remain elevated in ectopic ACTH secretion
115
Q

How do you distinguish Cushing syndrome caused by exogenous corticosteroids from other causes?

A

Low ACTH and atrophy of bilateral adrenal cortex

116
Q

Hormones produced by Zonular Glomerulosa, Fasciculata, and Reticularis of adrenal cortex

A
  • Aldosterone
  • Cortisol
  • Androgens

*STUDY AID: GFR

117
Q

Destruction of adrenal glands due to autoimmune disease, leading to suppressed mineralocorticoids and glucocorticoids & increased ACTH production from the pituitary gland; presents with hypotension, hyperpigmentation, weight loss, and hypoandrogenism (lack of pubic hair)

A

Primary Adrenal Insufficiency

aka. Addison Disease

118
Q

Why does Addison disease present with weight loss?

A

lack of cortisol production

119
Q

What causes hyperpigmentation in Primary adrenal insufficiency (PAI)?

A

Increased ACTH (due to low cortisol and low aldosterone) which also induces melanin synthesis

120
Q

Atrophy of adrenal glands due to chronic corticosteroid therapy, leading to suppressed ACTH & CRH production; presents WITHOUT hyperpigmentation since no ACTH production; aldosterone production is not affected

A

Secondary Adrenal Insufficiency

121
Q

The most common cause of secondary AI

A

Glucocorticoid therapy

122
Q

A medical emergency (fever, shock, mental status changes) caused by a lack of cortisol in patients with adrenal insufficiency; triggered by stress

A

Adrenal Crisis

123
Q

A condition that decreases “CRH” (and therefore ACTH and cortisol) production due to sudden discontinuation of chronic STEROID therapy; aldosterone is NOT affected!

A

Tertiary Adrenal Insufficiency

124
Q

Increased secretion of aldosterone from adrenal gland due to adrenal adenoma or hyperplasia; presents with low renin, hypokalemia, metabolic alkalosis, and treatment-RESISTANT hypertension

A

Primary Hyperaldosteronism

aka. Conn Syndrome

125
Q

Evasion of edema and Na+ retention in primary Hyperaldosteronism due to secretion of ANP and natriuresis as compensatory mechanism

A

Aldosterone Escape

126
Q

Admin of metyrapone will cause a ↓ in cortisol synthesis via inhib of 11-β-hydroxylase. In pts w/ an intact HPA axis, this will cause a reactive ↑ in ACTH, 11-deoxycortisol, and urinary 17-hydroxycorticosteroid lvls.

A

Congenital Adrenal Hyperplasia

127
Q

A term to describe a triad that may indicate the presence of an insulinoma

  • low blood glucose
  • hypoglycemia symptoms (syncope, lethargy, diplopia)
  • abrupt resolution of symptoms after normal glucose level
A

Whipple Triad

128
Q

What is produced by an insulinoma in addition to insulin that distinguishes it from exogenous insulin use?

A

C-peptide

129
Q

Tx for insulinoma

A

surgical resection/removal

130
Q

Tumor of pancreatic a cells that overproduces glucagon, leading to hyperglycemia, diarrhea, weight loss (lipolysis) and dermatitis (necrolytic migratory erythema)

A

Glucagonoma

131
Q

Tx for Glucagonoma

A

Octreotide (for diarrhea) & surgical resection

132
Q

Tumor of pancreatic D cells that overproduces somatostatin, leading to inhibition of other hormone secretion (insulin, glucagon, secretin, and cholecystokinin); presents with diabetes/glucose intolerance, steatorrhea (fatty stool), and gallstones

A

Somatostainoma

133
Q

A hormone released into the bloodstream by the duodenum to inhibit the gastric acid secretion & stimulate the bicarbonate secretion

A

Secretin

134
Q

A hormone which is secreted by cells in the duodenum and stimulates the release of BILE into the intestine

A

Cholecystokinin

135
Q

Tx for Somatostainoma

A

Octreotide (somatostatin analog) & Surgical resection

136
Q

Tumor of pancreatic cells that overproduces VIP, leading to watery diarrhea (tea-colored, persistent even with fasting), achlorhydia, and hypokalemia

A

VIPoma

137
Q

Tx for VIPoma

A

Octreotide (somatostatin analog) & Surgical resection

138
Q

Tumor of neuroendocrine cells from GI (terminal ileum) that produces ↑ 5-HT (serotonin), leading to recurrent diarrhea, wheezing, flushing/reddening, RIGHT-sided valvular heart disease, and niacin deficiency (pellagra)

  • remember that serotonin and niacin are both derived from tryptophan!
A

Carcinoid Tumor

139
Q

Since Carcinoid tumor arises from NEUROENDOCRINE cells, it is + for what IHC stains?

  • think about SCLC!
A
  • Chromogranin A
  • Synaptophysin
  • Neuron-specific enloase
140
Q

Tx for Carcinoid tumor

A

Octreotide (somatostatin analog) & Surgical resection

141
Q

The chance that carcinoid tumor can metastasize, present with 2nd malignancy, and are multiple

A

All 1/3

  • rule of thirds!
142
Q

Caused by any drug that ↑ 5-HT, leading to ↑ neuromuscular activity (hyperreflexia, hypertonia, seizure), autonomic instability (diarrhea, diaphoresis, hyperthemia), and altered mental status

A

Serotonin syndrome

143
Q

In order to avoid Serotonin syndrome, what is required after discontinuing a MAOI and before initiating SSRI therapy?

A

2 week washout period to allow time for monoamine oxidase (MAO) regeneration

144
Q

Tx for serotonin syndrome

A

Cyproheptadine (5-HT receptor antagonist)

145
Q

MEN 1 are associated with what three tumors?

A
  • Pituitary tumor
  • Pancreatic tumor
  • Parathyroid tumor
  • 3 P’s
146
Q

MEN 2A are associated with what three tumors?

A
  • Parathyroid tumor
  • Pheochromocytoma
  • Medullary Thyroid Carcinoma
  • 2 P’s
147
Q

MEN 2B are associated with what three tumors?

A
  • Pheochromocytoma
  • Medullary Thyroid Carcinoma
  • Marfanoid habitus/Mucosal Neuroma (oral/GI neuroma)
  • 1 P
148
Q

Mutation associated with MEN 1

A

MEN1 (menin, tumor suppressor gene)

149
Q

Mutation associated with MEN 2A/2B

A

RET (oncogene, codes for tyrosine kinase)

150
Q

Inheritance pattern for all MEN syndromes

A

Dominant

  • STUDY AID: “all MEN are dominant”
151
Q

A neuroendocrine tumor arising from the chromaffin cells of the Adrenal Medulla characterized by excess production of catecholamines; presents with HTN, diaphoresis, and palpitations.

A

Pheochromocytoma

152
Q

Since Pheochromocytoma arise from NEUROENDOCRINE (chromaffin) cells, it is + for what IHC stains?

A
  • Chromogranin A
  • Synaptophysin
  • Neuron-specific enloase
153
Q

Adrenal medulla (chromaffin cells) arises from

A

Neural crest cells (ectoderm layer)

154
Q

Adrenal cortex arises from

A

Mesoderm

155
Q

A drug that decreases cortisol production by inhibiting 11ß hydroxylase

A

Metyrapone

156
Q

What lab change is expected in PRIMARY adrenal insufficiency after Metyrapone administration??

A

↑ ACTH

↑ 11-deoxycortisol (cortisol precursor)

157
Q

What lab change is expected in Secondary adrenal insufficiency after Metyrapone administration??

A

↓ ACTH
↓ CRH
↓ 11-deoxycortisol (cortisol precursor)

*both fail to rise since chronic steroid use ↓ the body’s ability to produce corticosteroids

158
Q

Blistering rashes/dermatitis that can occur with too much glucagon in glucagonoma

A

Necrolytic Migratory Erythema

159
Q

What is a metabolite of serotonin (5-HT); elevated in carcinoid tumor

A

5-hydroxyindoleacetic acid (5-HIAA)

160
Q

The most likely organ that carcinoid tumor will metastasize

A

Liver

161
Q

What unique heart presentation is associated with carcinoid tumor due to increased serotonin?

A

Right-sided heart valvular disease (tricuspid, pulmonic valves)

162
Q

Production of what adrenal hormone remains intact in secondary (corticosteroid-therapy) AI?

A

Aldosterone (mineralcorticoids)

  • zona glomerulosa is not affected by “secondary” AI
163
Q

All congenital adrenal “enzyme” deficiencies are what inheritance pattern?

A

AR

164
Q

Why does Congenital Adrenal Hyperplasia present with BILATERAL adrenal gland enlargement and hyperpigmentation?

A

due to ↑ ACTH stimulation on adrenal glands and (MSH) Melanocyte-stimulating hormone

165
Q

What CAH enzyme deficiency causes ↓ mineralocorticoids, ↓ glucocorticoids, and ↑ androgens –> hyponatremia, hypotension, hyperkalemia, and ambiguous genitalia (only in females) or precocious puberty (in males)

A

21-hydroxylase

166
Q

↑ _____ confirms the diagnosis of 21-hydroxylase deficiency

A

17-hydroxyprogesterone

167
Q

What CAH enzyme deficiency causes ↓ aldosterone, ↓ glucocorticoids, and ↑ androgens –> HYPERtension and hypokalemia, and ambiguous genitalia (only in females) or precocious puberty (in males)

A

11β-hydroxylase

168
Q

Why does 11β-hydroxylase deficiency lead to HYPERtension and hypokalemia despite decreased aldosterone production?

A

due to ↑ 11-deoxycortisol that acts as mineralocorticoids

169
Q

What CAH enzyme deficiency causes ↑ mineralocorticoids, ↓ glucocorticoids, and ↓ androgens –> Hypertension, hypokalemia, and hypogonadism (boys appear phenotypically female)

A

17α-hydroxylase

170
Q

Tx for CAH

A

Corticosteroids

171
Q

Diabetes Mellitus present with what 3 P’s as clinical symptoms/signs?

A
  • Polyuria
  • Polydipsia
  • Polyphagia
172
Q

Diabetes Mellitus Type 1 is caused by autoimmune T-cell mediated destruction of

A

“B” cells of pancreas islet cells

173
Q

4 types of antibodies found in DM1

A
  1. Islet Cell Antibodies (ICA)
  2. Glutamic Acid Decarboxylase (GAD) antibodies
  3. Insulin Autoantibodies (IAA)
  4. Protein Tyrosine Phosphatase (PTP) antibodies
174
Q

Human MHC (HLA) associated with DM1

A

HLA-DR4
HLA-DR3

  • STUDY AID: 4-3 is “type 1”
175
Q

Diabetes Mellitus Type 2 is caused by increased resistance to ____ and “progressive” pancreatic B-cell failure

A

Insulin

176
Q

Which DM is associated with obesity?

A

Type 2

177
Q

Which DM is associated with strong genetic predisposition?

A

Type 2

  • Type 1 is associated with HLA but has weak genetic predisposition
178
Q

Which DM shows histological finding of pancreatic islet AMYLOID deposition

A

Type 2

  • It’s suggested that progressive beta-cell failure in type 2 diabetes correlates with the formation of pancreatic islet amyloid deposits
179
Q

Which DM shows histological finding of pancreatic islet LEUKOCYTE infiltration

A

Type 1

180
Q

Cleavage of proinsulin in pancreatic β-cell secretory granules yields insulin and what other protein?

A

C-peptide

  • also amylin
181
Q

Insulin is (steroid/peptide) hormone

A

Peptide

182
Q

Circulating levels of _____ can be used as a marker of endogenous insulin secretion

A

C-peptide

183
Q

Fasting Plasma Glucose level to diagnose diabetes

A

≥ 126 mg/dL

  • STUDY AID: think of my maximum weight!
184
Q

HbA1c level to diagnose diabetes

A

≥ 6.5%

185
Q

2-hour oral glucose tolerance test level to diagnose diabetes

A

≥ 200 mg/dL

186
Q

The most effective tx intervention in patients with diabetes

A

Smoking cessation (if smoking)

187
Q

HbA1c level reflects average blood glucose over prior ___ months

A

3

188
Q

HbA1c assay uses the life span of circulating ____ to measure blood glucose

A

erythrocytes

*RBCs live about 3 months

189
Q

A group of hormones that is released from enteroendocrine cells of GI after eating and augment the secretion of insulin from pancreatic beta cells

A

Incretins

  • Glucose-dependent Insulinotropic Polypeptide (GIP)
  • Glucagon Like Peptide-1 (GLP-1)
190
Q

Does ↑ blood glucose level induce the release of incretins?

A

NO

  • Incretins are secreted only after consumption of food (glucose)!
191
Q

The most common complication of disease in diabetic patients

A

Coronary Artery Disease

192
Q

Insulin resistance in DM2 is caused by phosphorylation of ____ by serine kinase

A

insulin receptor substrate (IRS)

193
Q

Insulin is cleared by what two organs?

A

Renal and Liver

194
Q

A condition caused by increased ketone production due to insulin noncompliance or increased insulin requirement in diabetic patients; presents with delirium, Kussmaul breathing, abdominal pain/nausea/vomiting, and dehydration

A

Diabetic Ketoacidosis (DKA)

  • STUDY AID: “DKA is Deadly”
  • Delirium
  • Kussmaul breathing
  • Abdominal pain/nausea/vomiting
  • Dehydration
195
Q

Unique feature in diabetic ketoacidosis due to exhaled acetone from increased ketone production

A

Fruity breath

196
Q

Tx for Diabetic Ketoacidosis (DKA)

A
  • Normal Saline
  • IV Regular insulin
  • K+ (if < 3.3)
197
Q

Why is K+ must be given in patients with Diabetic Ketoacidosis and K+ < 3.3?

A

Insulin activates Na+/K+ ATPase, so giving IV regular insulin will quickly drive potassium into cells, further lowering serum potassium level –> potentially can cause hypokalemia

198
Q

A condition that often presents in elderly patients w/ type 2 DM with limited access to water –> hyperglycemia leading to osmotic diuresis –> polyuria –> increased serum osmolality and dehydration

A

Hyperosmolar Hyperglycemic State (HHS)

199
Q

How do you distinguish Hyperosmolar Hyperglycemic State (HHS) from Diabetic Ketoacidosis (DKA)?

A

HHS: some insulin is still present, so ketones are ABSENT (no fruity breath)

200
Q

Tx for Hyperosmolar Hyperglycemic State (HHS)

A
  • Normal Saline
  • IV Short Acting (regular) insulin
  • K+ (if < 3.3)
  • same as DKA
201
Q

Tumor of pancreatic b cells that overproduces insulin, leading to whipple’s triad

A

Insulinoma

STEP 1 (19 decks)

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