M2 Flashcards

Question

EPI & NE effects

Answer 1

* NE fxs primarily as a neurotransmitter for cardiac effects * both NE & EPI influence vascular tone * EPI affects metabolic processes (e.g carbohydrate metabolism) * ↑ RR * ↑ bf to skeletal muscles * intestinal muscles relax * pupils dilate * ↑BP * ↑BG * ↑HR

Answer 2

* 5 types of adrenergic receptors: ⍺1, ⍺2, β1, β2, β3 * located in diff parts of body * extent of action depends on how much of the hormone is present * at higher levels: catecholamines can also bind to receptors with lower affinity * GPCRs * at ↓[plasma]: EPI predominantly stimulates β-adrenergic receptors causing vasodilation * at ↑[plasma]: EPI stimulates ⍺-adrenergic receptors sufficiently to override vasodilation & cause vasoconstriction * each adrenergic receptor subtype is encoded by a diff gene

Answer 3

β2-adrenergic receptor

Answer 4

⍺2-adrenergic

Answer 5

Gq alpha subunit using phospholipase C to convert PIP2 to IP3 & DAG

Answer 6

Gi ⍺ subunit inhibiting adenylyl cyclase

Answer 7

Gs ⍺ subunit using adenylyl cyclase to convert ATP to cAMP

Answer 8

inhibitory: blocks adenylyl cyclase

Answer 9

phenylephrine

Answer 10

Gi ⍺ subunit inhibits adenylyl cyclase to ↓ cAMP

Answer 11

1. ↑ force & rate of contraction in myocardium 2. ↑ renin secretion in JGC cells of kidney

Answer 12

Gs protein using adenylyl cyclase to ↑ cAMP

Answer 13

Gs protein using adenylyl cyclase to ↑ cAMP

Answer 14

isoproterenol

Answer 15

EPI > > > NE

Answer 16

Gs alpha subunit using adenylyl cyclase to ↑ cAMP

Answer 17

dobutamine or isoproterenol

Answer 18

1. vasoconstriction (↑ BP) 2. contracts spleen expelling blood

Answer 19

Gq using phospholipase C to↑ IP3, DAG, & Ca

Answer 20

↓ neurotransmitter release in preganglionic neurons

Answer 21

1. vasodilation (↑ bf) 2. bronchial dilation 3. ↑ glycogenolysis & gluconeogenesis in liver

Answer 22

* not adrenergic receptors * GPCRs * subcategories: D1-like & D2-like

Answer 23

inhibits prolactin release in pituitary lactotrophs

Answer 24

important in the brain/CNS & as a paracrine signaling mol

Answer 25

- ↑ HR & inotropy (β1) - vasoconstriction in most systemic arteries & veins (⍺1) - vasodilation in muscle & liver vasculatures at low concentrations (β2) & vasoconstriction at high concentrations (⍺1) - @ low-to-moderate circulating [EPI]: ↑ CO & redistribution of CO to muscular & hepatic circulations w/ only a small change in MAP b/c systemic vascular resistance falls due to β2-adrenoceptor activation - @ ↑ plasma [EPI]: MAP ↑ b/c of binding to ⍺-adrenoreceptors on bv that offsets β2-adrenoceptor vasodilation

Answer 26

* **catecholamine-secreting tumors from chromaffin cells of adrenal medulla** * relatively rare: ≤0.5% of hypertensive patients * secrete mainly **NE** - episodes of ↑ catecholamine secretion cause **hypertension, palpitation, headache, & sweating**

Answer 27

* mineralocorticoid * synthesized in zona glomerulosa * steroidogenesis pathway: cholesterol (cholesterol desmolase) ➔ pregnenolone (3β-HSD) ➔ progesterone (21⍺-hydroxylase) ➔ 11-deoxycorticosterone (P450c11/11β-hydroxylase) ➔ corticosterone (p450aldo/adosterone synthase) ➔ aldosterone * NO p450c17 (17⍺hydroxylase or 17,20-lyase) * NO 17β-HSD

Answer 28

* intravascular space (lymphatic, blood) * interstitial space occupied by fluids

Answer 29

proximal tutbule & loop of Henle via countercurrent system (~94%) * not under endocrine control * remaining Na will be reabsorbed in the principle cells of the collecting duct in response to aldosterone

Answer 30

* kidney = major site * binds to MR in target cell & affects transcriptional changes typical of steroid hormone receptor * retains Na & water in body (water follows Na) * stimulates Na reabsorption in principal cell of collecting duct * facilitates **transcription of Na/K ATPase** pumps in basolateral membrane → pumps Na back into blood & K into cell * stimulates **Sgk1 to inactivate Nedd4-2 channels** → inactivated Nedd4-2 channels cannot destroy ENaC (Na channels) ∴ Na can re-enter cell via apical membrane * ↑ BP by ↑ ECF volume (intravascular fluid predominantly) * ↑ urine excretion of K & H+ * stimulates **expression of K channels** in apical membrane

Answer 31

man fx = conserving body Na to sustain ECF volume * when body Na is depleted, fall in ECF & plasma volume ↓ renal arterial bf & pressure * aldosterone is largely secreted in response to signals that arise from the kidney when a reduction in circulating fluid volume is sensed

Answer 32

* aldosterone facilitates K removal from ECF * ↑ K stimulates aldosterone synthesis * K depletion (hypokalemia) = ↓ aldosterone secretion * hyperkalemia = ↑aldosterone * aldosterone is critical for disposal of daily dietary K load to maintain normal plasma [K] * stimulation of aldosterone synthesis by K: depolarization of zona glomerulosa cell membrane opens Ca v-gated channels ➞ ↑ in intracellular Ca stimulates expression of CYP11B2 (P450aldo/aldosterone synthase

Answer 33

* stimulated by: * K * angiotensin II * ACTH (minimal) * inhibited by: atrial natriuretic peptide (ANP) ➔ involved in diuresis * renin: enzyme produced in juxtaglomerular cells on afferent arteriole that converts angiotensinogen ➔ angiotensin I * pathway to ↑BP, ↑[Na], ↑ECF V * control of renin release: 1. baroreceptors in JGC detect renal perfusion pressure 2. macula densa cell chemoreceptors detect levels of Na & Cl in filtrate & communicate with adjacent JGC cells to release renin at low [NaCl] * factors that stimulate renin release: 1. ↓BP 2. ↓[Na] * afferent arteriole brings unfiltered blood to kidney * efferent arteriole brings filtered blood out of kidney

Answer 34

1. macula densa cells in distal tubule detect ↓ [NaCl] & JGC detect ↓BP in afferent arteriole ➔ JGC release renin 2. renin converts angiotensinogen ➔ angiotensin I (precursor) 3. ACE (angiotensin converting enzyme) produced mainly in lungs converts angiotensin I ➔ angiotensin II (potent vasopressor) 4. angiotensin II stimulates: 1. SNS ➔ release catecholamines from adrenal medulla to stimulate vasoconstriction 2. transcription of P450aldo ➔ ↑ aldosterone: reabsorption of Na & Cl in kidney to retain water 3. vasoconstriction ➔ ↑ BP & ↑ renal bf 4. AVP secretion in neurohypophysis ➔ ↑ water reabsorption 5. normal perfusion removes stimulus & acts as ⊖ feedback

Answer 35

maintain normal ECF V & BP * ↑ transcription of P450aldo ➞ ↑ aldosterone production * vasoconstriction ➞ ↑BP ➞ ↑renal bf * release of EPI & NE from adrenal medulla ➞ enhance actitivty of SNS & NE release in nerve terminals * promote release of AVP ➞ water reabsorption in kidneys

Answer 36

AT1 & AT2 * AT1: - adrenal, CV, & renal - Gq GPCR * AT2 associated w/ other effects (e.g. growth, differentiation) that may be opposed to AT1

Answer 37

* atrial natriuretic peptide * inhibits aldosterone * secreted by atrial myocytes in response to volume expansion * binds to receptors in zona glomerulosa to directly inhibit aldosterone synthesis * ↓ aldosterone indirectly by inhibiting renin-release * **acts via intracellular cGMP which opposes cAMP** * effects: **vasodilation, hyperfiltration, & natriuresis** (Na excretion) * ↑ GFR * inhibits Na & water reabsorption in principal cells of collecting duct * **inhibits secretion of renin, aldosterone, AVP, & ACTH**

Answer 38

* primary overproduction of aldosterone with low renin * Conn's syndrome * characterized by ↑BP from ↑ retention of NaCl & H2O by kidneys + ↓ serum [K] (hypokalemia) from excess K secretion in urine * causes: - benign adrenal tumor (adenoma) - hyperplasia of 1 or both adrenal glands (idiopathic: unknown cause)

Answer 39

* main targets of aldosterone: principal cell in the collecting ducts, colon epithelial cells, & sweat glands * **↑ K channels in apical membrane** to excrete more K * **↑ Na/K ATPase pumps in basolateral membrane** to pump Na out of cell into blood & K into cell (out of blood) where it can move through channels in apical membrane to be excreted in urine * **↑ expression of Sgk1** to inactivate destruction complex for Na channels to keep them in membrane * **ENaC** = epithelial Na channel ➔ brings Na back from lumen into cell * **ubiquitin** = system cells use to recycle mol ➔ tags cells & targets for destruction * **Nedd4-2** = ubiquitin protein that targets & destroys Na channels * **Sgk1** (serum-and-glucocorticoid kinase) phosphorylates Nedd4-2 ➔ inactivates them * aldosterone stimulates Sgk1 ➔ Nedd4-2 cannot destroy ENaC

Answer 40

enzyme that converts cortisol ➔ cortisone (inactive form) * cortisol has good affinity for mineralocorticoid receptor & because plasma [cortisol] > than [aldosterone] cortisol would occupy all MCR * aldosterone ≠ substrate for 11β-HSD

Answer 41

synthesized in ER of thyrocyte & packaged into exocytosis vesicles that fuse w/ apical membrane releasing contents into colloid * contains tyrosyl residues that can be iodinated - stimulated by TSH

Answer 42

* surrounded by collagenous connective tissue where parathyroid glands are located * thyrocyte = TH producing cell (follicular cell) * functional unit of thyroid gland * produce & release TH in response to TSH * colloid = viscous gel composed of iodinated thyroglobulin * extracellular stoage of TH & thyroglobulin * storrage of iodine * where TH is synthesized

Answer 43

* production of TH * production of calcitonin

Answer 44

* TRH released from PVN * stimuli: * cold temp * adrenergic input * metabolism & energy balance from Arc nucleus * T3 is the main effector of negative feedback

Answer 45

thyroglobulin = TH precursor * glycoprotein synthesized in thyrocyte & packaged in exocytosis vesicles * contains tyrosil residues that can be iodinated

Answer 46

thyroxine (tetraiodothyronine) = prohormone * longer 1/2 life ➞ more stable * storage form * less affinity binding to THR than T3 * 5' iodine * only synthesized in thyroid gland

Answer 47

triiodothyronine = most potent active form * no 5' iodine

Answer 48

reverse T3 = inactive form * control mechanism for TH level regulation * no 5 iodine

Answer 49

follicular cell ➔ TH-producing cell * produce & release TH in response to TSH

Answer 50

* Gq ⍺ subunit GPCR * Ca & PKC involved in activation of transcription of TSH gene * TRH also promotes glycosylation of TSH gene making TSH biologically active

Answer 51

1. iodine uptake via NIS 2. Tg synthesis 3. Tg iodination 4. deposition of Tg in colloid 5. colloid uptake into follicular cells (thyrocytes) 6. proteolysis of Tg (T3/T4 production) 7. immediate release of T3/T4 from colloid storage 8. follicular cell metabolism & cell growth

Answer 52

activated PKA stimulates: 1. **hypertrophy of thyroid cells** 2. activation of iodine pumps (**NIS**) 3. Tg exocytosis 4. TPO activity 5. induces pseudopods to ↑ Tg reabsorption at colloid border 6. lysosome-mediated **proteolysis of Tg**

Answer 53

expression of (synthesis via transcription): * Tg * thyroid peroxidase (TPO)

Answer 54

Na/I symporter = pump that actively transports I (& Na) into thyrocyte across the thyrocyte **basolateral membrane** * activated by binding TSH to its receptor * disorders of NIS associated w/ **hypothyroidism** * inactivating mutation of the NIS gene: **congenital hypothyroidism** * autoimmune disease = antibiodies against NIS: **acquired hypothyroidism**

Answer 55

inactivating mutation of the NIS gene

Answer 56

autoimmune disease where the body produces antibodies against NIS

Answer 57

thyroid peroxidase: * oxidation of iodine * iodination (organification) of thyroglobulin * coupling of MIT & DIT to form T3 & T4

Answer 58

* T4 = primary secretory product of thyroid gland * thyroid = only source of T4 * T3 = most potent/active form * derived from 2 processes: 1. ~80% deiodination of T4 in peripheral tissues (primarily liver but also kidneys & others) 2. ~20% direct thyroid secretion

Answer 59

1. ~80% deiodination of T4 in peripheral tissues (primarily liver but also kidneys & others) 2. ~20% direct thyroid secretion

Answer 60

T3 & T4 made of iodinated Tg 1. iodine is oxidized by TPO activity 2. tyrosine residues on Tg are iodinated (iodination/organification) 3. **iodination** of tyrosines yields MIT & DIT: adding iodines 4. **coupling** = binding of MIT & DITs (catalyzed by TPO) to get T3 & T4 5. **pendrin channels** in apical membrane transport I into colloid (not TSH-dependent − always there on a [gradient])

Answer 61

* transported via plasma carriers: **thyroid-binding globulin (TBG)**, **albumin**, **transthyretin** (<0.5% is unbound) * plasma carrier fx: 1. occupy space on TH ∴ only free portion of TH not bound to carrier is available to enter target cell & become metabolically active 2. extend TH half-life by protecting from degradation 3. maintain large circulating pool of TH

Answer 62

* thyroid gland can modify its activity **independent** of TSH to adapt to changes in iodine availability * in response to **iodine deficiency**: * ↑ iodine transport efficiency * T3 preferentially synthesized over T4 * in response to **iodine excess**: * many thyroid fx suppressed (primarily by inhibiting NIS i.e. **Wolff-Chaikoff effect** aka **iodide block**)

Answer 63

* nuclear receptors ∴ intracellular * thyroid receptor superfamily ➞ form heterodimers w/ retinoic acid (retinoid x − RXR) inside nucleus * TRE = thyroid response element * 2 types: TR⍺ & TRβ w/ isoforms * TR⍺1 * TR⍺2 * TRβ1 * TRβ2

Answer 64

1. **monocarboxylate transporter (MCT8)** = highly specific transporter ➞ carries TH across PM 2. **binding of T3 dislocates co-repressors & activates co-activators** (or vica-versa) - **co-regulator proteins** = co-activators (CoA) & co-repressors (CoR) - CoR bind to TR inactivating it - T3-binding exchanges CoR with CoA - sometimes TR has a CoA bound already & is actively transcribing ➞ T3 binding changes CoA ➔ CoR so binding represses gene transcription 3. modulation of gene expression in target cells

Answer 65

* binding of TRs to DNA is **independent** of hormone binding * TRs bind to DNA as: * **homodimers**: combination of TR isoforms (⍺, β) * **heterodimers**: associated w/ other nuclear receptors − most commonly retinoid X receptor (RXR)

Answer 66

* # of TRs * relative expression of subtype of TR (TR⍺ &/or TRβ) * expression & activity of co-regulators

Answer 67

1. hormone synthesis can autoregulate depending on iodine availability 2. T4 converted to T3 on demand 3. multiple carrier proteins ensure that TH is stable in circulation: **thyroid-binding globulin (TBG), transthyretin, albumin** 4. **deiodinases** are present in a variety of tissues

Answer 68

synergistic response with cortisol: * maintaining/↑ levels of glucose * stopping immune system in response to stressor

Answer 69

viscous gel composed of iodinated thyroglobulin * extracellular storage of TH & thyroglobulin * storage of iodine * where TH is synthesized

Answer 70

1. **primary** ➔ problem is in the endocrine gland 2. **central** ➔ problem is in hypothalamus 3. **secondary** ➔ problem is in the pituitary gland

Answer 71

**hyperadrenocorticism** - **excess circulating cortisol or glucocorticoids** - **ACTH-independent**: ↑ cortisol but not from adrenal gland being overstimulated - most commonly iatrogenic: induced by tx given to animals by humans - **ACTH-dependent**: pituitary or non-pituitary tumors secreting ACTH or CRH ➔ **Cushing's disease** -

Answer 72

excess circulating cortisol or glucocorticoids from tumors **ACTH-dependent hyperadrenocorticism** - **pituitary-dependent:** pituitary tumor producing ACTH ➔ hyperstimulation of adrenal gland - ectopic ACTH expression by nonpituitary tumor cells: POMC precursor incorrectly cleaved to release ACTH - bilateral hyperplasia of zona fasciculata & zona reticularis **ACTH-independent hyperadrenocorticism** from adrenal tumor secreting excess cortisol/glucocorticoids

Answer 73

- **atrophy of epidermis & connective tissue** ➞ skin thinning & alopecia - **centripetal obesity**: visceral fat accumulation ➞ pendulous abdomen - dehydration - osteoporosis - muscle weakness - **polyphagia**: feeling of extreme insatiable hunger - **exophthalmos**: bulging eyes - bruising & poor healing - pruritus: itching - acne - hyperpigmentation

Answer 74

**hypoadrenocorticism**: - associated w/ mineralocorticoid deficiency - primary hypoadrenocorticism = **glucocorticoid deficiency at adrenal level** - **congenital adrenal hyperplasia** = deficiency of enzyme P450c21 → not producing enough GC - causes: - autoimmune - infectious - congenital - iatrogenic - symptom: hyperpigmentation

Answer 75

- hyperpigmentation - hypoglycemia - changes in body hair distribution - GI disturbances - weakness - weight loss - postural hypotension

Answer 76

family of enzymes that de-iodinate iodotyrosines in TH mol - no way to add I after synthesis - peripheral metabolism of TH - serves 2 purposes: 1. ensures availability of circylating & tissue-specific T3 2. ensures levels of TH remain w/in physiological range via deactivation of T4 & T3 - 5'-deiodinase (D1 & D2) removes the I at the 5' position to activate T3 - 5-deiodinase (D3) removes the I at the 5 position to convert it to rT3 & inactivate it

Answer 77

removes the I at the 5' position to activate T3 - D1: - kidney, liver, skeletal muscle (& small amount in the thyroid gland) - 5' monodeiodination forms T3 ➞ active form - most abundant - in PM of cells ➞ ensures adequate circulating levels of T3 - D2: - brain & pituitary gland - in ER close to nucleus - ensures adequate cellular levels of T3 w/in CNS - very sensitive to changing circulating levels of T4 - low levels of T4 ↑ [5'-deiodinase] - high levels of T4 ↓ [5'-deiodinase]

Answer 78

removes the I at position 5 to convert it into rT3 & inactivate it - removes circulating TH when excess (removes possibility of converting T4 ➔ T3 - highly expressed in fetal tissues, placenta, CNS - placenta = filter btwn mother & fetus - inactivates T4 by conversion to rT3 - inactivates T3 by conversion to T2 (no 5' or 5 I) - ↑ in hyperthyroidism - ↓ in hypothyroidism

Answer 79

- roles in terminal differentiation of brain cells & neural development - mostly mediated by TR⍺ → critical for life - development of the auditory system - human TH resistance syndrome (Refetoff syndrome) = mutation in TRβ ➔ deafness - congenital hypothyroidism = genetic/iodine deficiency - impairs terminal differentiation process ➔ severe mental & growth retardation - cretinism = most severe form of mental retardation caused by congenital hypothyroidism - development of sensory systems (auditory, visual) - neurogenesis - neural transmission (myelin sheath formation)

Answer 80

most severe form of mental retardation caused by congenital hypothyroidism

Answer 81

- stimulates protein expression & turnover - ↑ metabolism secondary to thermogenesis (↑ basal body temp) - stimulate expression of β-adrenergic receptors & G-proteins to enhance actions of EPI (↑ adrenergic activity in general) - net result: ↑ BMR accompanied by ↑ energy expenditure & ↑ need for O2 in tissues to support ↑ activity

Answer 82

- enhances O2 absorption by resp system - ↑ expression of erythropoietin to enhance RBC production - enhances β-adrenergic receptor-mediated effects in the heart (inotropic & chronotropic effects)

Answer 83

- ↑ GI motility tract - ↑ GI absorption efficiency - stimulate lipolysis - ↑ appetite ➔ stimulate CNS satiety/hunger centers - POMC neurons in Arc use ⍺MSH to signal PVN to secrete TRH & begin TH cascade - insulin & leptin inform brain that body has enough nutrients to ↑ metabolic rate - leptin produced by adipocytes ➞ ↑ adipocytes = ↑ leptin circulating = sufficient fat storage - insulin produced in response to food (during absorptive state) ➞ informs brain that body has food

Answer 84

- TH enhances adrenergic stimulation of brown adipose tissue by ↑ expression of genes coding for proteins that enhance the response to β3 stimulation - subsequent increase in cAMP ↑ D2 activity & ∴ intracellular T3 - TH & SNS synergistically ↑ brown adipose tissue thermogenesis & adrenergic activation of brown adipose tissue enhances intracellular D2 activity - higher thermogenic capacity in hibernation season - HPT-axis & HPT enhance thermogenic capacity

Answer 85

brown adipose tissue - rich in mitochondria ➞ gives brownish color - more efficient at using uncoupling proteins - site of non-shivering thermogenesis

Answer 86

**non-shivering thermogenesis** by UCP1 (uncoupling proteins) in mitochondria of brown adipose tissue - UCP1: brown adipose tissue (BAT) - UCP3: muscle - located in inner mitochondrial membrane - redirect H+ flow from the ATPase (final step of the respiratory chain) ➞ dissipates energy in the form of heat instead of ATP

Answer 87

- tiredness - weakness - fatigue - bradycardia - cold intolerance - constipation - mental impairment - depression - weight gain - muscle cramps - infertility - goiter (if primary hypothyroidism)

Answer 88

thyroid gland is not producing sufficient TH - anabolic state - ↓ T4 w/ low-high levels of TSH - ↓ levels of 5-deiodinase

Answer 89

replace T4 to mimic normal physiological levels & attain normal TSH levels

Answer 90

autoimmune hypothyroidism: body produces antibiodies against TPO, Tg, & TSHR * progressive destruction of the thyroid gland * symptoms: fatigue, weight gain, joint/muscle pain, feeling cold, bradycardia, slow metabolism * may present w/ goiter

Answer 91

overproduction of TH - body is in catabolic state - ↑ 5-deiodinase - ↑ T4 w/ low-high levels of TSH

Answer 92

- hx - ↓ T4 w/ low-high levels of TSH - test for specific autoimmune antibiodies

Answer 93

- nervousness - fatigue - tachycardia - palpitations - weight loss - heat intolerance - irritability - muscle weakness - tremor - sleep disturbance or insomnia - ↑ perspiration - ↑ GI motility - goiter if TG is overstimulated

Answer 94

- hx - ↑ T4 w/ low-high levels of TSH

Answer 95

- surgery - antithyroid rx: adjuvant therapy w/ no specific effect on TG can be useful to control peripheral manifestations of thyrotoxicosis (e.g. β-blockers)

Answer 96

**continuous activation of TSHR by antibodies** - autoimmune hyperthyroidism - LATS: long-acting thyroid stimulating antibody - symptoms consistent with hyperthyroidism: insomnia, weight loss, heat intolerance, tachycardia, exopthalmos - commonly presents with goiter

Answer 97

strategy to conserve energy by decreasing thermogenesis/metabolic activity & lower energy - episodes of torpor & euthermia (wake up for ~15h)

Answer 98

thyroid activity ↑ → TH ↑

Answer 99

- ↑ levels of albumin (main TH carrier proteins in blood → more can be bound: inactive & ready) - ↑ availability in D2 (intracellular conversion of T4 → T3) - NE-mediated by β-adrenergic receptors stimulates D2 - TH ↑ expression of UCP1 - more expression of β-adrenergic receptors in BAT - TH & SNS synergistically ↑ brown adipose tissue thermogenesis & adrenergic activation of brown adipose tissue enhances intracellular D2 activity - higher thermogenic capacity

Answer 100

* iodination occurs at apical colloid border * iodination of the tyrosyl residues (iodotorosines) forms monoiodotyrosine (MIT) & diiodotyrosine (DIT) * these are coupled to form T3/T4 * iodide must be oxidized by TPO to be able to iodinate tyrosine residues

Answer 101

- kidney, liver, skeletal muscle (& small amount in the thyroid gland) - 5' monodeiodination forms T3 ➞ active form - most abundant - in PM of cells ➞ ensures adequate circulating levels of T3

Answer 102

- brain & pituitary gland - in ER close to nucleus - ensures adequate cellular levels of T3 w/in CNS - very sensitive to changing circulating levels of T4 - low levels of T4 ↑ [5'-deiodinase] - high levels of T4 ↓ [5'-deiodinase]

M2 Flashcards

(133 cards)