Thyroid Gland Flashcards
(175 cards)
1
Q
Secretes thyroid hormones (tissue metabolism regulation) and secretes calcitonin (calcium level regulation)
A
Thyroid Gland
2
Q
Shape and Weight of Thyroid Gland
A
H-shaped, 15-20 g
3
Q
What happens if there is enlargement of the thyroid gland (goiter)?
A
Dysphagia (difficulty swallowing)
Dyspnea (difficulty breathing)
4
Q
Clinical Test of Thyroid Gland
A
Swallowing
5
Q
Usually 4 (3-6), located posteriorly and is often removed during thyroidectomy; it regulates calcium levels in the blood and tissues.
A
Parathyroid Glands
6
Q
Blood Supply of Thyroid Glands
A
Superior thyroid artery → external carotid
Inferior thyroid artery → thyrocervical trunk (subclavian)
Thyroidea ima artery → arch of aorta or brachiocephalic
7
Q
Venous Drainage
A
Superior, Middle, and Inferior Thyroid Veins
8
Q
Risk of Thyroidectomy
A
Laryngeal Nerve Injury → hoarseness or loss of voice
9
Q
Functional unit of the thyroid gland; Grape-like structure 100-300 um in diameter
A
Thyroid Follicles
10
Q
Composition of Thyroid Follicles
A
Follicular cells (cuboidal epithelium)
Colloid (central pink-staining area)
Parafollicular cells in between follicles
High vascularized → capillaries
11
Q
Follicular Cell Polarity – Key Orientation?
A
Apical → colloid
Basolateral → blood
12
Q
Key Organelles in Follicular Cells?
A
RER, Golgi, Mitochondria → protein secretion
13
Q
Iodide Uptake – Mechanism?
A
Active transport iodide from blood to cell
14
Q
Thyroglobulin – Synthesis Pathway?
A
RER (synthesis) → Golgi (processing) → Colloid (secretion)
15
Q
Thyroglobulin – Binds What?
A
Tyrosine residues (~70) → for iodination
16
Q
T3/T4 – Storage Form?
A
Bound to thyroglobulin in colloid
17
Q
T3/T4 – Release Steps?
A
Endocytosis → Proteolysis → Secretion into blood
18
Q
Functions of Follicular Cells
A
Iodide Uptake
Thyroglobulin Synthesis
Hormone Storage
Hormone Release
19
Q
Located between thyroid follicles; secrete calcitonin (regulates calcium levels)
A
Parafollicular Cells
20
Q
Central, pink-staining material in thyroid follicles
A
Colloid
21
Q
Main Component of Colloid?
A
Thyroglobulin (large glycoprotein)
22
Q
Thyroglobulin – Origin & Secretion?
A
Synthesized by follicular cells, secreted into colloid
23
Q
Thyroglobulin – Key Feature?
A
~70 tyrosine residues per molecule
24
Q
Substrate for thyroid hormone synthesis (T3/T4)
A
Thyroglobulin
25
Normal Thyroid Follicle – Cell Type & Colloid?
Simple cuboidal epithelium; moderate colloid
26
Hyperthyroidism – Follicular Cell Changes?
Columnar cells
Apical lacunae
↓ colloid
27
Hypothyroidism – Follicular Cell Changes?
Flattened cells
No lacunae
↑ colloid
28
Two Precursors of Thyroid Hormone
1. Iodine (plasma)
2. Tyrosine (thyroglobulin in colloid)
29
Limiting Factor in Thyroid Hormone Synthesis
Iodide availability
30
Effect of Low vs. High Iodide Levels
Low → ↓ T3/T4
High → ↑ synthesis (to a limit)
31
Minimum Daily Iodide Requirement
Adults: 150 µg
Children: 90–120 µg
Pregnant women: 200 µg
32
Yearly & Weekly Iodide Need
~50 mg/year ≈ 1 mg/week
33
Average Daily Iodide Intake
~400 µg/day (adequate)
34
Daily Iodide Turnover – Breakdown
Intake: 400 µg
Excretion: 400 µg
320 µg kidney
60 µg thyroid gland
20 µg other tissue
10 µg stool
35
Iodide Usage by Thyroid
Forms T3/T4 → used → iodide excreted via kidneys
36
Tissues That Concentrate Iodide
Thyroid
Salivary
Mammary
Lacrimal
Choroid plexus
Gastric glands
37
Where Is Iodine Deficiency Common? Why?
High-altitude areas – iodine washed away by rain
38
Where Is Iodine Abundant? Why?
Coastal areas & seafood – naturally high in iodine
39
Public Health Measure Against Iodine Deficiency
Iodized salt, promoted by Sen. Juan Flavier (former DOH Sec)
40
Target of anti-thyroid drugs
Thyroid hormone synthesis
41
4 steps in thyroid hormone synthesis
1. Iodide trapping
2. Oxidation of iodide
3. Iodination of tyrosine
4. Coupling reaction
42
Enzyme catalyzes steps 2–4 of thyroid hormone synthesis
Thyroid Peroxidase (TPO)
43
Hormone regulates all steps of thyroid hormone synthesis
TSH (Thyroid Stimulating Hormone)
44
Two main precursors for thyroid hormones?
Iodine
Tyrosine (in thyroglobulin)
45
Active transport of iodide into follicular cells
Iodide trapping
46
Which transporter mediates iodide trapping?
NIS (Sodium-Iodide Symporter)
47
NIS Transport Ratio?
2 Na⁺ : 1 I⁻
48
Where is NIS located on the cell?
Basolateral membrane of follicular cells
49
What drives NIS activity?
Sodium gradient → Secondary active cotransport
50
What hormone stimulates NIS?
TSH
51
How does LOW iodide affect NIS?
↑ NIS activity (adaptive upregulation)
52
How does HIGH iodide affect NIS?
↓ NIS expression
53
How does iodide enter the colloid?
Via Pendrin (Cl⁻/I⁻ exchanger) on apical membrane
54
Where else is NIS found (not TSH-dependent)?
Salivary
Gastric
Ciliary body
Choroid plexus
Mammary
Placenta
Lacrimal glands
55
NIS Inhibitors (anti-thyroid drugs)?
Thiocyanate (CNS⁻)
Perchlorate (ClO₄⁻)
Pertechnetate (TcO₄⁻) → ↓ iodide trapping
56
What happens during iodide oxidation?
I⁻ → I⁰ or I₃⁻ (oxidized iodine)
57
Where does iodide oxidation occur?
Apical membrane (facing colloid)
58
Enzyme responsible for iodide oxidation?
Thyroid Peroxidase (TPO)
59
Oxidizing agent used in this step 2?
H₂O₂ (hydrogen peroxide)
60
What enzymes generate H₂O₂?
DUOX1/DUOX2 (Dual oxidases with NADPH oxidase activity)
61
Purpose of oxidized iodine?
To bind tyrosine residues on thyroglobulin
62
What is organification in thyroid hormone synthesis?
Iodination of tyrosine residues on thyroglobulin
63
Products of tyrosine iodination?
MIT = 1 iodine + tyrosine
DIT = 2 iodine + tyrosine
64
Enzyme for iodination step?
Thyroid Peroxidase (TPO)
65
Is iodination TSH-dependent?
Yes
66
Are MIT and DIT biologically active?
No → must undergo coupling to become active hormones
67
What catalyzes the coupling reaction in thyroid hormone synthesis?
Thyroid Peroxidase (TPO)
68
What is formed from MIT + DIT?
T₃ (Triiodothyronine)
69
More active, less abundant
↑ during low iodide (adaptive)
T₃ (Triiodothyronine)
70
What is formed from DIT + DIT?
T₄ (Thyroxine)
71
More abundant, less active (prohormone)
T₄ (Thyroxine)
72
What are the percentages of iodinated products in the colloid (thyroglobulin-bound)?
MIT: 23%
DIT: 33%
T₃: 7%
T₄: 35% (most abundant)
73
Thyroid Synthesis Steps Summary
Step 1: Iodide Trapping
Location: Basolateral membrane
Enzyme: NIS
TSH-dependent, Na+ cotransport
Step 2: Oxidation
Location: Apical Membrane/ Colloid
Enzyme: TPO + DUOX1/X2
Requires H2O2
Step 3: Iodination
Location: Colloid
Enzyme: TPO
Forms MIT/DIT
Step 4: Coupling
Location: Colloid
Enzyme: TPO
Forms T3/T4
74
What is the direction of hormone synthesis in follicular cells?
Basolateral → Apical (into colloid)
75
What is the direction of hormone secretion?
Apical → Basolateral (into blood)
76
Which step occurs inside the follicular cell?
Step 1: Iodide Trapping
77
Where do Steps 2–4 occur?
In the colloid (extracellular)
78
How are T3 and T4 stored?
Bound to thyroglobulin in the colloid
79
What triggers hormone secretion?
TSH stimulation
80
Apical receptor that binds thyroglobulin, triggering pseudopod formation and endocytosis
Megalin
81
What happens to the endocytotic vesicle?
Fuses with lysosomes → proteolysis of thyroglobulin
82
What happens to released T3 and T4?
Freely diffuse through basal membrane → bloodstream
83
What happens to MIT and DIT?
Not secreted → deiodinated by intrathyroidal deiodinase
→ Iodide recycled, tyrosine reused
84
Thyroid Secretion Summary
T3 & T4
Secreted into blood
Vesicle fusion + diffusion
MIT & DIT
Deiodinated & recyled
Intrathyroidal deiodinase
85
Most abundant thyroid hormone in circulation
T4 (Thyroxine) — 90–93%
86
Is T4 active or a prohormone?
Prohormone → converted to T3 in tissues
87
What are the iodine positions on T4?
3, 3′, 5, 5′
88
Most biologically active thyroid hormone
T3 (Triiodothyronine) — 3–4× more potent than T4
89
What are the iodine positions on T3?
3, 3′, 5
90
What is reverse T3 (rT3)?
Inactive form of T4, ↑ during stress/illness
Iodine positions: 3, 5, 5′
91
Thyroid hormone is commonly used for hypothyroidism therapy
L-thyroxine (T4)
92
Why is L-thyroxine preferred over direct T3 therapy?
Longer half-life, allows physiologic T3 conversion, avoids overstimulation
93
Percentage of T3 and T4 are protein-bound in plasma
>99%
94
Form of thyroid hormone is biologically active?
Free (unbound) hormone
95
4 Binding Proteins
Thyroxine-Binding Globulin (70%)
Transthyretin (10-15%)
Albumin & Prealbumin (15-20%)
Lipoproteins (~3%)
96
High affinity, low capacity; Major circulating reservoir; conserves iodide & prevents renal loss; buffers acute hormonal changes
Thyroxine-Binding Globulin (70%)
97
Transports T4 in CSF; Provides thyroid hormones in the CNS
Transthyretin
98
CSF reservoir protein for thyroid hormones
Transthyretin (TTR)
99
Which proteins loosely bind thyroid hormones for quick release?
Albumin & Prealbumin — 15–20%
100
What happens to free T3 and T4 when TBG increases?
↓ Free T3 and T4 (more bound)
101
What happens to free T3 and T4 when TBG decreases?
↑ Free T3 and T4 (less bound)
102
two main roles of TBG
1. Prevents renal hormone loss (not filtered by kidneys)
2. Reservoir for rapid hormone mobilization
103
Converts T4 → T3 (extracellular); delivers T3 to circulation
🧠 Low affinity, ↑ in hyperthyroidism
Type I Deiodinase (D1)
104
Where is D1 found?
Liver, kidney, skeletal muscle, thyroid
105
Converts T4 → T3 intracellularly; regulates TSH via CNS feedback
🧠 Very high affinity, ↑ in hypothyroidism
Type II Deiodinase (D2)
106
Where is D2 found?
CNS (glia), pituitary, brown fat
107
Converts T4 → rT3 (inactive); limits T3 excess
🧠 High affinity; ↑ in hyperthyroidism
Type III Deiodinase (D3)
108
Where is D3 found?
Placenta, fetal tissues, brain, skin
109
Recycles iodide by deiodinating MIT/DIT inside the thyroid
Intrathyroidal Deiodinase
110
Secreted by the hypothalamus; a tripeptide (3 amino acids)
TRH (Thyrotropin-Releasing Hormone)
111
Secreted by thyrotropes in the anterior pituitary; stimulates the thyroid gland to produce T3 and T4
TSH (Thyroid Stimulating Hormone)
112
How is T3 involved in negative feedback?
T3 inhibits TSH and TRH secretion
🧠 T3 is the primary regulator of the feedback loop
113
How does Type II deiodinase contribute to the feedback loop?
Type II deiodinase in the pituitary converts T4 → T3 to regulate feedback
114
What happens when T3 levels are high?
Inhibits TSH and TRH secretion, reducing T3 and T4 production
115
What happens when T3 levels are low?
Loss of negative feedback → ↑ TRH and TSH → ↑ T3 and T4 production
116
Inhibits TSH secretion from the anterior pituitary; counteracts TRH
🧠 Similar to its inhibitory role in growth hormone regulation
Somatostatin
117
A biphasic autoregulatory response of iodide on thyroid function:
Low iodide → stimulates NIS → ↑ T3 and T4 synthesis
High iodide (≥2 mg/day) → inhibits hormone synthesis
Wolff-Chaikoff Effect?
118
How does excess iodide inhibit thyroid hormone synthesis?
↓ NIS gene expression
↓ TPO expression
↓ NADPH oxidase activity
🧠 Prevents thyroid hormone overproduction from high dietary iodide
119
What is the circadian rhythm of thyroid hormone secretion?
Peak: Late afternoon to early evening
Lowest: During sleep, gradually rises next day
Influenced by seasons: ↑ in cold weather to raise BMR
120
Stimulates every step of thyroid hormone synthesis and secretion
Thyroid Stimulating Hormone
121
Target of TSH
Thyroid Gland → increased T3, T4 production
122
Mode of action of TSH
Immediate
Intermediate
Long-term
123
IMMEDIATE Effects (Seconds to Minutes):
🧠 Rapid stimulation of secretion machinery
🟢 ↑ NIS (Na⁺/I⁻ Symporter) → Iodide uptake
🟢 ↑ TPO activity → Steps 2–4:
Oxidation (Step 2)
Iodination (Step 3)
Coupling (Step 4)
🟢 ↑ Pseudopod extension + Colloid endocytosis
🟢 ↑ Colloid droplet formation + Lysosomal fusion
🟢 ↑ Proteolysis of thyroglobulin → Releases T3 & T4
🟢 ↑ NADPH production (oxidative support)
124
INTERMEDIATE Effects (Hours to Days):
🧠 Stimulates gene transcription & translation
🟡 ↑ Protein synthesis (notably within several hours)
🟡 ↑ Gene expression of:
Megalin (for colloid uptake)
TPO
Thyroglobulin
NIS
125
LONG-TERM Effects (Days to Weeks):
🧠 Structural/vascular remodeling of thyroid
🔴 Occurs with chronic TSH elevation (e.g., low T3/T4 or TSH tumors):
🔴 Hypertrophy (↑ cell size)
🔴 Hyperplasia (↑ cell number)
🔴 ↑ Capillary proliferation
➡️ Goiter formation
126
Where do thyroid hormones exert their effects inside the cell?
Nucleus — binding to Thyroid Hormone Receptors (TRs).
127
Which thyroid hormone is the most active form?
T3 is the active form — binds more strongly to TRs than T4.
128
What are the two main types of thyroid hormone receptors and where are they found?
🫀 TRα1 → Heart, Skeletal Muscle
🧠 TRβ1 → Brain, Liver, Kidney
🎤 TRβ2 → Pituitary (key for negative feedback)
129
How do T3 and T4 enter cells?
Through specific membrane transporters — they cannot freely diffuse.
130
Main transporters for thyroid hormones?
💛 MCT8 & MCT10 → Transport T3 and T4 into cells
❤️ OATP1C1 → Specializes in transporting T4 into the brain
131
Major functions of thyroid hormones
✅ ↑ Oxygen consumption in cells
✅ ↑ ATP production & Basal Metabolic Rate (BMR)
✅ Regulate lipid and carbohydrate metabolism
✅ Promote growth & development, especially of the CNS
✅ Help convert beta-carotene to vitamin A
132
What symptom may result from poor conversion of beta-carotene due to low thyroid hormone?
Carotenemia (yellowish skin), especially in hypothyroidism
133
💥 Metabolic Effects
↑ BMR (Basal Metabolic Rate)
↑ O₂ use (except brain, gonads, spleen)
↑ Heat production
↑ Mitochondria
↓ Body weight
134
🍭 Carbohydrate Metabolism
↑ Glucose absorption (GIT)
↑ Glucose turnover
↑ Glycolysis (glucose breakdown)
↑ Gluconeogenesis (glucose formation)
↑ Insulin secretion
135
🥓 Lipid Metabolism
↑ Lipolysis (fat breakdown)
↑ FFA oxidation
↑ Cholesterol & FA synthesis
↑ Chylomicron clearance (fat transport cleanup)
136
🍖 Protein Metabolism
↑ Protein turnover
↑ Proteolysis (breakdown > synthesis)
↑ Urea production
💡 Summary: Hyperglycemic, Lipolytic, Proteolytic
137
❤️ Cardiovascular System
↑ HR (chronotropic), ↑ contractility (inotropic)
↑ SV, CO (Stroke Volume, Cardiac Output)
↓ TPR (vasodilation)
↑ Pulse pressure (↑ SBP, ↓ DBP)
↑ RAAS activity → ↑ blood volume
↑ Lusitropic effect (better relaxation)
138
🌬 Respiratory System
↑ Respiratory rate & minute ventilation
↑ Response to hypoxia/hypercapnia
↑ Erythropoietin → ↑ Hemoglobin
139
💧 Renal System
↑ Renal blood flow
↑ GFR (Glomerular Filtration Rate)
↑ Kidney size
140
🍽 Gastrointestinal System
↑ Motility
↑ Secretions
141
🧒 Growth & Development
↑ Bone growth & maturation
↑ Brain development
Essential for auditory development
⚠️ Deficiency → cretinism, deaf-mutism
142
🧬 Autonomic Nervous System
↑ Sensitivity to catecholamines
Synergistic effect (↑ HR, metabolism, CNS)
Permissive action
143
🧠 Central Nervous System
↑ Alertness, responsiveness, memory
↑ Mental excitation
⚠️ Excess → insomnia, anxiety
144
🦴 Endocrine System
↑ GH secretion
↓ Prolactin, PTH, calcitriol
↑ Sensitivity to cortisol, glucagon, catecholamines
145
💪 Muscular System
↑ Performance
↑ Glycolysis & glycogenolysis
146
🧖 Skin, Bone, Connective Tissue
↑ Bone & tooth development
↑ Skin, hair, nail turnover
↓ Mucopolysaccharide → prevents myxedema
147
Cause: ↑ T3 & T4
Common Signs:
Goiter
Tachycardia, palpitations
Heat intolerance, weight loss
Nervousness, tremors
Exophthalmos (Graves’)
Labs:
↑ T3/T4
↓ TSH (primary)
± ↑ TSI (if autoimmune)
HYPERthyroidism
148
Diagnosis for HYPERthyroidism
Free T4 (± T3): Most accurate
TSH: Axis involvement
TSI: Graves’ (autoimmune)
RAIU: Detect hot nodules
Imaging (US, CT, MRI): Tumors, cysts
149
Treatment Options for HYPERthyroidism
1. Surgery
💉 Subtotal/Total Thyroidectomy
💉 Lifelong hormone replacement if total
💉 Risk: parathyroid damage
2. Radioactive Iodine (RAI)
🪫 Low dose: diagnostic
🔋 High dose: destroys thyroid tissue
3. Pharmacologic
💊 TPO inhibitors: PTU, Methimazole, Carbimazole
💊 Iodides: ↓ blood flow before surgery
💊 NIS inhibitors: Rare use
150
Types of Primary HYPERthyroidism (Thyroid Gland itself)
1. Graves' Disease
2. Toxic Multinodular Goiter (Plummer’s Disease)
3. Thyroid Adenoma
151
TSI mimics TSH → ↑ T3/T4
Women (20–50 yrs)
Signs: Diffuse goiter, exophthalmos, heat intolerance, weight loss
Labs:
🟩 ↑ T3/T4
🟥 ↓ TSH
🟩 ↑ TSI
🟥 ↓ TRH
Graves’ Disease (Autoimmune)
152
Autonomous nodules → T3/T4 w/o TSH
Older patients, long-standing goiter
Signs: Nodular goiter, no exophthalmos
Labs:
🟩 ↑ T3/T4
🟥 ↓ TSH
🟥 ↓ TRH
TSI: normal or mildly ↑
Toxic Multinodular Goiter (Plummer’s Disease)
153
Benign, solitary nodule
Painless, mild-moderate hyperthyroid symptoms
No autoimmune markers
Labs:
🟩 ↑ T3/T4
🟥 ↓ TSH
🟥 ↓ TRH
TSI: Normal
Thyroid Adenoma
154
TSH-secreting pituitary adenoma
Signs: Hyperthyroid + pituitary mass (HA, vision loss)
Labs:
🟩 ↑ T3/T4
🟩 ↑ TSH
🟥 ↓ TRH
TSI: Normal
Secondary HYPERthyroidism (Pituitary cause)
155
Hypothalamic tumor → ↑ TRH
Very rare
Signs: Similar to secondary
Labs:
🟩 ↑ T3/T4
🟩 ↑ TSH
🟩 ↑ TRH
TSI: Normal
Tertiary HYPERthyroidism (Hypothalamic cause)
156
Key Feature: ↓ T3/T4 → Slowed metabolism
Common Symptoms:
Fatigue, cold intolerance
Weight gain, bradycardia
Constipation, dry skin
Depression, memory issues
HYPOthyroidism
157
Causes:
Hashimoto’s thyroiditis (autoimmune)
Iodine deficiency
Post-surgery/radiation
Idiopathic goiter
Hormones:
🟥 ↓ T3/T4
🟩 ↑ TSH
🟩 ↑ TRH (no feedback)
Hashimoto's Key Points:
Initial transient hyperthyroidism
Lymphocytic infiltration → thyroid failure
Primary HYPOthyroidism (Thyroid Problem)
158
Cause: ↓ TSH secretion
Hormones:
🟥 ↓ T3/T4
🟥 ↓ TSH
🟩 ↑ TRH (hypothalamus still functional)
Secondary HYPOthyroidism (Pituitary Failure)
159
Cause: ↓ TRH secretion
Hormones:
🟥 ↓ TRH
🟥 ↓ TSH
🟥 ↓ T3/T4
Tertiary HYPOthyroidism (Hypothalamic Failure)
160
Diagnostic Differentiation Test for HYPOthyroidism
1. TSH Test
2. TRH Stimulation Test
161
T3/T4 ↑ = Thyroid is functional → problem is pituitary or hypothalamus
TSH Test
162
↑ TSH → Hypothalamic cause (pituitary responds)
No TSH ↑ → Pituitary cause
TRH Stimulation Test
163
Cause: Long-standing hypothyroidism
Mechanism: Mucopolysaccharide buildup
Signs:
Mental slowness, fatigue ("myxedema madness")
Coarse hair, dry/yellow skin
Slow speech, husky voice
Constipation, bradycardia
Hypercholesterolemia
Myxedema (Severe Adult HYPOthyroidism)
164
Onset: Neonatal or fetal
Causes:
Maternal iodine deficiency
Thyroid agenesis/dysgenesis
Inborn hormone synthesis errors
Hypopituitarism
Maternal anti-thyroid Abs
Signs:
Mental + growth retardation
Coarse face, protruding tongue
Potbelly, deaf-mutism
Key: Mental retardation → distinguishes from dwarfism
Dx: Newborn screening → treatable early with T4
Cretinism (Congenital HYPOthyroidism)
165
Causes:
🟩 ↑ TSH (Primary Hypothyroidism)
🟩 ↑ TSI (Graves’ Disease / Hyperthyroidism)
🟩 Multiple Nodules (Multinodular Goiter)
Goiter / Enlarged Thyroid Gland
166
Clinical Exam for Goiter
Ask patient to flex neck and swallow → thyroid rises visibly if enlarged
167
Hypothyroid Goiter Treatment
Levothyroxine (T4) – long-acting, standard
Liothyronine (T3) – fast-acting, shorter half-life
👉 Goal: Restore T3/T4 → ↓ TSH → Shrink goiter
168
Purpose: Assess thyroid functionality (not structure)
Method:
✔ Use iodine isotopes: I-123 (preferred), I-131, I-125
✔ Uptake measured at 6 hr & 24 hr
✔ Normal 24-hr uptake: ~25%
Radioactive Iodine Uptake (RAIU)
169
↑ RAIU (>60%)
Hyperthyroidism
170
↓ RAIU (<5%)
Hypothyroidism
171
Hot Nodule
↑ Uptake – usually benign
172
Cold Nodule
↓ Uptake – malignancy risk
173
🧪 RAIU CURVES (Uptake Trends)
🟩 Normal (Green): ~25% at 24 hrs
🟪 Hypothyroid (Purple): Low at 6 hrs, <5% at 24 hrs
🟦 Hyperthyroid (Blue): High at 6 hrs, >60% at 24 hrs
🟥 Elevated Turnover (Red): Higher uptake at 6 hrs than 24 hrs (due to fast hormone release)
174
Treatment of HYPOthyroidism
💊 Levothyroxine (T4) – preferred for stable, long-term control
💊 Liothyronine (T3) – rapid onset, used in special cases
175
Treatment Goals for HYPOthyroidism
✔️ Normalize T3, T4, TSH
✔️ Reduce symptoms
✔️ Shrink goiter (if present)
