Transcript CLINICAL ENDOCRINOLOGY & METABOLISM—INTRODUCTION

CLINICAL ENDOCRINOLOGY &
METABOLISM—INTRODUCTION
AND GENERAL CONCEPTS(总论)
Institute of Metabolism & Endocrinology
A. The rapidity and extensiveness of
advances in endocrinology have
made it increasingly difficult for
the students and physicians to take
full advantage of information
available for the understanding,
diagnosis, and treatment of clinical
disorders, not only of diseases in
endocrinology, but also of that in
all clinical specialties.
B. What easy to handle is that the
general knowledge and the principles
of endocrinology and metabolism.
C. For interest, be interested in the
interesting medical branch.
D. Main subjects
I.
Regulation systems of
extracellular communication
II. Endocrine gland and hormonesecreting cells
III. Hormones
IV. Hormone secretion rhythms
V. Hormone synthases and its
regulation
VI. Endocrine regulation axes
VII. Mechanisms of hormone action
VIII. Nutrient metabolism
IX.
X.
XI.
Systemic examination
Laboratory and special
examinations
Therapeutic principles
I. Regulation Systems of ExtraCellular Communication
nervous system
endocrine system
immune system
II. Endocrine Gland and HormoneSecreting Cells（激素分泌细胞）
A. Endocrine gland
a. hypothalamus & posterior pituitary
b. pineal gland (松果体)
c. anterior and intermedial pituitary
d. thyroid
e. parathyroid
f. endocrine pancreas (内分泌胰腺)
g. adrenal cortex and medulla
h. sexual gland (testis or ovary)
i. others: thymus (胸腺)，placenta
B. Diffuse neuro-endocrine cells
APUD(amine precursor uptake and
decarboxylation) cells in GI,
pancreas, adrenal medulla, etc.)
C. Hormone-secreting cells in tissues
atrium, endothelium, fibroblast,
lipocytes, lymphocytes
D. Structure of hormone-secreting cells
peptide/protein hormone-secreting cells:
hormone-containing granules
(激素颗粒)
steroid hormone-secreting cells:
lipid droplet (脂质小滴)
III. Hormones
A. Classification
a. as peptide/protein
b. as derivatives of amino acid (catecholamine,
5-HT, melatonin, T3/T4)
c. as derivates of cholesterol (cortisol,
aldosterone, estrogen, androgen,
progesterone, 1, 25-(OH)2D3)
B. Storage
hormone granules
thyroglobulin (甲状腺球蛋白)
C. Types of hormone secretion
endocrine (内分泌)
paracrine (旁分泌)
autocrine (自分泌)
intracrine (胞内分泌)
neurocrine (神经分泌)
juxtacrine (并邻分泌)
solinocrine (腔分泌)
amphicrine (双重分泌)
D. Hormone transportation
soluble hormone+binding protein:
insulin, GH. IGF. Glucagon-like peptide
insoluble hormone+binding protein:
T3, T4, sex steroids, cortisol, vitamin D.
E. Hormone degradation and half-life
half-life: peptides and protein:
minutes steroids: variable,
hrs degradation in liver,
kedney, other tissues, or in
hormone-secreting cells.
IV. Secretion Rhythms
A: Biological rhythms（生物节律）
milliseconds: nerve impulse, membrane
electrolytes.
minutes: neurotransmitters
hours: LH, TRH, testosterone, cortisol,
GH, prolactin, TSH, etc
days: FSH peaks
weeks: menorrhea
months: T4, 1,25-(OH)2D3, pregnancy
B. Circadian rhythms (昼夜节律)
biological “clock” in hypothalamus
(melatonin), but lost in Cushing disease
and psychosis
C. 24-hr changes of serum and urine
hormone (metabolic products)
D. Heterogeneity of serum hormones
hormone, pro-hormone (激素原),
prepro-hormone (前激素原)
monomer, dimer, trimer tetramer, etc.
fragement of peptides.
V. Hormone Synthases and Its Regulation
A. Endocrine regulation
active hormone molecule
hormone-binding protein
hormone receptor on membrane
in cytoplasma
in nucleolus (nucleoplasm)
post-receptor transduction (cascade reaction)
tropic-hormone (促激素) feedback cycle
target cell reaction
B. Paracrine/autocrine regulation
exist almost in all tissues.
“point-line” (点-线式) regulation
network
VI. Endocrine Regulation Axes
nerve impulses/cytokines
CNS
A
hypothalamus
B
pituitary gland
D
target gland
A. Hormone regulation
A: ultra-short feedback (超短反馈) B: short feedback (短反馈)
C: positive feedback (正反馈)
D: long negative feedback (负反馈)
: stimulating;
: inhibitory
B. Regulation axes (调节轴)
a. hypothalamus-pituitary-thyroid (adrenal
cortex, sexual gland)
b. GIH/GHRH-GH/GHBP-IGFs/IGFBPSIGFBP/IGFBPase
c. renin-AT-ALD
involved in renin, AT, ALD, ANP, AVP,
AM (adrenomedullin, 肾上腺髓质素)
d. axis of endocrine pancreas-energy metabolism
and body weight
involved in insulin, glucagon, glucagon-like
peptide-1, somatostatin, leptin, etc.
e. PTH-CT-1,25-(OH)2D3
involved in PTH, CT,1,25-(OH)2D3, serum Ca2+,
Pi3f. AVP-AVP receptor-AQP (aquaporin, 水孔蛋白)
V1 receptor: related to regulation of BP
V2 receptor: related to H2O reabsorption
VII. Mechanisms of Hormone Action
A. Acted as transcription- regulatory
factors
steroid hormone bindin with receptor
(cytoplasm or nucleoplasm)
H-R complex+DNA
binding domain
gene expression
protein
B. Acted at cell surface
a. peptide hormone + membrane R
postreceptor
cascade reaction
b. types of membrane R
– G-protein coupled receptor (transmenbrane 7
times) involved in PTH, AT, glucagon, LH, FSH,
TSH, AVP, CT, HCG, etc.
– receptor kinases (transmembrane 1 time), with
tyrosine kinase (activity), involved in insulin, IGF,
EGF, etc.
– receptor-linked kinases, involved in GH, PRL,
leptin
– receptors of ligand-gated ion channels
(transmembrane 4 or 6 times), involved in 5-HT,
GABA, etc.
VIII.
Nutrient Metabolism
A. General concepts:
a. metabolism, anabolism and catabolism
b. metabolic diseases (related to enzymes,
hormones, or ion channels, etc).
c. macroelement and microelement (traced
element)
d. micronutrient (Fe, F, Zn, Cu, Mn, I, Cr,
Co, etc)
e. vitamins
IX. Systemic Examination
A. Symptom and signs
a. body height (genetic factors, GH, TH, sex
hormones, IGF-1, nutrition, systemic
diseases)
b. obesity and weigh loss (genetic constitution,
nutrition, systemic disease, GH, TH, insulin,
leptin, cortisol, sex hormones)
c. polydipsia and polyuria (DM, ALD ,
hyperparathyroidism, DI)
d. hypertension with hypokalemia (primary
hyperaldosteronism, reninoma, Cushing
syndrome)
e. hyperpigmentation (ACTH, MSH, estrogen,
progesterone, androgen)
f. hair loss or hypertrichosis (hairy, 多毛症)
genetics, race, androgen.
hypertrichosis: PCOS, congenital adrenal
hyperplasia, Cushing disease, ovarian
tumors, hypothyroidism, drugs.
hair loss: cortisol , androgen ,
g. gynecomastia (男性乳腺发育):
Klinefelter syndrome, testicular
tumors, drugs.)
h. exophthalmos (突眼)：Graves disease,
chronic lymphocytic thyroiditis, eye
diseases.)
i. bone pain and fractures (osteoporosis,
hyperparathyroidisim, bone or hematologic
diseases)
X. Laboratory and Special Examinations
A. hormones and biomarkers (生化标志物)
in serum and urine: hormones,
electrolytes, sugar
B. hormone derivatives: VMA, 17-OHCS,
17-KS
C. Dynemic tests (动态试验)
stimulation test (兴奋试验)：
hypofunction (hypocortisolism)
inhibitory states (TSH in GD)
suppression test (抑制试验)：
hyperfunction (DXM for Cushing disease)
therapeutic test (治疗试验):
(spironolactone treatment in suspected
hyperaldosteronism)
provocation test (glucagon test for diagnosis
of pheochromocytoma)
X-ray film (bone diseases, kedney stones)
CT&MRI (morphologic changes)
radionuclear tomography (thyroid, pancreas,
adrenal cortex and medulla, parathyroid,
etc)
type B US (thyroid, adrenal cortex, ovary,
testis)
XI. Therapeutic Principles
A. Pathogenic therapy: supplement of nutrients,
gene treatment.
B. Hypofunction:
1. hormone replacement therapy (Addison
disease, hypothyroidism; hypogonadism)
2. drugs to stimulate hormone secretion
(sulfonylurea for type 2 DM)
3. transplantation (organ, tissue, cells)
C. Hyperfunction
1. drugs to suppress hormone secretion
(iodide for GD, spironolactone
for hyperaldosteronism. SS for
insulinoma)
2. radioactive therapy (131I for GD, γknife for pituitary tumors)
HYPERTHYROIDISM
(THYROTOXICOSIS, 甲亢)
Hyperthyroidism is only a diagnosis of
excessive thyroid hormone status, not a
concrete disease or a syndrome.
It is wrong to say “Graves disease (Graves
病)” as “hyperthyroidism (甲亢)” in brief.
Pathogenesis of Hyperthyroidism
Thyroidal origin
Graves disease
multiple nodular thyrotoxicosis (多结节性毒性甲状腺肿)
Plummer disease (toxic thyroid adenoma)
automatic hyperfunctional thyroid nodules (自主
功能性甲状腺结节)
multiple autoimune endocrine syndrome with
hyperthyroidism (多发性自身免疫性内分泌腺
病伴甲亢)
thyroid carcinomas
neonatal hyperthyroidism
genetic toxic thyroid hyperplasia/goiter
iodine-induced hyperthyroidism (碘甲亢)
Pituitary origin
pituitary TSHoma
thyroid hormone insensitivity syndrome
(pituitary type, 垂体型TH不敏感综合征)
paracarcinoma syndrome
HCG-related hyperthyroidism
carcinomas (lung, GI, pancreas) with
hyperthyroidism
Ovarian goiter with hyperthyroidism
Iatrogenic hyperthyroidism (医源性甲亢)
Transient hyperthyroidism
Subacute
de Quervian thyroiditis (肉芽肿性甲状腺炎)
hymphocytic thyroiditis (postpartum, IFN, IL, Li)
trumatic thyroiditis
radioactive thyroiditis
Chronic
chronic lymphocytic thyroiditis
GRAVES DISEASE (GD)
I.
II.
III.
IV.
V.
Pathogenesis
Histopathology
Clinical presentation
Laboratory and special exams
Diagnosis and differential
diagnosis
VI. Treatment
Graves Disease (GD)
GD is also called: diffuse toxic goiter
Basedow disease
Subclinical hyperthyroidism is usually
referred to a GD state with (ab)normal T3,T4,
decreased TSH, and no clinical symptoms of
hyperthyroidism
I. Pathogenesis
A. Abnormalities of immune system
a. TSH-R-Ab + TSH-R
mimic the action of
TSH
hyperfunction and goiter.
b. functioning of Ig
Th hypersensitivity + IL-1,
IL-2
B cells produce TSH-R-Ab (TRAb)
c. TRAb
stimulating IgG
hyperfunction(TSAb)
inhibitory IgG
hypofunction and antagonist
of TSHR andTSAb (TF1Ab, TGBAb)
growth-stimulating IgG (TGI)
B. Other factors
genetic factors
infective factors
stress (physical or emotional)
C. Thyroid-associated ophthalmopathy
(TAO)
unknown
GAG (葡萄聚糖) accumulation, T cell
infiltration, edema, fibrosis and sight
loss.
II. Histopathology
A. Thyroid
goiter: symmetrical, diffuse, soft enlarged
after treatment: lobular
follicles: hyperplastic column with scant colloid,
papillary projections,
vascularity increased
lymphocytes and plasma cells infiltration
B. Eyes
orbital contents increased, containing mucoprotein,
GAG (glycosaminoglycan, 葡糖聚糖), lymphocytes.
C. Skin (dermopathy)
hyaluronic acid (透明质酸), chondroitin sulfates
(硫酸软骨素) increased,
collagen fibers separated
nodular and plaque formation
lymphatic drainage decreased
III.Clinical Presentation
A. General considerations
male: female ≈ 1: 4~6, common in
30~40yrs.
B. Hypermetabolic states
nervousness (99%). irritability (90%),
palpatation (88%), tachycardia (82%),
insomnia (60%), fatigue (70%), heat
intolerance (70%), excessive sweating
(40%), weight loss (75%), with
voracious appetite (65%), menstrual
pattern changed (50%)
C. Thyroid
diffuse goiter: absent in the elderly,
consistency: soft, firm, rubbery,
symmetrical enlarged,
surface: smooth, lobular, thrill with audible
bruit
eyelid spasm or retraction
D. Eyes
a. non-infiltrative orbitopathy:
fissure widened, sclera exposed,
lid retraction, lid tremor, lid lay,
globe lay.
b. infiltrative orbitopathy:
excessive tearing
exophthalmos (asymmetrical)
eyelids unclosed
blurred vision
double vision
visual acuity decreased
corneas ulcerated, infected
sight loss
c. Classification of Graves orbitopathy: NOSPECS
(from: American Thyroid Association)
Class
0
1
2
3
4
5
6
Definition
No physical signs or symptoms
Only signs, no symptoms (signs limited to
upper lid retraction, stare, lid lag, and
proptosis to 22mm)
Soft tissue involvement (symptom and sign)
Proptosis>22mm
Extraocular muscle involvement
Corneal involvement
Sight loss (optic nerve involvement)
E. Others
tremor of the hands and tongue
muscle wasting
rapid reflex response
diarrhea
liver function
wbc , and anemia,
vitiligo (白癜风), hair loss
pretibial myxedema (胫前粘液性水肿)
F. Complications
a. cardiopathy and heart failure
thyrotoxicosis ,arrhythmia, heart enlargement and
heart failure, and all disappeared after treatment
b. Thyrotoxic crisis
symptoms and signs exaggerated abruptly
precipitating factors: infection, trauma, surgery
radiation thyroiditis, DKA, parturtion
Additional pictures: arrhythmias, pulmonary edema,
congestive heart failure, restlessness, delirium,
nausea, vomiting, abdominal pain, apathy, stupor,
coma, hypotension, shock, etc.
c. hypokalemic periodic paralysis
more common in Asia
abruptly paralysis with hypokalemia
precipitated by dextrose, oral carbohydrate
or vigorous exercise.
attacks last 7-27 hrs.
some companied by myasthenia gravis.
IV. Laboratory and Special Exams
A. Serum TH and TSH
a. FT3 and FT4
b. TT3 and TT4
c. rT3
d. TSH
B. TSH receptor antibodies
C. TRH stimulation test
euthyroid Graves ophthalmopathy
GD medication
D. 131I uptake and T3 suppression test
E. pathological exams
V. Diagnosis and Differential Diagnosis
A. Functional diagnosis
GD suspected: (1)weight loss; (2)slight
fever; (3)diarrhea; (4)tachycardia; (5)atrial
fibrillation; (6)fatigue; (7)dysmenorrhea;
(8)with difficult in control of DM, TB, heart
failure, CHD, liver disease
B. Types
FT3 、FT4 , sTSH (uTSH) : hyperthyroidism
FT3(orTT3) , FT4(TT4) normal, sTSH : T3 hyperthyroidism
FT4(orTT4) , FT3 (TT3) normal, sTSH : T4 hyperthyroidism
FT3 and FT4 (ab)normal, sTSH : subclinical hyperthyroidism
C. Pathogenic diagnosis
TRAb, TgAb, TPOAb, HCG, 131I uptake, TSH
VI. Treatment
A. General management
rest enough, energy and nutrients supplement,
sedatives for restlessness and insomnia.
B. Management of hyperthyroidism
a. medical
antithyroid agents: methylthiouracil (MTU) or
propylthiouracil (PTU)
300~600mg/d
methimazole (MM) or
carbimazole (CMZ)
30~60mg/d
b. dosage and course
1st stage (ca.6 wks):
full dosage to control symptoms
2nd stage (ca. 4~8wks):
dosage decrease gradually
1/6 dosage/wk
3rd stage (ca 1yr or more)
PTU 50mg(or MM 5mg), Qd
c. “block-replace” regimens
TH added to prevention of
hypothyroidism. T4 50µg, Qd.
d. drug withdrawal
goiter subsides
minimal dosage to maintain treated
effects
TSH return to normal
TSAb negative
normal response to TRH
e. drug side-effects
primary and secondary failure
agranulocytosis (<1%, within 2 mos)
WBC count/ wk or mo
C. Radioiodine (131I)
a. more active than before, more(USA) VS less
(Euro)
b. contraindications:
pregnant thyrotoxicosis
young people (<20yrs)
severe exophthalmos
thyrotoxic crisis
failed to I uptake
dosage should be calculated by specialist
C. Complications
hypothyroidism
radiation thyroiditis
thyrotoxic crisis
exaggarated proptosis (smoking)
D. Surgery
indications: failed to antithyroidal agent
huge thyroid or suspected with
tumors
retrosternal goiter
contraindications: severe proptosis
severe systemic diseases
early and late pregnancy
thyrotoxicosis not controlled
E. Treatment decision-making
a. firstly, treated with medications for all patients
b. after controlled, decided by
age
run course of disease
severity & complications
thyroid states
doctor’s experience
patient’s willings and special entities
F. Special concerns
a. minimal iodide supplement, iodo-NaCl is
not suitable for GD
b. severe proptosis treated with caution,
including TH supplement and prednisone
c. thyroid crisis treated with NaI, PTU,
DXM, and propranolol
d. PTU is the treatment of choice for
hyperthyroidism in pregnancy, never
makes TSH <0.5U/L
e. heart failure treated with digoxin may be
dangerous in some cases
高敏TSH检测在甲状腺功能诊断及
监测中的意义
甲状腺功能异常是临床上常见的一组疾病。有研究表明，高
敏TSH在甲状腺功能诊断方面最为敏感。1999年9月~2000年11月
在我科实验室所做的5100人次甲状腺功能检查，以了解三项检测
指标在甲状腺功能诊断及监测中的意义。
1 资料和方法
1.1 实验对象
我科临床诊断为甲亢①的病人及甲亢服药复查的病人共4518份血标
本。
1.2 实验方法
标本收集每次抽肘静脉血3ml，离心后取血清置–20℃保存。检测
方法FT3，FT4用放免法，药盒由天津协和试剂公司提供，TSH用
免放法，药盒由天津协和试剂公司提供。
1.3 统计学处理
率的比较采用X2检验。
2 结果
4518份标本中，FT3、FT4均增高，TSH降低者有1596份，占总数
的35.25%；FT3增高，TSH降低，FT4正常者有564份，占总数的
12.46%；FT4、FT4正常，仅有TSH降低者有736份，占总数的
16.25%；三项结果均正常者有820份，占总数的18.11%；FT3、
FT4正常，而TSH升高者有338份，占总数的7.46%；FT3、FT4降
低，TSH升高者有46份，占总数的1.02%；FT4降低，TSH升高，
FT3正常者有314分，占总数的6.93%；FT4增高，TSH降低，FT3
正常者有46份，占总数的1.02%；其他各种组合有29份，占总数的
0.64%。
2.1 在诊断甲亢方面
以TSH降低为诊断指标，其阳性率为65.33%② （2952/4518），以
FT3升高为诊断指标，阳性率为47.80%（2160/4518）经X2检验，
差异有显著性（P<0.001），说明以TSH降低为诊断指标，阳性率
为 36.56% （ 1652/4518 ） ， 明 显 低 于 TSH 和 FT3 的 阳 性 率 （ 均
P<0.001），提示在诊断甲亢时，FT4的敏感性最低。
2.2 在诊断甲低方面
以TSH升高为诊断指标，其阳性率为15.45%③ （698/4518），以
FT4降低为诊断指标，其阳性率为7.97%（360/4518），明显低
于前者（P<0.001）；如以 FT3降低为诊断指标 ，其阳性率为
1.02%（46/4518），远低于前二者的阳性率（均P<0.001）。
3 讨论
甲状腺功能异常是一组常见的临床症群，它已成了继溏尿病之后
的第二个常见的内分泌疾病，包括有甲状腺机能亢进症、亚临床
甲亢、甲状腺机能减退症和亚临床甲减。典型的甲亢或甲减因有
其明显的临床症状而不易漏诊，但亚临床甲状腺疾病常常没有典
型的临床症状或仅有一些非特异的临床表现，易被误或漏诊。此
时，恰当的实验室检查对诊断十分有益。Volpe在复习了大量文
献后提出，如果为了筛选甲状腺功能异常的患者，TSH是最开始
需要做的，若TSH降低，则需进一步做FT3和FT4，必要时还可
做TRH兴奋试验；若TSH升高，则需进一步做FT4和甲状腺抗体
（TAb）。从本文的统计结果亦可看出，高敏TSH对依断甲亢或
甲低的敏感性均高于FT3、FT4，提示临床上需判断甲状腺功能
时，应首选TSH检查。
甲亢患者服药治疗，其间甲状腺功能的监测对药物剂量的调整
十分重要。从本文的统计结果可看出，当TSH已经升高时，其
FT3、FT4水平尚在正常范围（338/4518），如果此时药物剂
量不改变，可能会加重药物性甲低；相反，FT3、FT4水平在
正常范围的一部分病人，TSH水平低于正常，如此时仅根据
FT3、FT4水平而停用抗甲亢药，又会导致甲亢复发，提示在
治疗监测过程中，也应以TSH为首选检查。
此外，TSH检查在甲低的诊断及治疗监测中也十分重要 。
Ayala等认为，对只有TSH升高的甲低患者也应予甲状腺素治
疗，以纠正血脂异常或改善临床神经系统症状；Smallridge也
认为，当TSH大于10mIU/L高度提示应使用甲状腺素治疗，且
治疗的目的是使TSH恢复正常。我们的结果提示，在体外试验
中，判断甲状腺功能方面，TSH是最敏感的，而FT3对诊断甲
亢最敏感，FT4对诊断甲减最敏感④ ，与国外报道一致。
思 考 题
一、判断
1、甲亢 = Graves 病
2、甲状腺性甲亢时，TSH降低的阳性率为65.33%
3、原发性甲减时，TSH升高的阳性率为15.45%
4、判断甲状腺功能时，TSH最敏感，而FT3对诊
断甲亢最敏感，FT4对诊断甲减最敏感。
二、论文评价
5、如根据科学性（50%）、先进性（10%）、实
用性（20%）和创新性（20%）来评价此文，
您给多少分？
×××教授：
我于2000年5月在附二院检查出甲亢，经治疗，到10月
指标基本正常。后到北京工作，经中日友好医院检查发现有
反复，药物（丙硫）的用量降不下来。2001年6月20日在中
日友好医院做碘131治疗。12月13日检查：FT3：6.84（3.6713.5），FT4：3-91（7.46~71.1），TSH：32.69（0.34~5.6）。
原主治医师诊断为甲低，处方为优甲乐：50µg/日，2002年1
月16日检查FT3：8.92；FT4：15.76；TSH：0.19。
今年2月27日检查FT3：8.13，FT4：20.85，TSH：0.14。经
电话请教原131治疗主治医师，建议改为优甲乐：25µg/日。3
月 27 日 检 查 ： TSH ： 0.05 （ 0.49-4.67 ） ； FT3 ： 3.29
（1.45~3.48）；FT4：1.62(0.71~1.85)。内分泌科教授要求作
TRH兴奋试验。4月2日，另一位教授用她的经典处方（心跳
88次/分，甲状腺不大）治疗，处方为他巴唑（3次/日，5mg/
次）和维生素AD。
建 议 二 个 月 后 复 查 。 6 月 5 日 检 查 ： 游 离 T3 ： 4.3
（ 3.67~20.1 ） ， 游 离 T4 ： 3.04 （ 7.46~21.1 ） ， TSH ：
83.67（0.34~5.6），山东德州市一个医院又诊断为甲低，
处方为甲状腺片40mg/日，多抗甲素片5mg/日。7月5日检
查：FT3：10.15；FT4：9。39；TSH：2.46，要求服药量
不变。8月16日检查：FT3：10.94；FT4：12.29，TSH：
0.09，心跳72次/分，甲状腺不大。医师认为，FT3、FT4
处于中间值，TSH偏低没问题，可照常服药。日前TSH为
0.09，按2002年1、2、3月的检查的经验，又将是甲亢的
预兆，应该如何办才好？
病人：张新根
问题：①目前的基本诊断是什么？
②处理中存在哪些问题？
诊断 甲亢 正常
甲低
甲低
优甲乐
50µg/d
建议
TRH Test
处理
PTU
I131治
疗后
A
B
C
D
E
A
B
C
D
E
FT4
0 4
0 3
0 2
0 1
FT3
F
G
5 1
0 1
5
F
83.7mU/L
G
uTSH
0 3
5
0.1
0.09
A
B
C
D
E
F
G
时间
问题：①目前的基本诊断是什么？
②处理中存在哪些问题？