Download Endocrine System Education Syllabus

Endocrine system diseases
Introduction
Teaching purposes
Enables students to appreciate general understanding of endocrinology and endocrine
diseases through an overview of related knowledge about endocrinology, endocrine
hormones and endocrine diseases.
Teaching Requirements
1. Master the principles of the diagnosis of endocrine diseases. Emphasizes the
clinical syndrome as main diagnosis evidence and the importance of hormone
secretion regulation mechanism in the diagnosis of endocrine metabolic diseases.
2. Be familiar with the immunity – neuron– endocrine network regulation. Grasp the
names and roles of hormones secreted by hypothalamus, pituitary and target gland
(tissue), the concepts of positive feedback, negative feedback about the hypothalamus
- pituitary - target gland axis and its regulation mechanism.
3. Be familiar with the principles of diagnosis and therapy of endocrine diseases.
4. Understand the function and importance of the endocrine system and the history of
the endocrinology development.
5. Understand the classification, etiology of endocrine diseases.
6. Understand the classification and main mechanism of endocrine hormones.
Teaching contents
1. The endocrine system, organs and tissues: endocrine concept; endocrine system,
organs and tissues.
2. The function and importance of the endocrine system and the history of the
endocrinology development.
3. The classification of endocrine hormones, the main mechanism of hormones.
4. Mutual regulation among neuron - endocrine – immunity; mutual regulation
between the nervous system and endocrine system; the hormones secreted by the
hypothalamus, pituitary and target glands (tissues); the concepts and mechanisms of
positive and negative feedbacks of the hypothalamus - pituitary - target glands axis;
immune system and endocrine function
5. Classification of endocrine system diseases by function, location and etiology.
6. Diagnosis principles of endocrine disease: typical symptoms, physical sign,
laboratory examinations, including evidence of metabolic disorders, hormone levels
and dynamic function test; pathological diagnosis: imaging, radionuclide, ultrasound,
cytology, intravenous catheter inspection; etiological diagnosis: antibody detection,
chromosome, HLA identification.
7. Prevention and cure principles of endocrine diseases: emphasizing the importance
of prevention and the therapy principles can be classified into two types by function
of hyper- or hypo-. Hyper-type: surgical resection, radiotherapy suppressing and
chemotherapy drugs suppressing; Hypo-type: to supplement a physiological dose of
hormones, most of them need lifelong supplementation and etiology therapy.
Simple goiter
Teaching purposes
Master the etiology, pathogenesis, clinical manifestations, diagnosis, prevalence and
therapy measures of simple goiter basing on understanding the epidemiology.
Teaching requisition
1. Master etiology and pathogenesis of simple goiter: mainly because of iodine
deficiency.
2. Master the diagnosis and differential diagnosis (emphasizing importance of
differential diagnosis to thyroid cancer).
3. Master the treatment of simple goiter.
4. Be familiar with the prevention of simple goiter.
5. Be familiar with the clinical manifestation of simple goiter.
6. Understand the pathology of simple goiter.
7. Understand the concepts of simple goiter, endemic goiter and sporadic goiter.
Teaching content
1. Etiology and pathogenesis
Iodine deficiency
thyroid hormone synthesis or secretion disorder
thyroid hormone requirements increasing
2. Pathology
3. Clinical manifestations: thyroid can be diffused or nodular tumescent, functions of
most of them are normal or low. 131I uptake rate is increased; urinary iodine is
significantly decreased or disappeared. T4 is low or normal; sometimes T3 is high and
TSH is elevated or normal.
Diagnosis and differential diagnosis: diagnosis based primarily on the goiter and
normal thyroid function. The prevalence history of endemic goiter areas is helpful to
the diagnosis. Chronic lymphocytic thyroiditis and thyroid cancer (particularly
nodules) should be identified from it. Present diagnosis purpose is to exclude thyroid
tumors, thyroid cancer; chronic lymphocytic thyroiditis is the most common cause.
And cytology is an important diagnostic tool.
4. Prevention: iodized salt or iodized oil injection
5. Treatment: thyroid hormone can be used for mild cases (young). The cases can be
followed up if malignant tumor excluded. On general, surgery is tabooed. Tumor or
suspected cancer should be operated.
Hyperthyroidism
Teaching purposes
Enable students to have a better understanding of etiology, pathogenesis, clinical
manifestations, diagnosis and treatment of chronic toxic goiter with hyperthyroidism
(Graves' disease) on the basis of understanding physiology of thyroid.
Teaching requisition
1. Master the Graves' disease in clinical manifestations (including general and special).
2. Master laboratory and differential diagnosis of hyperthyroidism.
3. Master Graves' Disease drug therapy principles and their common adverse drug
effects.
4. Master hyperthyroidism crisis principles.
5. Be familiar with the classification of hyperthyroidism.
6. Be familiar with the isotope treatment indications, contraindications, complications.
7. Understand the surgical treatment indications, contraindications, complications.
8. Understand the etiology and pathogenesis of hyperthyroidism (difficulties).
Teaching content
1. Overview: definitions and classification: mainly description of diffused goiter with
hyperthyroidism. Note the difference between thyrotoxicosis and hyperthyroidism.
2. Etiology and Pathogenesis: the modern point of view on the mechanism of
autoimmune disease in this disease.
3, Pathology: briefly state pathological changes of thyroid, anterior tibial myxedema
and infiltrative exophthalmos of.
4. Clinical manifestation: state manifestation in the nervous, mental, cardiovascular,
gastrointestinal, musculoskeletal, reproductive, endocrine, hematopoietic system with
more thyroid hormone secreted basing on the physiological role of thyroid hormone.
Focus on teaching manifestation due to high metabolism and increased sympathetic
activity symptoms and signs of thyroid and eyes (simple exophthalmos and infiltrative
exophthalmos). Emphasize the main clinical evidence for diagnosis of Graves' disease,
hyperthyroidism.
5. special clinical manifestations:
Thyroid crisis (focal point)
Hyperthyroid heart disease
Apathy hyperthyroidism
Subclinical hyperthyroidism
Pretibial myxedema
Thyrotoxic periodic paralysis
6. Laboratory examination:
(1) Test of the blood thyroid hormones: clinical significance and impact factors of the
test of free thyroxine (FT4), free triiodothyronine 3 (FT3), total thyroxine (TT4), total
triiodothyronine (TT3) and anti-T3 (rT3).
(2). thyroid stimulating hormone (TSH) test: emphasize the sensitivity of the TSH
reflecting the hypothalamus - pituitary - thyroid axis function, especially important for
subclinical hyperthyroidism or hypothyroidism diagnosis.
(3) Thyroid uptake rate of 131I measurement:
1> two categories of high and low uptake rates can be classified, helpful to diagnosis
of etiology of thyrotoxicosis.
2> estimate absorption amount of iodine.
(4) TRH stimulation test. (little done)
(5) 3 triiodothyronine suppression test (T3 suppression test): almost given up now.
(6) Determination of thyroid autoantibodies: emphasize TSAb as an indication of
early diagnosis of Graves disease, determining disease activity, whether relapse and
whether withdrawal. The clinical relevance is not very significant.
(7) Imaging examination: ultrasound, radionuclide scanning, CT, MRI.
7. Diagnosis and differential diagnosis: for the majority of cases, the initial diagnosis
can be made according to symptoms, physical signs and tests of thyroid hormones and
other laboratory tests.
(1) diagnosis: including functional and etiological diagnosis.
(2) differential diagnosis: with simple goiter, pheochromocytoma, neurosis and
tuberculosis, malignant tumors, chronic colitis and so on.
8. Therapy
(1) General treatment: mainly free from iodine's “three high diet” (high sugar, high
protein, high vitamin), emphasizing psychological nursing and some symptomatic
treatment (sedatives, and adrenergic β-blockers).
(2) Drug treatment.
Mechanism of anti-thyroid drugs，treatment indications, dosage, duration, side effects,
relapse and withdrawal problems.
β-blocker usage, indications and usage of compound iodine.
(3) 131 I treatment indications, contraindications and complications.
(4) Indications, contraindications, complications and preoperative preparation for
surgical treatment.
Prevention and treatment of thyroid crisis
Improper operation preparation or other emergency conditions that may induce
thyroid crisis. Understand the early manifestation of thyroid crisis and early treatment
that can block the disease development.
Treatment principle: elucidate the importance and the mechanism of dose thiourea
and iodine, adrenergic β-receptor blockers, adrenal cortex hormone therapy for hyroid
crisis; emphasize the key to rescuing measures are the applications of iodine with
other supporting and assistant treatment in crisis prevention and treatment.
9. Infiltrative exophthalmos treatment
Hypothyroidism
Teaching purposes
Understand the etiology clinical manifestations, prevention and treatment of
hypothyroidism.
Teaching requisition
1. Understand the etiology of hypothyroidism
2. Understand the clinical manifestations of hypothyroidism
3. Master laboratory examination of hypothyroidism
4. Master treatment of hypothyroidism
Teaching content
1. Concepts: systemic low metabolic syndrome caused by a variety of reasons for low
thyroid hyperlipidemia or thyroid hormone resistance.
2. Etiology: the causes of adult hypothyroidism: (1), autoimmune damage; (2) thyroid
damage; (3) Iodine excess; (4) anti-thyroid drugs
3. Clinical manifestations:
(1). general manifestation
(2). muscle and joint
(3). cardiovascular system
(4). hematological system
(5). digestive system
(6). the endocrine system
(7). pretibial myxedema
4. Laboratory examination
(1) biochemical tests
(2) serum thyroid hormone and TSH
(3) thyroid autoantibodies
(4) TRH exciting experiment
5. Treatment
(1) hormone replacement therapy
(2) hormone replacement therapy notes
(3) the treatment of myxedema coma
Diabetes
Teaching purposes
A better understanding on the classification, clinical manifestations, diagnostic
criteria and treatment of diabetes on the basis of understanding of diabetes
epidemiology.
Teaching requisition
1. Master the diagnosis of diabetes; be familiar with the differential diagnosis.
2. Master diabetes complications.
3. Master the treatment principles of diabetes.
4. Master the diagnosis and treatment of diabetic ketoacidosis.
5. Be familiar with the clinical manifestations of diabetes
6. Be familiar with the classification of diabetes mellitus.
7. Be familiar with the laboratory examination.
8. Understand the definition and of epidemiology of diabetes.
9. Understand the etiology, pathogenesis and natural history diabetes.
10. Understand the pathophysiology of diabetes.
11. Understand the diabetes prevention.
12. Understand the diagnosis and treatment of diabetic hyperosmolar coma.
Teaching content
1. Overview: definitions, epidemiology
2. Diabetes Category: be familiar with the 1997classification criteria of ADA.
3. Etiology, pathogenesis and natural history
(1) type 1 diabetes: six stages in its development
1) Section 1 - genetic susceptibility: HLADQ, DR gene-related.
2) Section 2 - autoimmune response starts.
3) Section 3 – Immunological reaction abnormal: there may be autoantibodies. And
GAD antibody has most sensitivity and specificity, helpful to distinguish type 1
between type 2 diabetes.
4) Section 4 - progressive loss of function of islet β cells.
5) Section 5 - clinical Diabetes.
6) Section 6 - complete destruction of islet β cells function, significant clinical
manifestations of diabetes.
(2) Type 2 diabetes: the development of its can be divided into four stages
1) genetic susceptibility and environmental factors interaction: Type 2 diabetes is a
polygenic disease with extensive genetic heterogeneity. Environmental factors play an
important role in the pathogenesis of type 2 diabetes, including population aging,
nutritional factors, central obesity, lack of physical activity, urbanization, the
intrauterine environment and stress, chemical poisons and so on.
2) hyperinsulinemia and / or insulin resistance: insulin resistance and insulin secretion
dysfunction are the two basic aspects and features in the pathogenesis of type 2
diabetes, and related with atherosclerotic cardiovascular disease, hypertension,
dyslipidemia, central obesity and other factors, and one aspect of the so-called
"metabolic syndrome".
3) impaired glucose tolerance (IGT): the majority of patients with type 2 diabetes
have this phase.
4) clinical Diabetes
4. Pathophysiology: metabolic disorders of diabetes are mainly due to biological
activity or effect of insulin caused by absolute or relative lacking, which in turn
causes three major metabolic disorder characterized by continuing high blood sugar.
5. Clinical manifestations
1) metabolic disorder syndrome: “3 poly and one less” is polydipsia, polyuria,
polyphagia and weight loss.
2) complications and / or concomitant disease.
3) reactional hypoglycemia.
4) surgical treatment for various diseases, hyperglycemia is found in the perioperative
stage.
5) high pleural sugar is found as only in physical examination with no obvious
symptoms.
6. Complications
(1) acute complications.
l) diabetic ketoacidosis.
2) hyperosmolar nonketotic diabetic coma.
3) lactic acidosis.
4) infection: boils, carbuncle, skin fungal infections, tuberculosis and urinary tract
infections, renal papillary necrosis.
(2) chronic complications
Macrovascular disease: large and medium-sized artery atherosclerosis.
Microangiopathy.
1) diabetic nephropathy.
2) diabetic retinopathy.
3) Other: Diabetic cardiomyopathy.
neuropathy: autonomic nervous system, peripheral nerves and cranial neuropathy
other eye diseases: macular degeneration, cataracts, glaucoma, refractive changes, and
ciliary body of iris lesions.
diabetic Foot
7. Laboratory examination
Test of urinary glucose: no confirmed meaning
Pleural glucose test: an important diagnostic test
glucose tolerance test (OGTT)
glycosylated hemoglobin A1c (GHA1c) and glycated albumin (fructosamine) test
plasma insulin and C-peptide
other: blood lipids
8. Diagnosis and differential diagnosis
Diagnostic criteria: Since 1985, diagnostic criteria is from the general international
WHO standard, the new one in 1997 from ADA.
Differential diagnosis:
⑴positive urine glucose due to other reasons
⑵the impact of drugs on glucose tolerance
⑶differential diagnosis between various types of diabetes
9. treatment: the current emphasis is on the principle of early treatment, long-term
treatment, combined therapy, individual treatment measures, and the key to treatment
is to control the blood glucose.
l) Education
2) Diet therapy: development of total calories, carbohydrate content, protein and fat
percentage, a reasonable allocation and follow-up visit.
3) physical exercise
4) oral hypoglycemic agents:
Sulfonylurea drugs: mechanism of action, indications, types and side effects
Biguanide: mechanism of action, contraindications, indications and side effects α
glucosidase inhibitors: mechanism of action, indications and side effects
Thiazolidinedione: mechanism of action, indications and side effects
Benzoic acid derivatives
5) insulin: indications, preparation type, using the principles and dose adjustment and
side effects
6). pancreas transplantation and islet cell transplantation
7) the treatment of diabetic pregnancy
10. Prevention: a reasonable diet, adequate exercise to prevent from obesity, advocate
non-smoking, less alcohol, less salt eating.
Primary prevention: intervention to those risk groups preventing from diabetes
Secondary prevention: early detection and effective treatment on diabetes
Third prevention: delay and / or prevention and treatment of diabetic complications
11. Diabetic ketoacidosis
1). Etiology: such as infection, trauma, pregnancy and the discontinuation of insulin
therapy.
2). Pathophysiology and clinical manifestations: acidosis, different degrees of water
loss (dehydration), electrolyte balance disorder, oxygen transporting system disorders,
peripheral circulatory failure, renal dysfunction and central nervous system
dysfunction
3). laboratory examination
4). Diagnosis and differential diagnosis: identification on the coma, acidosis,
dehydration, shock, low blood sugar and so on. Contrast with hyperosmolar
nonketotic diabetic coma.
5). Prevention and treatment: emphasis on prevention and importance of early
diagnosis and early treatment. Fluid replacement, small doses of insulin and
correction of water, electrolyte, acid base balance disorders and other principles, and
compare to hyperosmolar nonketotic diabetic coma.
teaching methods
The best way is according to slide and strengthen the teaching in demonstration.
Pituitary hypofunction
Teaching purposes
Learn pituitary hypothyroidism in particular the cause, clinical manifestations,
diagnosis and treatment of Sheehan's syndrome, basing on understanding of anterior
pituitary function
Teaching requisition
1. Master the etiology of Sheehan's syndrome.
2. Master the diagnosis and differential diagnosis of adult impaired pituitary function.
3. Master the principles adult impaired pituitary function treatment and the order of
hormone replacement therapy.
4. Be familiar with clinical manifestation of the adult impaired pituitary function and
emphasize on Sheehan's syndrome.
5. Be familiar with laboratory examinations of the adult impaired pituitary function.
6. Understand etiology and pathogenesis of adult impaired pituitary function of
hypothyroidism
Teaching content
1. Etiology and pathogenesis of the adult impaired pituitary function, with Sheehan's
syndrome as a representative.
(1) pituitary tumors
(2) hypothalamic lesions
(3) pituitary necrosis: pituitary necrosis and fibrosis because of postpartum hemorrhage called Sheehan (Sheehan) syndrome in clinical practice.
(4) sellar surgery, radiotherapy and trauma
(5) infection and inflammation
(6) long-term glucocorticoid treatment
(7) pituitary apoplexy
(8) Other: lymphocytic hypophysitis, vacuolus sella, etc.
2. Clinical manifestations: Sheehan syndrome tend to have the whole pituitary dysfunction, but no space-occupying lesion
The manifestation of gonadal dysfunction
The manifestation of hypothyroidism
Addison's performance
Pituitary crisis:
Motivations: a variety of stress such as infection, sepsis, diarrhea, vomiting,
dehydration, hunger, cold, acute myocardial infarction, cerebrovascular accident,
surgery, trauma, anesthesia and the use of sedatives, hypnotics, hypoglycemic agents,
etc..
Clinical manifestation
⑴a high fever type (T> 40 ℃)
⑵low temperature type (T <30 ℃)
⑶low blood sugar type
⑷circulatory failure type
⑸water intoxation ⑹mixed type
3. Laboratory and other tests:
Gonadal function examination: decreasedFSH, LH, E2, or T.
Adrenal cortex function test: decreased,ACTH, cortisol, 24-hour urinary free cortisol,
and 17 - hydroxy corticosteroids
Thyroid function test: decreased TSH, T3, T4
Pituitary stimulation test used to know about the reserve function of endocrine cells,
and helpful in diagnosis of the dysfunction sites: such as the ACTH stimulation test,
GRH, TRH, CRH, GHRH stimulation tests
Imaging: CT, MRI, X ray and CT and sella photographs
4. Diagnosis and differential diagnosis
Diagnosis: the diagnosis can be confirmed through disease history, symptoms,
physical examination, combined with laboratory examinations and imaging.
Differential Diagnosis: it should be differentiated from multiple endocrine
dysfunction and anorexia nervosa
5. Treatment:
long-term or even life-long target gland hormone replacement therapy: emphasis on
glucocorticoid replacement first in the treatment process followed by thyroid hormone,
preventing from the occurrence of adrenal crisis.
Treatment of pituitary crisis: intravenous injection of 40 ~ 60ml 50% glucose solution
to rescue low blood sugar firstly, then intravenous corticosteroids-hydrocortisone is
added. Circulatory failure - anti-shock, sepsis infection - anti-infection, edema enhancing diuretic, prednisone or hydrocortisone can be used, low body temperature
person - a small dose of thyroid hormone and incubation. Narcotics, sedatives,
hypnotics, or hypoglycemic agents are prohibited or cautiously used.
Cushing syndrome (hypercortisolism)
Teaching purposes
Study the pathophysiology, clinical manifestations, diagnosis and treatment x on the
basis of understanding the adrenocortical physiology.
Teaching requisition
1. Master pathophysiology and clinical manifestations of Cushing syndrome.
2. Master the diagnosis and differential diagnosis of Cushing's syndrome.
3. Be familiar with etiology, pathology and clinical features of all types of Cushing
syndrome.
4. Be familiar with the principles of the treatment of Cushing's syndrome, and
understand the prognosis.
5. Understand the definition of Cushing's syndrome and be familiar with their
classification.
Teaching content
1. Emphasize the concept, definition and etiology of Cushing's disease;
ACTH-dependent and-independent.
2. Pathophysiology and clinical manifestations
(1) lipid metabolism disorders: central obesity
(2) Protein metabolism disorders: purple stripes, ecchymosis, muscle atrophy
Metabolic disorders: impaired glucose tolerance, some of then have steroids diabetes.
Electrolyte disturbances: hypokalemia alkalosis
Cardiovascular disease: high blood pressure
Reduced resistance to infection
Hematopoietic system and blood changes: sanguine
Sexual dysfunction
Nerve, mental disorders
Skin pigmentation
3. Etiology, pathology and clinical features of various types of Cushing syndrome
pituitary ACTH-dependent Cushing disease
Ectopic ACTH syndrome
Adrenocortical adenoma
Adrenocortical carcinoma
ACTH-independent bilateral small nodular hyperplasia (dysplasia)
ACTH-independent macronodular adrenal hyperplasia
Iatrogenic Cushing syndrome
4. Diagnosis and differential diagnosis:
Diagnosis is based on:
① clinical manifestations,
② whether the Cushing's syndrome exist determined by: 24-hour urinary free
cortisol measure, cortisol rhythm measure, and low-dose dexamethasone
suppression test. If Cushing's syndrome diagnosed, locations (causes) should be
found whether in the pituitary? Adrenal? (Which side? the adrenal adenoma or
cancer?), Or whether ectopic? High-dose dexamethasone suppression test,
saddle MRI, adrenal CT, lung CT can be done to find specific lesion.
Differential diagnosis: with simple obesity, type 2 diabetes and alcoholic liver
functional lesion with false identification of Cushing's syndrome.
5. Treatment:
Cusing's disease:
① transsphenoidal resection of pituitary microadenomas;
②
subtotal adrenal microadenomas + pituitary irradiation (Nelson syndrome occurs
carefully) if no microadenomas were found:
③ craniotomy for resection of pituitary macroadenomas combined with
radiotherapy;
④therapy or preoperative preparation with inhibiting cortisol synthetic drugs.
Adrenal adenoma: resection after diagnosis of adenoma location, and the gradual
reduction of hormone replacement, promoting recovery of the atrophy adrenal with
ACTH.
Early surgical resection of adrenal carcinoma is needed and radical chemotherapy for
those who fail to radical cure.
Bilateral resection and postoperative hormone replacement are done for ACTH
independent bilateral adrenal hyperplasia,
Iatrogenic Cushing syndrome withdrawal, drug change (taken at a draught, every
other day, etc.)
Primary cancer should be the treated for ectopic ACTH syndrome.
Drugs
that
block
synthesis
of
adrenal
hormones:
O,P'-DDD
(2,4'-dichlorodiphenyldichloroethane(mitotane,Lysodren-antineoplastic), Metyrapone,
aminoglutethimide, ketoconazole and so on.
It should be noted treatment before and after surgery to remove tumors or hyperplasia
adrenal in treatment of Cushing's syndrome.
6 Prognosis: It may gradually improve after a few of months’ effective treatment. The
therapeutic effect of Cushing's patients is different, recurrence and should be regularly
observed, or whether there is the occurrence of adrenal insufficiency or Nelson's
syndrome.
Primary aldosteronism
Teaching purposes
Understand the etiology, clinical manifestations and treatment of primary
aldosteronism based on understanding the function of the adrenal cortex.
Teaching requisition
1.
2.
3.
4.
Master pathophysiology and clinical manifestations.
Master principle of treatment.
Be familiar with the diagnosis and differential diagnosis
Understand the relevant laboratory examinations
Teaching content
1. Etiology and pathology: APA (aldosterone-producing adenoma.), idiopathic
hyperaldosteronism, glucocorticoid-remediable aldosteronism, aldosterone cancer,
aberrant aldosterone secretion organizations, most of them are aldosterone tumors.
2. Pathophysiology: clinical manifestations caused by excess aldosterone which
induces storage of sodium and elimination of potassium.
3. Clinical manifestations:
(1) Hypertension: The most common manifestation
(2) neuromuscular dysfunction: usually related with hypokalemia
(3) kidney manifestation: increased nocturia, polyuria, polydipsia and other
related chronic hypokalemia
(4) Cardiac manifestation: usually secondary to hypertension
(5) Other manifestations: impaired glucose tolerance or diabetes, etc.
4. Laboratory examinations
(1) blood and urine biochemical tests
(2) blood renin, angiotensin, aldosterone tests
(3) spironolactone test
4. diagnosis and etiological diagnosis
(1) dynamic tests: decubitus and erect position tests, sodium (salt) stress test, etc.
(2) imaging examination
5. Treatment
(1) surgical treatment: for those who has adrenal adenoma
(2) drug therapy: spironolactone for preparation of adenoma operation and the
long-term treatment for idiopathic hyperaldosteronism.
Primary chronic adrenocortical insufficiency (Addison's disease)
Teaching purposes
Know about the etiology, clinical manifestations and treatment of Primary chronic
adrenocortical insufficiency base on understanding the function of the adrenal cortex.
Teaching requisition
1. Master pathophysiology and clinical manifestations.
2. Master principle of treatment.
3. Be familiar with the diagnosis and differential diagnosis.
4. Be familiar with chronic primary adrenal hypofunction of the etiology and
pathology.
5. Be familiar with the diagnosis and differential diagnosis and know about laboratory
tests.
Teaching content
1. Etiology and pathology:
Adrenal Tuberculosis: common causes in our country.
Idiopathic adrenal atrophy: usually related to autoimmunity, common causes in
developed
countries.
2. Pathophysiology and clinical manifestations:
manifestation of lack of aldosterone
manifestation of lack of Cortisol
Clinical manifestations of adrenal crisis
3. Laboratory examination:
Biochemistry: hyponatremia, hypokalemia, hyperkalemia.
Blood routine: usually normocelluar, normochromic anemia, hypereosinophilic.
Imaging tests: heart shrink, tubercle and calcification shown in imaging films of the
adrenal.
Test of hormones: basic cortisol, 17-OH cortisol, plasma ACTH, ACTH stimulation
test,
4. Diagnosis and differential diagnosis: weight loss, skin darkening, low blood
pressure, debilitation helpful to the diagnosis of this disease. It should be
differentiated with chronic liver disease and other wasting disease.
5. Treatment:
Basic treatment: education of patients - medication for life, card for the disease on the
body, glucocorticoid replacement, using salt, if necessary, mineral corticoids.
Cause treatment: active tuberculosis should be actively treated if it exists, other glands
dysfunction for autoimmunity.
Treatment of Adrenal Crisis: mainly intravenous corticosteroids, saline water and
glucose supplement, and treatment of some stress.
Pheochromocytoma
Know about etiology, pathology, clinical manifestations, diagnosis and treatment on
the basis of understanding the function of adrenal medulla.
Teaching requisition
1. master pathophysiologial and clinical manifestations
2. master principle of treatment
3. be familiar with the diagnosis and differential diagnosis
Teaching content
1. The definition and overview of pheochromocytoma.
2. Tumor location and biochemical characteristics.
3. Clinical manifestations: 1. cardiovascular system manifestations: (1) hypertension:
two types including paroxysmal hypertension or persistent high blood pressure. (2)
hypotension, shock. (3) cardiac performance.
2. Metabolic disorders, diabetes, etc.
3. Other clinical manifestations, such as high metabolic manifestation
4. Diagnosis and differential diagnosis
1). test of catecholamines and their metabolites of blood and urine
2). pharmacological test: phentolamine test and provocation test, etc.
3). the imaging examination
5. Treatment: mainly through surgical excision, lowering blood pressure through
medication and correcting low blood volume before operation.
Diabetes insipidus
Teaching purposes
Study etiology, clinical manifestations, laboratory examination and treatment of
diabetes insipidus based on understanding the physiological function of antidiuretic
hormones.
Teaching requisition
1. Master the diagnosis and differential diagnosis of diabetes insipidus.
2. Master the treatment of diabetes insipidus.
3. Be familiar with the clinical manifestations of diabetes insipidus.
4. Understand the definition, etiology and pathogenesis of diabetes insipidus.
Teaching content
1. The definition of diabetes insipidus. Describe the concepts of central and
nephrogenic diabetes insipidus.
2. The etiology and pathogenesis of diabetes insipidus.
Causes of central diabetes insipidus:
Secondary diabetes insipidus: cancer, trauma, infection.
Idiopathic diabetes insipidus.
Hereditary diabetes insipidus: autosomal dominant inheritance.
3. Clinical manifestations: polyuria, polydipsia and polydipsia, low specific gravity of
urine.
4. Diagnosis and differential diagnosis:
(1) water deprivation test: mainly used for identification of diabetes insipidus and
psychogenic polydipsia.
(2) water deprivation - vasopressin test: mainly used for identification of central
diabetes insipidus and nephrogenic diabetes insipidus.
(3) Determination of plasma arginine vasopressin
(4) other inspections: sellar X-ray, visual field examination, CT or MRI may be used
to exclude whether there are tumors in the pituitary or in the vicinity of that.
5. Differential diagnosis: psychogenic polydipsia, nephrogenic diabetes insipidus,
chronic kidney disease
6. Treatment
Hormone replacement therapy: vasopressin agent, tannic acid vasopressin injection
(Vasopressin Tannate), desmopressin.
other anti-diuretic drugs: hydrochlorothiazide, carbamazepine, chlorpropamide
treatment of Cause
7. Prognosis: depends on treatment of Cause.
Hypoglycemia
Teaching purposes
Study the etiology, classification, clinical manifestations, laboratory examination and
treatment on the basis of understanding blood glucose regulation mechanism.
Teaching requisition
1. Master clinical manifestations, diagnosis and differential diagnosis of
hypoglycemia.
2. Master the treatment of hypoglycemia.
3. Be familiar with the etiology and classification of hypoglycemia.
4. Know about blood sugar regulation mechanism.
Teaching content
1. The definition of hypoglycemia.
2. Blood sugar regulation mechanism.
3. Common causes, classification of low blood sugar
pathophysiologial and clinical manifestations
over-excited symptoms of autonomous (sympathetic)
nerve symptoms of neurological hypoglycemia
diagnosis and differential diagnosis
hypoglycemia can be determined by triad syndrome of hypoglycemia
the laboratory evaluation of hypoglycemia
test of plasma insulin
48 ~ 72 hours starvation experiment
glucagon stimulation test
differential diagnosis:
Prevention and treatment:
treatment of low blood sugar attack
treatment according to etiology
prevention of low blood sugar.
[Attached] frequent hypoglycemia
Drug-induced hypoglycemia: very common, and anti-diabetes treatment is the main
reason.
Insulinoma.
Other tumors that induces low blood sugar
Introduce the prevention of the disease.
Pituitary tumor
Teaching purposes
Study classification, clinical manifestations, diagnosis, and treatment principles of
pituitary tumor based on understanding different types of hormones secreted by
pituitary.
Teaching requisition
1. Master classification pituitary tumors according to the cells which secret different
hormones.
2. Master the two clinical manifestations of pituitary tumors: space seized
compression manifestation and manifestation of abnormal hormone secretion
3. Be familiar with the clinical manifestations of prolactinoma: space seized
compression manifestation, male sexual dysfunction, women amenorrhea and
galactorrhea.
4. Be familiar with the diagnosis of prolactinomas: clinical presentation and
laboratory and imaging features of prolactin levels
5. Be familiar with the principles of treatment of pituitary tumors: In addition to
prolactinomas, drug treatment is generally preferred, surgical treatment should be
considered for all pituitary tumors, especially large adenoma and functional tumors.
6. Understand pituitary apoplexy.
7. Understand the complications of pituitary tumor.
Teaching content
1. The classification of pituitary tumors
by origin classification of hormone-secreting cells
classification according to tumor size
2. Clinical manifestations:
(1). pituitary tumors, especially functional pituitary tumors may have two clinical
manifestations: space seized compression manifestation; abnormal hormone secretion,
or excessive, or increased pituitary tumors oppressing other normal tissues of pituitary,
reducing hormone secretion.
(2). pituitary internal bleeding can occur in tumor development, and it causes pituitary
apoplexy, manifested as severe headache, vision sharp declining, extraocular muscle
paralysis, drowsiness, coma, meningeal irritation sign and intracranial hypertension.
(3). prolactinoma is the most common pituitary tumor, patients often see the doctor
because of female amenorrhea and galactorrhea, male sexual dysfunction, or
compression symptoms, and the majority are large adenomas when found.
3. Prolactin diagnosis: clinical manifestations and laboratory test of prolactin and
imaging
4. Treatment principles: drug treatment is generally preferred for prolactinomas, and
all othert pituitary adenoma especially large and functional tumors should be
considered surgery.