Internal medicine 2: Endocrinology important questions

Endocrinology important questions 1. WHAT ARE MAJOR PITUITARY HORMONES?  Anterior lobe (9) o ACTH & related peptides (LPH, MSH, Endorphins) o Glycoproteins (TSH, LH, FSH) o Somatomammotropins (GH, PRL)  Posterior (2) o ADH, OT

2. ETIOLOGY OF HYPOPITUITARISM?  Hypopituitarism: Absence of one or more pituitary hormones.  Etiology & pathogenesis a. Invasive (Neoplasms)  Pituitary tumors  Hypothalamic tumors (eg: cranio-pharyngioma)  Metastatic tumors, lymphoma etc b. Infarction (Ischemic damage to the pituitary)  Postpartum necrosis (Sheehan’s syndrome)  Hemorrhagic infarction of pituitary tumor  Aneurysm of the carotid artery c. Infiltrative  Hemochromatosis  Histiocytosis X  Sarcoidosis d. Injury  Head trauma e. Immunologic f. Iatrogenic  Surgery  Radiation therapy g. Infections  Tuberculosis  Syphilis  Mycotic  Meningitis

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i. Isolated

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h. Idiopathic

3. WHAT ARE CLINICAL FEATURES OF HYPOPITUITARISM?  Symptoms & signs related to causes i. Postpartum (Sheehan’s syndrome) ii. Pituitary tumor: headache, loss of vision, extended sella turcica, CSF rhinorrhea, galactorrhea after pituitary stalk section iii. Others: trauma, history, surgery scar  Hormone deficiency features (1st loss of GH & Gonadotropin  TSH  ACTH  finally PRL) i. Hypogonadism  Female : Absence of lactation & cyclic menustration, breast atrophy,  vaginal secretions, infertility  Male

: Testes  in size,  muscular strength, loss of axillary & pubic hair

ii. Hypothyrodism  Cold intolerance, dry skin, pallor, mental slowing, bradycardia, hoarseness, constipation iii. Hypoadrenalism  Weakness, postural hypotension, malaise, dehydration, nausea, vomiting, depigmentation iv. GH deficiency   muscle mass & ↑ fat mass, growth retardation, worsening hypoglucemia v. PRL deficiency  Failure of postpartum lactation  Other findings i. Anemia, hypoglycaemia, hyponatremia ii. Adult GH deficiency:  RBC; ↑ LDH, cholesterol;  bone mass

4. WHAT ARE THE THREE GENERAL LABORATORY TESTS FOR HYPOPITUITARISM? i. Pituitary hormone : FSH, LH, PRL, TSH, ACTH, GH ii. Target gland hormone a. Thyroid hormone b. Adrenal cortex hormone c. Gonadal hormone iii. Assessment of pituitary reserve (stimulation test) a. TRH Stimulating TSH Test b. CRH Stimulation ACTH Test c. GHRH (LHRH) Stimulation Test

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d. Insulin hypoglycaemia test (dangerous)

5. TREATMENT PRINCIPLES OF HYPOPITUITARISM? i. Nutrition : ↑ calorie, rich in protein & vitamins ii. Hormonal replacement  Glucocorticoids i. Hydrocortisone: 10-30 mg/d, Prednisone 2.5-7.5 mg/d ii. Morning dosage > afternoon dosage, 2/3 dosage am, 1/3 pm iii. During stress, the dose should be increased 2-3 folds iv. Used before thyroid hormone iii. Etiology: tumor

6. PITUITARY CRISIS: PREDISPOSING FACTORS, CLINICAL MANIFESTATIONS, TREATMENT. i. Predisposed factors: - infection, sedative or hypnotic medicine, stress ii. Clinical manifestation: - weakness, hypotension, low or high temperature, depression, lethargy, hypoglycemia iii. Treatment a. 50% Glucose 60cc.iv, 10% Glucose 500cc i.v drip continued b. Hydrocortisone 100-200 mg/d divided c. 0.9% NaCl 500cc i.v (in patients with  Na) d. L-T4 50ug/d (was given after the use of glucocorticoids)- keep warm for patients with low T e. Antibiotics f. Symptomatic therapy: shock, infection, fever g. Inhibit use of sedative

7. REASONS FOR PRIMARY HYPOTHYROIDISM? REASONS FOR SECONDARY HYPOTHYROIDISM?

DIFFERENCE BETWEEN PRIMARY AND SECONDARY HYPOTHYROIDISM?  Primary Hypothyroidism + Secondary Hypothyroidism  Hypothyroidism SECONDARY HYPOTHYROIDISM

- HOSHIMOTO’s THYROIDITIS

- Pituitary necrosis (SHEEHAN’s SYNDROME)

- Surgical removal

- Pituitary or hypothalamic neoplasm

- Irradiation of thyroid

- Congenital hypopitutarism

- Iodine deficiency - Idiopathic hypothyrodism- probably old Hoshimoto’s - Late stage invasive fibrous thyroiditis

- Hemochromatosis

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- Drug therapy (Lithium, Interferon)

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Reasons

PRIMARY HYPOTHYROIDISM

Hormone

Grave’s diease

excess

Multinodular goitre

TSHoma

Adenoma Subacute thyroditis Hormone

Hashimoto’s thyroiditis

deficiency

Atrophic hypothyroidism

Diagnosis

TSH ↑

TSH 

Free TH  (depressed)

Free TH  (low)

Levothyroxine given

Glucocorticoid given

Treatment

Hypothyroidism

8. WHAT IS MOST COMMON CAUSE OF HYPOTHYROIDISM?  The most common cause of hypothyroidism  Hashimoto's thyroiditis (or autoimmune hypothyroidism)  Primary hypothyrodism  HOSHIMOTO’s THYROIDITIS  Secondary Hypothyroidism  Pituitary necrosis (SHEEHAN’s SYNDROME)

9. CLINICAL FEATURES OF HYPOTHYROIDISM? <not in ppt>        

Fatigue, loss of energy, lethargy.

Weight gain.

Decreased appetite.

Cold intolerance.

Dry skin.

Hair loss.

Sleepiness.

Muscle pain, joint pain, weakness in the extremities

10. WHAT IS THERAPY OF HYPOTHYROIDISM? Treatment: Thyroid Hormone Replacement  Primary hypothyrodism  HOSHIMOTO’s THYROIDITIS  Levothyroxine  Secondary Hypothyroidism  Pituitary necrosis (SHEEHAN’s SYNDROME)  Glucocorticoids  Levothyroxine can cause ↑ resting heart rate & blood pressure  So replacement should start at low doses in older & patients at risk for cardiovascular compromise  Younger patients: can be started at target dose usually 0.075 mg/day  Elderly & high risk patients : start low & go slow, usually 0.025 mg/day

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 Increase in increments of 0.025 mg q 4 weeks until TSH returns to normal

11. DIFFERENCE BETWEEN HYPERTHYROIDISM AND THYROTOXICOSIS?  Hyperthyrosim: Overproduction of TH by thyroid  Thyrotoxicosis: Excessive quantity of TH

GRAVES DISEASE Definition: Its an autoimmune disease that affect the thyroid o

Thyrotoxicosis

o

Hyperthyrodism

o

Graves disease: TR Ab

Clinical Manifestation o

Thyrotoxicosis

o

Thyroid Goiter

o

Consequence of autoimmunity

12. SPECIAL MANIFESTATIONS IN GRAVES’ DISEASE?  Exophthalmos

 symmetrical enlargement

 pretibial myxedema

 non-nodular gland

 hyperthyroidism

 mobile,soft, NON-TENDER

 thyroid bruit

13. THYROTOXICOSIS SYMPTOMS AND SIGNS?  Symptoms & signs o Heat intolerance

o Palpitations

o Warm moist skin

o Fast heart rate

o Hyper-appetite

o Breathlessness

o Fatigue

o Staring gaze

o Muscle weakness

o ↑ bowel movements

o Insomnia

o Light or absent menstrual periods

o Nervousness o Trembling hands

14. HOW TO DO DIAGNOSIS OF GRAVES’ DISEASE?  Confirmation of Thyrotoxicosis – Function diagnosis: o Symptoms & signs

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o Lab testing: T3, T4

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o BMR

 Confirmation of primary hyperthyroidism – Anatomical diagnosis: o TSH  Confirmation of Grave’s disease – Etiological diagnosis o Positive TRAb (TRAb, TPOAb, possible) antibodies o Imaging study o Often a personal or family history of autoimmune disorder

15. WHAT ANTIBODIES ARE SEEN IN GRAVES’ DISEASE? 

Positive TRAb,



maybe positive TPOAb,



maybe positive TGAb

16. WHAT KIND OF TREATMENTS ARE AVAILABLE FOR GRAVES ’ DISEASE?  TRIAD i. Anti-thyroid drugs: PTU (propylthiouracil) or methimazole ii. Surgery iii. Radioactive iodine treatment

17. WHAT ARE THE ADVERSE EFFECTS OF ANTI-THYROID-DRUGS “THIONAMIDES”?  Agranulocytosis  Skin Rash  Liver toxicity

18. MAJOR DIFFERENCES BETWEEN DIABETES MELLITUS I AND DIABETES MELLITUS II? DM Type 1

DM Type 2

Age at diagnosis

Usually < 40

Usually > 40

Weight

Thin (recent weight loss)

Obese

Ketonuria

Yes

No

Rapid death without

Yes

No

Family history of diabetes

Uncommon

Common

Autoimmune etiology

Yes

No

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treatment with insulin

19. DEFINE DAWN PHENOMENON AND SOMOGYI EFFECT?  Dawn Phenomenon: o High morning blood glucose o Is not caused by hypoglycaemia, but by random release of triggering hormones o Avoid intake of carbohydrates at bedtime.  Somogyi Effect: o is caused by nocturnal/night-time hypoglycaemia o leads to rebound hyperglycemia in early morning hours o it is due to having extra insulin before bedtime o mainly with type 1 diabetics 20. DIAGNOSIS CRITERIA OF DIABETES MELLITUS?  At least 2 tests on separate days with:  Diabetes o HbA1c > 6.5 % o OR Random plasma glucose ≥ 11.1 mmol/l o OR 2 hr OGTT glucose

≥ 11.1 mmol/l

o OR Fasting plasma glucose

≥ 7.0 mmol/l

 Abnormal o 2 hr OGTT glucose (IGT)

≥ 7.8 - < 11.1 mmol/l

o Fasting plasma glucose (IFG) ≥5.6 - < 7.0 mmol/l  Normal o Fasting plasma glucose

< 5.6 mmol/l

o Postprandial plasma glucose < 7.8 mmol/l

21. WHAT ARE THE TYPES OF TREATMENTS AVAILABLE FOR DIABETES MELLITUS? o Diabetes Self-management Education o Medical Nutrition Therapy o Exercise Treatment o Antihyperglycemic Agents

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o Patient's Condition Monitoring

22. WHAT ARE THE COMPLICATIONS OF DIABETES MELLITUS? INCLUDE ACUTE AND

CHRONIC COMPLICATIONS.  Complication of Diabetes Mellitus o Acute: DKA, NKHCC, hypoglycaemia, LA o Chronic: Long term poisoning by hyperglycaemia - MICROvascular: eyes, kidneys, peripheral nerves - MACROvascular: cardiovascular disease (or)  Acute complication (Short term complication) o

Low blood sugar (hypoglycaemia)

o

Diabetic Ketoacidosis (DKA)

o

Hyperglycemic Hyperosmolar State (HHS)

o

Lactic acidosis

o

Bacterial/fungal infections

 Chronic complication (Long term complications) o Microvascular Complications of Diabetes  Eye disease (Diabetic retinopathy)  Kidney disease (nephropathy )  Nerve disease (neuropathy) o Macrovascular Complications of Diabetes  coronary artery disease,  peripheral arterial disease, and stroke

23. WHAT ARE THE GENERAL TYPES OF ORAL HYPOGLYCEMIC DRUGS AVAILABLE?  Sulfonylurea

Secretagogue

 Glinides  Metformin  TZDs  Alpha glucosidase inhibitors  Incretin mimetics  DPP IV inhibitors  Amylin analogues

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 Cannabinoid receptors blocker

24. WHAT ARE THE TYPES OF INSULIN AVAILABLE FOR DIABETES MELLITUS (ACCORDING TO

DURATION OF ACTION)?

Insulin

Onset

Peak

Duration

Rapid-acting

< 0.5 hr

0.5 – 2.5 hrs

3 – 4.5 hrs

0.5 – 1 hr

1 - 4 hrs

4 - 8 hrs

1 – 3 hrs

3 - 8 hrs

7 - 14 hrs

2 – 4 hrs

6 - 12 hrs

12 – 30 hrs

1 - 2 hrs

none

18 - 24 hrs

(Insulin analogues: lispro, aspart, glulisine Short-acting (Soluble – regular) Intermediate-acting (Isophane, lente) Long-acting (Bovine ultralente) Long-acting

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(Insulin analogues: glargine, detemir)