Endocrinology: Pituitary,hypothalamus, Thyroid Flashcards

Question

CF of cushing syndrome

Answer 1

``` Obesity or weight gain (>115% ideal body weight) Thin skin Moon facies Hypertension Purple skin striae Hirsutism Menstrual disorders (usually amenorrhea) Plethora Abnormal glucose tolerance Impotence Proximal muscle weakness Truncal obesity Acne Bruising Mental changes Osteoporosis Edema of lower extremities Hyperpigmentation Hypokalemic alkalosis Diabetes mellitus ```

Answer 2

Diatinguish bw pituitary ACTH producing adenoma from ectopic ACTH producing tumor Level of ACTH is measured in IPS and peripheral veins in response to CRH

Answer 3

selective transsphenoidal resection

Answer 4

SOMATOSTATIN ANALOGUE Pasireotide S/e: diabetes ( supressed pancreatic secretion of insulin ,incretins) rest git GLUCOCORTICOID RECEPTOR ANTAGOINIST Mefiprostone STEROIDOGENIC INHIBITORS Metyrapone( inhibitis and 11b-hydroxylase) Ketaconazole(inhibits CYP 450)

Answer 5

Adrenalectomy in the setting of residual corticotrope adenoma tissue. characterized by rapid pituitary tumor enlargement and increased pigmentation secondary to high ACTH.

Answer 6

Nonfunctional

Answer 7

V2 receptors- G protein- adenylate cyclase -inc cAMP- more insertion of AQP2 V1 receptors-phospholipase C- contraction of smooth muscle in blood vessels in the skin and gastrointestinal tract,

Answer 8

``` Lithium Demeclocycline Methoxyflurane Amphotericin Aminoglycosides Cisplatin Rifampin Foscarnet ```

Answer 9

three different types of salt and water imbalance: (1) an increase in total body water that exceeds the increase in total body sodium (hypervolemic hyponatremia) Causes: CHF, cirrhosis , nephrosis (2) a decrease in body sodium greater than the decrease in body water (hypovolemic hyponatremia) Causes:diarrhoea , diuretic abuse, mineralocorticoid deficiency (3) an increase in body water with little or no change in body sodium (euvolemic hyponatremia) Cause: * nausea, cortisol deficiency * SIADH

Answer 10

Increased in all

Answer 11

PITUITARY DI Desmopressin NEPHROGENIC DI Thiazide diutetics, amiloride Low Na diet , PG synthsesis inhibitor PRIMARY POLYDYPSIA No way to correct Desmopressin, antidiuretic will cause water intoxication because it does not inhibit urge to drink V2 RECEPTOR MUTATION

Answer 12

DYPSOGENIC characterized by inappropriate thirst caused by a reduction in the set of the osmoregulatory mechanism. It sometimes occurs in association with multifocal diseases of the brain such as neurosarcoid, tuberculous meningitis, and multiple sclerosis but is often idiopathic PSYCHOGENIC POLYDYSIA is not associated with thirst, and the polydipsia seems to be a feature of psychosis or obsessive compulsive disorder IDIOPATHIC results from recommendations to increase fluid intake for its presumed health benefits

Answer 13

Increase TBG Inc total T3 and T4 But free T3 and T4 normal Androgens,: dec

Answer 14

Because the free thyroxine binds to TBG(as it is raised idue to effect of estrogen)which can cause hypothyroidism

Answer 15

A protein responsible for efflux of iodine in the follicle

Answer 16

A primary deficiency of plasma AVP also can result from increased metabolism by an N-terminal aminopeptidase produced by the placenta. It is referred to as gestational DI because the signs and symptoms manifest during pregnancy and usually remit several weeks after delivery

Answer 17

increase in plasma osmolarity and sodium will stimulates thirst and a compensatory increase in water intake. hypernatremia and other overt physical or laboratory signs of dehydration do not develop unless the patient also has a defect in thirst or fails to increase fluid intake for some other reason.

Answer 18

DEIODINASE 1 low affinity for T4 DEIODINASE 2 Converts T4 to T3 DEIODINASE 3 Inactivates T4 and T3

Answer 19

Nuclear though it is a peptide

Answer 20

Iodine deficiency

Answer 21

Congenital hypothyroidism Thyroid hormone synthesis normally begins at about 11 weeks of gestation. If there is no thyroid gland/hormone mothers thyroid will compensate till birth so chances creatinism will be in first few yrs of life. If mother is also hypothyroid during pregnancy the child will be born with creatinism.

Answer 22

TSH excursions are modest in comparison to those of other pituitary hormones, in part, because TSH has a relatively long plasma half-life (50 min)

Answer 23

Excess iodide transiently inhibits thyroid iodide organification

Answer 24

``` INCREASE TBG: inc in estrogens Pregnancy OCP Hormone therapy Tamoxifen Serm Inflammatory liver ds ``` DECREASE TBG Androgens Nephrotic syndrome

Answer 25

Thyrotoxicosis factitia | Caused by self administration of thyroid hoemones

Answer 26

Oxidation of iodide to iodine Coupling of MIT/DIT and DIT/DIT

Answer 27

TPO Tg TSH-R(blocking ,not stimulatory like TSI) iseful markers of autoimmunity

Answer 28

Increased dermal glycosaminoglycan content traps water, giving rise to skin thickening without pitting (myxedema)

Answer 29

SYMPTOMS Tiredness weakness Dry skin Feeling cold Hair loss Difficulty concentrating and poor memory Constipation Weight gain with poor appetite (due to fluid retention) Dyspnea(dec ventilation ,muscle weakness) Hoarse voice (tissue deposition) Menorrhagia (later oligomenorrhea or amenorrhea) Paresthesia Impaired hearing (fluid accumulation) ``` SIGNS Dry coarse skin cool peripheral extremities (blood flow directed away from skin due to inc PVR) Puffy face,hands, and feet (myxedema) Diffuse alopecia Bradycardia Peripheral edema Delayed tendon reflex relaxation Carpal tunnel syndrome Serous cavity effusions ```

Answer 30

Dec in SV Inc in PVR So, Hypertension particularly diastolic

Answer 31

PRIMARY Autoimmune hypothyroidism: Hashimoto’s thyroiditis atrophic thyroiditis Iatrogenic: 131I treatment subtotal or total thyroidectomy external irradiation of neck for lymphoma or cancer Drugs: iodine excess (including iodine-containing contrast media and amiodarone) lithium antithyroid drugs p-aminosalicylic acid interferon α and other cytokines, aminoglutethimide tyrosine kinase inhibitors (e.g., sunitinib) Congenital hypothyroidism: absent or ectopic thyroid gland dyshormonogenesis TSH-R mutation Iodine deficiency ``` Infiltrative disorders amyloidosis sarcoidosis hemochromatosis scleroderma cystinosis Riedel’s thyroiditis ``` Overexpression of type 3 deiodinase in infantile hemangioma and other tumors TRANSIENT Silent thyroiditis, including postpartum thyroiditis Subacute thyroiditis Withdrawal of supraphysiologic thyroxine treatment in individuals with an intact thyroid After 131I treatment or subtotal thyroidectomy for Graves’ disease ``` SECONDRY Hypopituitarism: tumors pituitary surgery irradiation infiltrative disorders Sheehan’s syndrome trauma genetic forms of combined pituitary hormone deficiencies Isolated TSH deficiency or inactivity Bexarotene treatment ``` ``` Hypothalamic disease: tumors trauma infiltrative disorders idiopathic ```

Answer 32

Long standing hypothyroidism Patient took no medication ``` S/s Bradycardia Hypotension Hyoothermia Stupor Coma Seizures Delayed deep tendon reflex Other feature of hypothyroidism ``` PRECIPITATING FACTORS Myxedema coma almost always occurs in the elderly and is usually precipitated by factors that impair respiration, such as drugs (especially sedatives, anesthetics, and antidepressants), pneumonia, congestive heart failure, myocardial infarction, gastrointestinal bleeding, or cerebrovascular accidents. Sepsis should also be suspected. Exposure to cold may also be a risk factor. TREATMENT Iv.bolus of levothyroxine Liothyronine(T4 to T3 conversion is impaired in myxedema , but high dose can cause artythmia) Hydrocortisone(due to impaired adrenal reserve) Treat precipitating factor

Answer 33

Due to short half life 3 -4 daily doses have to be given leading to fluctuating T3 levels

Answer 34

``` PRIMARY HYPERTHYROIDISM Graves’ disease Toxic multinodular goiter Toxic adenoma Functioning thyroid carcinoma metastases Activating mutation of the TSH receptor Activating mutation of GSα (McCune-Albright syndrome) Struma ovarii Drugs: iodine excess (Jod-Basedow phenomenon) ``` THYROTOXICOSIS WITHOUT HYPERTHYROIDISM Subacute thyroiditis Silent thyroiditis Other causes of thyroid destruction: amiodarone, radiation, infarction of adenoma Ingestion of excess thyroid hormone (thyrotoxicosis factitia) or thyroid tissue SECONDRY HYPERTHYROIDISM TSH-secreting pituitary adenoma Thyroid hormone resistance syndrome: occasional patients may have features of thyrotoxicosis Chorionic gonadotropin-secreting tumors Gestational thyrotoxicosisa

Answer 35

THYROTOXICOSIS state of thyroid hormone excess HYPERTHYROIDISM Result of excessive throid function

Answer 36

TSI TPO are also.present

Answer 37

Yes(not Ab Against TPO, Tg) So can cause thyrotoxicosis in fetus. Antityhroid drugs given to mother will protect the fetus also as they will also cross placenta

Answer 38

``` OPHTHALMOPATHY eye sign Grittiness Tearing Proptosis Corneal damage Periorbital edema Scleral injection Chemosis Optic nerve compression ``` DERMOPATHY Most frequent over ant and lateral aspects of lower leg So aka Pretibial myxedema Noninflamed indurated plaque ACROPATHY Form of clubbing

Answer 39

Propylthiouracil Carbimazole Methimazole MOA All inhibit the function of TPO, reducing oxidation and organification of iodide. These drugs also reduce thyroid antibody levels by mechanisms that remain unclear, and they appear to enhance rates of remission. Propylthiouracil inhibits deiodination of T4 → T3.

Answer 40

Propylthiouracil

Answer 41

Hepatotoxicity

Answer 42

Preadministeration of antithyroid drugs to decrease the hormone level but these drugs should be discontinued 3- 5 days before radionucleotide Rx because it will prevent its uptake and hence the effect

Answer 43

``` S/s Fever Delerium Seizures Coma Vomiting Diarrhoea Jaundice Hyperthermia Arrythmia Cardia failure ``` ``` PRECIPITATING FACTORS acute illness (e.g., stroke, infection, trauma, diabetic ketoacidosis), surgery (especially on the thyroid), or radioiodine treatment of a patient with partially treated or untreated hyperthyroidism. ``` DRUGS Propylthiouracil(DOC: inhibit T4 to T 3 conversion) If not available: methimazole Iodine :block thyroid hormone synthesis via the Wolff-Chaikoff effect (the delay allows the antithyroid drug to prevent the excess iodine from being incorporated into new hormone) Propanolol,esmolol (adrenergic manifestations, also prevent T4 to T3 conversion)

Answer 44

``` SYMPTOMS Hyperactivity irritability dysphoria Heat intolerance sweating Palpitations Fatigue and weakness Weight loss with increased appetite Diarrhea Polyuria (hypercalciuria) Oligomenorrhea, loss of libido Insomnia ``` ``` SIGNS Tachycardia atrial fibrillation Tremor Goiter Warm, moist skin Muscle weakness proximal myopathy Hyperreflexia Lid retraction, lag Gynecomastia Osteopenia Alopecia ```

Answer 45

Sinus tachycardia Palpitations Inc SBP especially Inc stroke vol(high output cardiac failure) So, bounding pulse, widened pulse pressure, aortic systolic murmer) Atrial fibrillation

Answer 46

``` Suppurative Rare Thyroid pain Fever Dysphagia Erythema Systemic symptoms ``` Inc ESR Inc WBC Fna'neutrophils

Answer 47

1) the transient increase in hCG during the first trimester, which stimulates the TSHR (dec TSH and inc thyroid hormones leading to transient gestational hyperthyroidism) (2) the estrogen-induced rise in TBG during the first trimester, which is sustained during pregnancy (3) alterations in the immune system, leading to the onset, exacerbation, or amelioration of an underlying autoimmune thyroid disease (4) increased thyroid hormone metabolism by the placenta (5) increased urinary iodide excretion, which can cause impaired thyroid hormone production in areas of marginal iodine sufficiency

Answer 48

Can cause both hypo/hyperthyroidism INITIALLY, Hypothyroidism due to wolf-chaikoff effect THAN, inhibitory effects on deiodinase activity and thyroid hormone receptor action become predominant. Inc T4, dec T3 , inc rT3, inc TSH SOMETIMES , jod-basedow phenomenon occurs: Thyroid hormone synthesis becomes excessive as a result of inc iodine exposure due to underlying thyroid abnormality (graves, nodular goitre) that results in inc in iodine uptake Wolf chaikoff effect will not occur

Answer 49

Aka de Quervain’s thyroiditis granulomatous thyroiditis viral thyroiditis. CAUSE: virus THREE DISTINCT PHASES 1. thyrotoxic: inc Tg,thyroid hormones , dec TSH, dec Radioactive iodine uptake 2. hypothyroid: low T3/T4 , inc TSH , inc RIU 3. recovery ``` C/m Pain Refered to jaw, ear Swelling Fever Features of thyrotoxicosis/hypothyroidism H/o URT infection Sore throat Tender ``` ``` TREATMENT Aspirin large dose Prednisone B adrenergic blockers No role of antityroid drugs in thyrotoxic state ```

Answer 50

3 differentiating feature from subacute thyroiditis are 1. painless 2. normal ESR 3. positive TPO

Answer 51

``` Insidious Painless Nontender Hard Asymmetric Fixed Local symptoms due to compression: Esophagus Trachea Neck veins RLN ``` Dense fibrosis even outside thyroid capsule CONFUSED WITH MALIGNANCY

Answer 52

Due to acute severe illness Due to release of cytokines such as IL-6 Most common hormone pattern: Low T3(total,free both) Normal T4 Normal TSH Cause:due to impaired peripheral conversion of T4 to T3 via 5'deiodination leading to inc rT3 and decreased clearance. So inc production and dec clerance of rT3. Help as:limit the catabolism in starved and ill patient Very sick patients: dec in total T3 and T4 (low T4 syn) Cause: accelerated degradation of T4 and T3 Altered binding to TBG

Answer 53

Diffuse nontoxic/simple/colloid goitre No nodules and hyperthyroidism Diffuse enlargement Nontoxic multinodular goite Toxic multinodular goitre(functional autonomy) Hyperfunctioning solitary nodule/toxic adenoma

Answer 54

cassava root, which contains a thiocyanate; vegetables of the Cruciferae family (known as cruciferous vegetables) (e.g., Brussels sprouts, cabbage, and cauliflower); and milk from regions where goitrogens are present in grass.

Answer 55

``` Variable nodule size Hypercellular regions Cystic areas filled with colloid Fibrosis Haemorrhage Lymphocytic infilteration ```

Answer 56

Malignancy

Answer 57

History of head and neck irradiation, including total-body irradiation for bone marrow transplant and brain radiation for childhood leukemia Exposure to ionizing radiation from fallout in childhood or adolescence Age <20 or >65 years Increased nodule size (>4 cm) New or enlarging neck mass Male gender Family history of thyroid cancer, MEN 2, or other genetic syndromes associ-ated with thyroid malignancy (e.g., Cowden’s syndrome, familial polypo-sis, Carney complex) Vocal cord paralysis, hoarse voice Nodule fixed to adjacent structures Extrathyroidal extension Lateral cervical lymphadenopathy

Answer 58

Enhanced thyroid hormone production by autonomous nodule(graves, toxic goitre) on giving contrast agents and other iodine containing substances

Answer 59

FOLLICULAR Hematogenous PAPILLARY Lymphatic

Answer 60

Medullary ca of thyroid

Answer 61

SPORADIC FAMILIAL MEN 2A MEN2B Familial MTC without other features of MEN

Answer 62

these include psammoma bodies, cleaved nuclei with an “orphan-Annie” appearance caused by large nucleoli, and the formation of papillary structures.

Answer 63

Papillary thyroid ca

Answer 64

FTC is difficult to diagnose by FNA because the distinc-tion between benign and malignant follicular neoplasms rests largely on evidence of invasion into vessels, nerves, or adjacent structures.