Endocrine Flashcards

Question

Primary Hyperparathyroidism

Answer 1

common - parathyroid adenoma, PTH high / normal Ca High

Answer 2

**SIADH Cannot Void** S: SSRIs (Sertaline) I: Indomethacin (Analgesics) A: Antidepressants (Tricyclics) D: Diuretics (Thiazides) H: Haloperidol Cannot: Cyclophosphamide, Carbamazepine Void: Vincristine

Answer 3

ibcrease urine outout low urine osmolality raised plasma osmolality hypernatremia polyuria (excessive urination), polydipsia (excessive thirst), and confirmation that the kidneys are not properly concentrating urine despite sufficient ADH (antidiuretic hormone) levels Urine Osmolality: Typically low, below 300 mOsm/kg, even when not fluid-restricted. Serum Osmolality: Usually within normal limits (280-290 mOsm/kg) when not fluid-restricted, but may be elevated with fluid restriction. Urine Specific Gravity: Low, below 1.005. 24-hour Urine Collection: Demonstrates significantly high urine volume. Urine and Serum Sodium: May be elevated. Serum Potassium: May be elevated. Serum Calcium: May be elevated. Water Deprivation Test Copeptin Measurement Desmopressin (DDAVP) Stimulation Test:

Answer 4

low urine output low sodium Low plasma osmolality High urine osmolality **Diagnosis criteria of SIADH** decreased serum osmolality (<275 mOsm/kg) increased urine osmolality (>100 mOsm/kg) euvolaemia. increased urine sodium (>20 mmol/L) no other cause for hyponatraemia (no diuretic use and no suspicion of hypothyroidism, cortisol deficiency, marked hyperproteinaemia, hyperlipidaemia or hyperglycaemia).

Answer 5

* <100 = Addisons or hypoadresalism likely * 100500 = Addisons unlikely

Answer 6

Hypercalemia hyponatremia hypoglicemia metabolic acidosis Addison's disease disrupts the body's ability to produce adequate levels of cortisol, leading to various physiological problems and symptoms, including impaired stress response, metabolic disturbances, and blood pressure irregularities

Answer 7

central obesity insulin resistance hypertension, and dyslipidemia poses a significant risk for the development of atherosclerotic cardiovascular diseases type II diabetes mellitus other conditions - raised Uric acid levels, Polysisctic ovarian syndrome, fatty liver disease

Answer 8

Glucose >11 pH<7.3 Bicarbonate <15 Blood ketones >3 or urine ketones 2+

Answer 9

Mirabegron - Mirabegron is a selective beta-3 adrenergic receptor agonist. oxybutinin can cause confusion in elderly

Answer 10

Marfanoid habitus, edullary thyroid cancer, pheochromocytoma, and mucosal neuromas RET proto onco gene present

Answer 11

3 P's Parathyroid gland Pancreas Pituitary gland

Answer 12

medullary thyroid cancer >70% 2Ps Pheochromocytoma - Adrenal Parathyroid RET proto onco gene present

Answer 13

Propylthiouracil inhibits the production of new thyroid hormone in the thyroid gland. [2] It acts by inhibiting the enzyme thyroid peroxidase, which usually converts iodide to an iodine molecule and incorporates the iodine molecule into amino acid tyrosine. to treat hyperthyroidism in pregnancy or breast feeding, and when surgery or radioactive iodine therapy are not suitable carbimazole is the first choice treatment

Answer 14

1st line - Transphenoidal surgery if unsuccessfull medications 1. somatosatin analogue 2. pegvisoman 3. dopamine agonists colorectal cancer risk increased

Answer 15

- same clinical presentation as Cushings, but with severe hypokalemia and very high ACTH - doesnt respond to high dose dexa suppression

Answer 16

8- cushings syndrome + elevated 9 am cortisol and high ACTH - respond to high dose Dexa (2mg 6hr for 48hr) -dexa respond to pituirary only, CRH - increasse cortisol (0nly in piturory )

Answer 17

80% Solitory Adenoma 10% Hyperplasia 1% cancer 80% symptomatic - polydipsia, polyurea, depression, constipation, peptic ulcers, pancreatitis, bone pain fractures, kidney stones, hypertension - high Ca+, low Ph+, PTH could be normal - Scan - Techniciam Mibi substraction - X ray - paper pot skull, ostiitis, fibrosa cystica - Management - parathiroidectomy, non - surgical = cinacalcet

Answer 18

Fetal loss maternal heart failure premature labor

Answer 19

Replace GLP-1 mimetic instead of gliclazide

Answer 20

- Ketoacidosis - Severe gastro-intestinal disease (not for liraglutide and semaglutide) - Liraglutide: diabetic gastroparesis, inflammatory bowel disease

Answer 21

Ketoacidosis No Hypoglycaemia risk

Answer 22

IGF 1 level followed by OGTT + serial GH measurements

Answer 23

1. - Shakiness, sweating, dizziness, or lightheadedness. - Hunger, confusion, or difficulty concentrating. - Rapid heartbeat, blurred vision, or headache. - In severe cases, seizures, loss of consciousness, or coma 2. Glucagan increase - adrenalin, cortisol increase

Answer 24

1: Hexokinase/glucokinase, 2: Glycogen synthase, 3: Phosphorylase, 4: Phosphofructokinase, 5: Pyruvate kinase, 6: Pyruvate carboxylase, 7: Phosphoenolpyruvate carboxykinase, 8: Fructose-1,6-biphosphatase, 9: Glucose-6-phosphatase.

Answer 25

eastrogen - Liver TBG increases and bind to FT3 & FT4 rerduce free T3, T4 Secondary Increase increase in TSH

Answer 26

Male phenotype, Karyotype (47, XXY), Long/tall, Infertile, gyenicomastia Nondisjunction, Eunuchoid body proportions, FSH elevated, High LH (Elevated Gonadotropins) Minimal facial & axillary hair, Estradiol/testosterone ratio elevation

Answer 27

Pretibial Myxedema (Thyroid Dermopathy) Hyperpigmentation Vitiligo

Answer 28

Diagnosis - Neontal screening - elevated levels of galactose-1-phosphate Classic Galactosemia: Mutation in enzyme galactose-1-phosphate uridyltransferase (GALT). Variant Galactosemia: GALK1 and GALE. clinical manifestations - oor feeding, jaundice, liver damage, and cataracts, Sepsis if not treated - failure to thrive and interlectual difficulties

Answer 29

1. The thiazolidinedione, reduces peripheral insulin resistance, leading to a reduction of blood-glucose concentration. PPAR Gamma 2. History of heart failure, previous or active bladder cancer, uninvestigated macroscopic haematuria, causes weight gain, liver imparement

Answer 30

Blocks thyroid hormonogenesis by inhibiting the action of thyroid peroxidase, organification of iodide and their uptake by tyrosyl radicals as well as the coupling of iodotyrosines with iodothyronine residues (T3 and T4) which in turn suppress the synthesis of thyroid hormones

Answer 31

Anticancer agents - Vinca alkaloids (e.g. Vincristine), platinum compounds (e.g. Cisplatin), Alkylating agents (e.g. Cyclophosphamide) Anti-depressants - Tricyclic antidepressants, SSRIs, MAOI Anti-epileptic medications - Carbamazepine, Sodium Valproate Anti-hypertensives - ACEi, ARB, Amlodipine Anti-pyschotic medications - henothiazines, Butyrophenones Diuretics - Thiazides, Indapamide, Amiloride, loop diuretics Proton pump inhibitors - Omeprazole

Answer 32

1. Medications (most commonly thiazide diuretics). 2. Syndrome of inappropriate antidiuresis. 3. Underlying medical conditions (such as heart failure, kidney disease, and liver disease).

Answer 33

Mild — serum sodium concentration 130–135 mmol/L. Moderate — serum sodium concentration 125–129 mmol/L. Severe — serum sodium concentration less than 125/120 mmol/L.

Answer 34

false low serum Na+ concentration due to hyperproteinaemia - multiple myeloma or hypertriglyceridaemia

Answer 35

- Severe hyperglycaemia (the high levels of glucose draw intracellular water into the extracellular space) - Administration of an active osmolyte (such as mannitol)

Answer 36

- Medications, especially thiazide diuretics. - Endocrine disorders (primary adrenal insufficiency). - Cerebral salt-wasting (a rare cause of hyponatraemia resulting from a central nervous system insult such as aneurysmal subarachnoid haemorrhage). - Severe diarrhoea and/or vomiting (gastrointestinal sodium loss). - Sweating (for example during exercise) and extensive skin burns (transdermal sodium loss). - Salt-wasting nephropathies, for example tubulopathy after chemotherapy. - Third space losses — bowel obstruction, pancreatitis, severe hypoalbuminaemia, sepsis, or muscle trauma

Answer 37

- Congestive heart failure. - Liver disease (cirrhosis with ascites). - Kidney disease (acute kidney injury, chronic kidney disease, nephrotic syndrome).

Answer 38

- Drugs (for example selective serotonin-reuptake inhibitors and thiazide diuretics). - Syndrome of inappropriate antidiuretic hormone secretion (SIADH). - Endocrine disorders (secondary adrenal insufficiency and hypothyroidism [very rare cause]). - High water low solute intake — primary polydipsia, anorexia nervosa, and beer potomania (excess beer consumption with a low solute diet).

Answer 39

OGTT test fasting >5.6 2 Hour >7.8

Answer 40

Metformin (fasting Glucose <7, not controlled by diet/ fasting) Insulin (if not treated with insulin) Treated with short acting (no long acting)

Answer 41

Macrosmia polyhydro amnio

Answer 42

QT Interval Prolongation: rare : Peaked T waves, Torsades de pointes, Atrial Fib

Answer 43

Rare, aggressive, spreads rapidly, often leading to a poor prognosis >60 years

Answer 44

- Slow-growing, palpable lump, Asymptomatic - Risk Factors: Radiation Exposure, Genetic Factors, Family History - young females - treatable -

Answer 45

- autosomal dominant - high LDL **Simon Broome Criteria ** 1. adult - total chol- 7.5, LDL- 4.9 Child- total - 6.7, LDL - 4 2. tendon xanthoma, 3. Family histiory tretatment - high dose statin

Answer 46

PH - high Bp, Low K+, high Na+, low Renin (diagnosed from treatment resistent hypertension with low K+), aldesterone renin ratio high RTS - kow k+, high Aldesterone, High Na+, High Renin Renal artery stenosis, a narrowing of the arteries supplying the kidneys, can lead to secondary hyperaldosteronism Renal Artery Stenosis: This condition, often caused by atherosclerosis, narrows the arteries that bring blood to the kidneys. This reduced blood flow can be mistaken by the kidneys as a sign of low blood volume, leading to the activation of the renin-angiotensin-aldosterone system (RAAS). Hyperaldosteronism: Aldosterone is a hormone that regulates blood pressure and electrolyte balance. When there's too much aldosterone, it can lead to high blood pressure, low potassium levels, and other complications. There are two main types: Primary Hyperaldosteronism: This is caused by problems within the adrenal glands, often due to tumors or overgrowth, leading to independent aldosterone production. Secondary Hyperaldosteronism: This is triggered by external factors, such as renal artery stenosis, that activate the RAAS, causing the adrenal glands to produce more aldosterone

Answer 47

in renal failure, low vit D, low Ca, raised PTH, raised ALP due to bone resoption Primary hyperthyroidism arises from a problem within the thyroid gland itself, causing it to produce too much hormone. Secondary hyperthyroidism, on the other hand, is caused by issues in the pituitary gland or hypothalamus, which regulate thyroid-stimulating hormone (TSH) production, indirectly affecting thyroid function Primary Hyperthyroidism: Cause: The thyroid gland is the primary source of the excess thyroid hormone production. This can be due to various factors, including Graves' disease (an autoimmune condition), toxic multinodular goiter, or toxic adenoma. Mechanism: In primary hyperthyroidism, the thyroid gland produces excessive amounts of T3 and T4, which then suppress the production of TSH by the pituitary gland. This is a negative feedback mechanism. Diagnosis: In primary hyperthyroidism, TSH levels are low or suppressed, while free T4 and/or free T3 levels are elevated. Secondary Hyperthyroidism: Cause: The pituitary gland or hypothalamus, not the thyroid, is the source of the problem. A tumor or other issue in these areas can lead to overproduction of TSH. Mechanism: Excess TSH stimulates the thyroid gland, causing it to produce more thyroid hormones. Diagnosis: In secondary hyperthyroidism, TSH levels are high, while free T4 and/or free T3 levels are elevated

Answer 48

long standing secodnary hyperpara result in hyperplasia of parathiroid gland. raised Ca, raised PTH, high Ph

Answer 49

changes in color vision - urgent decompression surgery

Answer 50

pancreatic tumors that produce excess insulin lead to hypoglycemina diagnosis- supervised fasting (72 hrs) nuroendocrine tumor in pancreartic beta cells in langhanns MEN 1 associated primary treatment for insulinoma is surgical removal of the tumor. hypoglycemia, including sweating, tremors, palpitations, confusion, and in severe cases, seizures or loss of consciousness A diagnosis of insulinoma is often suspected when a patient presents with Whipple's triad, which includes: Symptoms of hypoglycemia Documented low blood sugar (glucose) at the time of symptoms Improvement of symptoms after glucose administration

Answer 51

pregnancy prolactinoma' PCOS primary hyporthiroidism metacropanide domperidone phenothiozene

Answer 52

men - loss of libido, impotence,galactoria female- amenohria, galactoria

Answer 53

Anti eastrogen

Answer 54

metabolic alcolosis with hypocalemia small cell lung cancer - Ectopic ACTH

Answer 55

XY along with inability of body cells to responds to andregens, rudimentory testes Bi lateral groin swelling

Answer 56

amitriptiline, deuloxitine, gaba pentin

Answer 57

risk of vitriuos haemorrage treatment- lasor photocoagulation

Answer 58

secretory - prolactinoma nonsecretory -

Answer 59

Insulin aspart: Available as Fiasp, NovoRapid, and Trurapi. Insulin lispro: Available as Admelog, Humalog, and Lyumjev. Insulin glulisine: Available as Apidra. Key features: Faster Onset: within 15 minutes. Shorter Duration: 2-5 hours. Improved Glucose Control: manage blood sugar levels after meals, reducing postprandial glucose excursions. Convenience: flexibility in meal timing and bolus dosing. Safe

Answer 60

Morphine is primarily metabolized in the liver, mainly through glucuronidation, forming morphine-3-glucuronide (M3G) and morphine-6-glucuronide (M6G Mechanism of Action: Morphine binds to opioid receptors, primarily mu receptors, in the CNS side effects like respiratory depression. Morphine travels through the blood and crosses the blood-brain barrier to reach its targets in the brain. Excretion: Morphine is metabolized in the liver into M3G and M6G, which are then excreted in the urine. A small amount of unchanged morphine is also excreted in the urine. Some metabolites may also be excreted in the bile and undergo enterohepatic recycling. The metabolites are generally excreted renally, so renal function can impact morphine and its metabolites. Around 70-80% of an administered dose is excreted within 48 hours, primarily in the urine.