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 - Normal response: Urine concentrates (>600 mOsm/kg). NDI (Lithium-induced): Urine remains dilute (<300 mOsm/kg) even after ADH injection. Copeptin Measurement Desmopressin (DDAVP) Stimulation Test: become high osmolality

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 Other possible manifestations: Adrenal tumors (nonfunctional or cortisol-secreting) Foregut carcinoids (thymic, bronchial, gastric) Facial angiofibromas, collagenomas (cutaneous markers) Clinical Features & Tumor Types 1. Primary Hyperparathyroidism (PHPT) Most common & earliest manifestation (90% by age 50). Multiglandular hyperplasia (unlike sporadic single adenomas). Symptoms: Kidney stones, osteoporosis, fatigue, hypercalcemia. Treatment: Subtotal parathyroidectomy (recurrence common). 2. Pancreatic Neuroendocrine Tumors (pNETs) Gastrinoma (Zollinger-Ellison syndrome, ~40%) Recurrent peptic ulcers, diarrhea, GERD. Diagnosed by elevated fasting gastrin + secretin stimulation test. Managed with high-dose PPIs (omeprazole) and surgery if localized. Insulinoma (~10%) Fasting hypoglycemia, neuroglycopenic symptoms. Diagnosed by 72-hr fast (confirm insulin abuse first)+ elevated insulin/C-peptide. Treated with surgical resection. Nonfunctional pNETs (~20-30%) May metastasize (liver); monitored with CT/MRI & chromogranin A. 3. Pituitary Adenomas Prolactinoma (most common) → galactorrhea, amenorrhea. Somatotroph (GH-secreting) → acromegaly. Corticotroph (ACTH-secreting) → Cushing’s disease. Diagnosis: MRI pituitary + hormone testing. Treatment: Dopamine agonists (prolactinoma), surgery, or radiation. 4. Other Tumors Adrenal adenomas (usually nonfunctional; rarely cortisol-secreting). Thymic/bronchial carcinoids (aggressive; screen with chest CT). Facial angiofibromas (benign, but pathognomonic).

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 (Gold St) + serial GH measurements (normal people GH suppressed while Acromegaly not)

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

PA - high Bp, Low K+, high Na+, low Renin (diagnosed from treatment resistent hypertension with low K+), aldesterone renin ratio high Diagnostic Tests - Aldosterone-to-Renin Ratio (ARR), - Saline Suppression Test RAS - kow k+, high Aldesterone, High Na+, High Renin, ↑ Angiotensin II Diagnostic Tests - Duplex Ultrasound (1st-line), CTA/MRA (gold standard) 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 Clinical Clues to Differentiate Renal Artery Stenosis: Flash pulmonary edema, ↑ Cr on ACEi/ARB, asymmetric kidney size on US. Atherosclerotic RAS: Older age, PVD/CAD risk factors. Fibromuscular Dysplasia: Young women, "string-of-beads" on angiography. Primary Hyperaldosteronism: Hypokalemia without diuretics, family history of early HTN. Adenoma (APA): Unilateral adrenal nodule on CT.pai Hyperplasia (BAH): Bilateral adrenal thickening. ✅ RAS = ↑ Renin, ↑ Aldosterone, vascular bruit, ACEi-induced renal dysfunction. ✅ Conn’s = ↓ Renin, ↑ Aldosterone, hypokalemia, adrenal lesion. ✅ Test renin/aldosterone early in resistant HTN!

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 - Hormone secretion: Functional (secreting) adenomas (about 70% of cases): Prolactinomas (most common, secrete prolactin) Growth hormone-secreting (cause acromegaly or gigantism) ACTH-secreting (cause Cushing's disease) TSH-secreting (cause central hyperthyroidism, rare <1%) FSH/LH-secreting (gonadotroph adenomas) Non-functional adenomas (about 30% of cases) Invasiveness: Non-invasive (remain within sella turcica) Invasive (extend into surrounding structures like cavernous sinus) Medical Therapy Prolactinomas: Dopamine agonists (cabergoline, bromocriptine) - first line Acromegaly: Somatostatin analogs (octreotide, lanreotide) GH receptor antagonist (pegvisomant) Cushing's disease: Steroidogenesis inhibitors (ketoconazole, metyrapone) Pasireotide (somatostatin analog) TSHomas: Somatostatin analogs (octreotide, lanreotide) normalize thyroid function in >90%

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.

Answer 61

An autonomous overproduction of aldosterone by the adrenal glands, leading to hypertension, hypokalemia, and metabolic alkalosis. Causes Adrenal Adenoma (Aldosterone-Producing Adenoma, APA) – 60-70% (unilateral). Bilateral Adrenal Hyperplasia (BAH) – 30-40%. Rare Causes: Familial Hyperaldosteronism (Type I, II, or III). Adrenal carcinoma (very rare). Clinical Features 1. Hypertension (Resistant to multiple drugs) Often severe, early-onset (<40 years). 2. Hypokalemia (Not always present! ~40% are normokalemic) Symptoms: Muscle weakness, cramps, fatigue, palpitations (arrhythmias). ECG: U waves, flattened T waves. 3. Metabolic Alkalosis (High serum HCO₃⁻). 4. Other Effects of Aldosterone Excess: Hypernatremia (mild). Low plasma renin (suppressed by aldosterone). Diagnosis Step 1: Screening (For High-Risk Patients) Resistant hypertension (≥3 drugs). Hypertension + hypokalemia (spontaneous/diuretic-induced). Early-onset HTN (<40) or family history of hyperaldosteronism. Initial Test: Aldosterone-to-Renin Ratio (ARR): High aldosterone + low renin suggests Conn’s. Step 2: Confirmatory Tests (If ARR Elevated) Saline Infusion Test (gold standard): Failure to suppress aldosterone (<5 ng/dL after 2L saline) confirms diagnosis. ✅ Suspect in resistant HTN ± hypokalemia → check ARR. ✅ AVS is gold standard to guide surgery vs. meds. ✅ Spironolactone/eplerenone for BAH; surgery for APA.

Answer 62

Competitive inhibition of TPO → blocks: Iodination of tyrosine residues on thyroglobulin. Coupling of MIT/DIT into T3/T4. No effect on pre-formed thyroid hormones (takes weeks to deplete stores). Both are thioamide antithyroid drugs (ATDs) that inhibit thyroid hormone synthesis, but with key differences: Carbimazole (CMZ) Active Form Converted to methimazole (MMI) in the body. Inhibits thyroid peroxidase (TPO) → blocks iodination & coupling of tyrosines (T3/T4 synthesis). Propylthiouracil (PTU) Same as CMZ, but weaker TPO inhibition Blocks type 1 deiodinase (reduces T4→T3 in tissues) Faster (hours, due to T4→T3 inhibition).

Answer 63

Subclinical hypothyroidism (SCH) - characterized by elevated thyroid-stimulating hormone (TSH) with normal thyroxine (T4) levels Consequences of Non-Compliance While most cases of mild SCH (TSH <10 mIU/L) may not require immediate treatment, poor adherence in indicated cases can lead to: Progression to overt hypothyroidism (2-6% annual risk, higher with thyroid antibodies) 16 Potential cardiovascular risks including diastolic hypertension and dyslipidemia 13 Adverse pregnancy outcomes in women of reproductive age (when untreated

Answer 64

1. Risk Factors Duration of diabetes (most important; >10 years significantly increases risk). Poor glycemic control (high HbA1c). Hypertension & dyslipidemia (worsen vascular damage). Pregnancy (can accelerate retinopathy). Renal disease (diabetic nephropathy correlates with severity). 2. Pathophysiology Hyperglycemia → endothelial dysfunction → breakdown of blood-retinal barrier. Microaneurysms (earliest sign) → leakage (edema, exudates). Capillary occlusion → retinal ischemia → hypoxia-driven VEGF release → neovascularization (proliferative stage). Classification & Stages A. Non-Proliferative Diabetic Retinopathy (NPDR) (Early to Moderate Disease) Mild NPDR: Microaneurysms only. Moderate NPDR: Microaneurysms + retinal hemorrhages, hard exudates, cotton-wool spots. Severe NPDR ("4-2-1 Rule"): 4+ quadrants of hemorrhages 2+ quadrants of venous beading 1+ quadrant of IRMA (intraretinal microvascular abnormalities) High risk of progression to PDR. B. Proliferative Diabetic Retinopathy (PDR) (Advanced Disease) Neovascularization (new fragile vessels at optic disc [NVD] or elsewhere [NVE]). Vitreous hemorrhage (bleeding from ruptured vessels). Tractional retinal detachment (fibrovascular scarring pulls retina). C. Diabetic Macular Edema (DME) (Vision-Threatening Complication) Fluid leakage into macula → blurred vision. Can occur at any stage of DR. Clinical Presentation Early stages: Often asymptomatic (detected only on screening). Later stages: Blurred or fluctuating vision. Floaters (vitreous hemorrhage). Sudden vision loss (retinal detachment, severe hemorrhage). Diagnosis Dilated fundus exam (gold standard): Assess hemorrhages, exudates, neovascularization. Optical Coherence Tomography (OCT): Detects macular edema (retinal thickness). Fluorescein Angiography: Identifies leaking vessels, ischemia, neovascularization. 4. Diabetic Macular Edema (DME) Anti-VEGF therapy (first-line). Focal laser (if persistent edema). Steroid implants (e.g., dexamethasone) in refractory cases. Complications Vitreous hemorrhage → sudden vision loss. Retinal detachment → permanent blindness.

Answer 65

Key Features: Etiology: Most commonly associated with diabetes mellitus (diabetic neuropathy). Other causes include: Spinal cord disorders (e.g., syringomyelia, tabes dorsalis from syphilis). Peripheral neuropathy (e.g., alcoholism, leprosy, hereditary neuropathies). Chronic steroid use or post-transplant neuropathy. Pathophysiology: Loss of protective sensation (neurotrauma theory) leads to unnoticed repetitive microtrauma. Neurovascular theory suggests autonomic dysfunction causes increased blood flow, leading to osteoclast activation and bone resorption. Results in bone destruction, fractures, dislocations, and severe joint deformity. Clinical Presentation: Acute phase: Swelling, warmth, redness (mimics infection or gout). Pain (mild or absent due to neuropathy). Chronic phase: Foot deformity (e.g., "rocker-bottom" foot, midfoot collapse). Instability, ulceration, and recurrent infections. Diagnosis: Clinical suspicion in a neuropathic patient with a warm, swollen foot. Imaging: X-rays: Bone destruction, fragmentation, dislocation, sclerosis. MRI: Helps differentiate from osteomyelitis (bone marrow edema pattern). Bone scan (if infection is a concern). Lab tests: Rule out infection (WBC, ESR, CRP may be elevated in both Charcot and infection). Treatment: Acute Phase: Immobilization: Total contact cast (TCC) or non-weight-bearing with crutches/wheelchair. Offloading: Reduce stress on the affected joint. Bisphosphonates (e.g., IV pamidronate) may help reduce bone turnover (controversial). Chronic Phase: Custom orthotics, braces (e.g., Charcot Restraint Orthotic Walker, CROW). Surgical reconstruction (if severe deformity or instability). Prevent complications (ulcers, infections, amputations). Complications: Chronic ulcers (leading to osteomyelitis). Foot deformity causing gait abnormalities. Increased risk of amputation if untreated. Key Differential Diagnoses: Osteomyelitis (often coexists, may require biopsy). Cellulitis/gout (acute inflammation mimics Charcot). Septic arthritis

Answer 66

Autoimmune origin: Caused by autoantibodies (especially TSH receptor antibodies, TRAb) targeting orbital fibroblasts, leading to inflammation, swelling, and tissue remodeling. Bilateral (but often asymmetric): Typically affects both eyes, though one eye may appear worse. Active (inflammatory) and inactive (fibrotic) phases: Active phase (6-24 months): Inflammation, swelling, redness, and progression. Inactive phase: Scarring, stable but sometimes permanent changes (e.g., double vision, eyelid retraction). Common Symptoms Eye bulging (proptosis/exophthalmos) – Due to increased orbital fat and muscle swelling. Eyelid retraction – Upper lid pulled up, giving a "staring" appearance. Redness and swelling (periorbital edema, conjunctival injection). Dry eyes, grittiness, excessive tearing (due to exposure keratopathy). Double vision (diplopia) – From extraocular muscle inflammation/fibrosis. Pain with eye movements (especially upward gaze). Vision loss (rare but serious) – From optic nerve compression (dysthyroid optic neuropathy). Severe Complications Corneal ulceration (due to severe exposure). Optic neuropathy (compression from swollen muscles). Restricted eye movements leading to permanent strabismus. Risk Factors for TED Graves’ hyperthyroidism (~90% of cases). Smoking (strongest modifiable risk factor; worsens severity). Radioactive iodine (RAI) therapy (can exacerbate TED if not managed properly). High TSH-receptor antibody (TRAb) levels. Poor thyroid control (both hyper- and hypothyroidism can worsen TED).

Answer 67

Estradiol > 1000 pg/mL outside pregnancy → rule out ovarian tumor Postmenopausal E2 > 50 pg/mL → investigate for malignancy Sudden breast enlargement, severe pelvic pain, or abnormal bleeding → urgent evaluation Causes of Very High Estradiol 1. Physiological (Benign) Causes Ovulation (transient peak) Pregnancy (estradiol rises progressively, reaching thousands of pg/mL in the third trimester) Obesity (adipose tissue converts androgens to estrogen via aromatase) 2. Medications & Exogenous Hormones Fertility treatments (e.g., ovarian stimulation for IVF) Estrogen therapy (oral, patches, or gels) Tamoxifen (SERM that can increase E2 in some women) Certain oral contraceptives 3. Pathological Causes Ovarian tumors (granulosa cell tumors, thecomas – secrete estrogen) Adrenal tumors (rare, may produce estrogen precursors) Liver cirrhosis (reduced estrogen metabolism) Aromatase excess syndrome (genetic condition causing excess estrogen production) Polycystic ovary syndrome (PCOS) (some women have high E2 due to follicular cysts) Primary hypothyroidism (can elevate SHBG, increasing bound estradiol)

Answer 68

Postpartum thyroiditis is an autoimmune thyroid disorder that occurs within 12 months after childbirth, characterized by transient thyroid dysfunction (hyperthyroidism → hypothyroidism → recovery or permanent hypothyroidism). 2. Pathophysiology Autoimmune destruction of thyroid follicles (similar to Hashimoto’s thyroiditis). Three phases: Hyperthyroid phase (1-4 months postpartum) – due to thyroid hormone leakage from damaged follicles. Hypothyroid phase (4-8 months postpartum) – due to depleted thyroid hormone stores. Recovery phase (most recover by 12 months, but ~20-30% develop permanent hypothyroidism). Hyperthyroid Phase (Weeks 1-4 Postpartum) Symptoms: Fatigue, palpitations, anxiety, heat intolerance, weight loss. Mild or asymptomatic (often mistaken for postpartum stress). Key difference from Graves’ disease: No orbitopathy or severe symptoms. Low/normal radioactive iodine uptake (vs. high uptake in Graves’). Hypothyroid Phase (Months 4-8 Postpartum) Symptoms: Fatigue, depression, weight gain, dry skin, cold intolerance, poor milk supply. Often misdiagnosed as postpartum depression. Recovery Phase (By 12 Months) Most return to euthyroid state, but some develop permanent hypothyroidism. Diagnosis Thyroid Function Tests (TFTs): Hyperthyroid phase: ↓ TSH, ↑ FT4/FT3 (mild elevation). Hypothyroid phase: ↑ TSH, ↓ FT4. Thyroid Antibodies: Anti-TPO antibodies (positive in ~80% of cases). Ultrasound (if needed): Diffuse hypoechogenicity (similar to Hashimoto’s). Management (NICE & ATA Guidelines) 1. Hyperthyroid Phase Usually mild and self-limiting (no treatment needed). If severe symptoms (rare): Beta-blockers (e.g., propranolol) for palpitations/anxiety. Avoid antithyroid drugs (not effective, as it’s a destructive process). 2. Hypothyroid Phase If symptomatic or TSH >10 mIU/L: Levothyroxine (25-50 mcg/day, adjust based on TSH). If planning another pregnancy: Treat even mild hypothyroidism (TSH >2.5). Re-evaluate at 6-12 months: Taper and stop levothyroxine if TSH normalizes. Continue lifelong if persistent hypothyroidism (~20-30% of cases). 3. Monitoring Check TSH at 3, 6, and 12 months postpartum (especially in high-risk women). Complications Permanent hypothyroidism (20-30% of cases). Recurrence in future pregnancies (up to 70% if TPO antibodies positive). Postpartum depression (linked to hypothyroid phase). Differential Diagnosis Condition Key Features Graves’ disease Orbitopathy, high RAI uptake, TRAb positive Postpartum anxiety/depression No thyroid abnormalities Subacute thyroiditis Painful thyroid, viral prodrome

Answer 69

PTH is the primary hormone responsible for maintaining calcium balance in the body. It achieves this by: Increasing Calcium Absorption in the Kidneys: PTH acts on the kidneys to promote calcium reabsorption in the thick ascending loop of Henle, distal convoluted tubule, and collecting ducts, reducing calcium excretion in the urine. Releasing Calcium from Bone: PTH stimulates osteoclasts, which break down bone tissue, releasing calcium into the bloodstream. Increasing Vitamin D Synthesis: PTH also stimulates the production of the active form of vitamin D (1,25-dihydroxyvitamin D or calcitriol) in the kidneys, which enhances calcium absorption from the gu

Answer 70

Diagnosis & Screening Diagnostic criteria: Use HbA1c (≥48 mmol/mol or 6.5%) or fasting plasma glucose (≥7.0 mmol/L). If results are inconclusive, perform an oral glucose tolerance test (OGTT) Risk assessment: Use tools like QDiabetes to identify high-risk individuals for screening 2. Glycemic Control Targets Individualized HbA1c targets: General target: ≤48 mmol/mol (6.5%) for most adults. Relaxed targets: Consider ≤53 mmol/mol (7.0%) for those at risk of hypoglycemia or with frailty/comorbidities Continuous glucose monitoring (CGM) may be considered for adults with recurrent hypoglycemia or impaired awareness 3. Pharmacologic Therapy First-Line Treatment Metformin remains first-line unless contraindicated (e.g., renal impairment) SGLT2 inhibitors (e.g., empagliflozin, dapagliflozin) are recommended for: Heart failure (reduce hospitalization). Chronic kidney disease (CKD) (eGFR ≥20 mL/min) GLP-1 receptor agonists (e.g., semaglutide, liraglutide) for: Obesity + high cardiovascular risk. Weight management (if BMI ≥35 kg/m² or ≥30 kg/m² with comorbidities) Second-Line & Beyond Dual therapy: Add SGLT2i or GLP-1 RA if HbA1c remains above target Triple therapy: Consider DPP-4 inhibitors, pioglitazone, or sulfonylureas if needed, but avoid sulfonylureas in high hypoglycemia risk patients 3. Insulin therapy: Basal insulin (e.g., glargine, degludec) for persistent hyperglycemia. Consider hybrid closed-loop systems for type 1 diabetes 4. Lifestyle & Non-Pharmacologic Interventions Diet: Emphasize Mediterranean-style diets, low glycemic index foods, and weight loss (if BMI ≥25) Exercise: ≥150 mins/week of moderate activity + resistance training Smoking cessation: Offer support to reduce cardiovascular risk 5. Complication Screening & Management Annual screenings for: Retinopathy (digital retinal imaging). Neuropathy (10g monofilament test). Nephropathy (UACR & eGFR) Cardiovascular risk: Statin therapy (atorvastatin 20mg) for primary prevention. Antiplatelet therapy (low-dose aspirin) only if high CVD risk Foot care: High-risk patients (previous ulcers, neuropathy) should have podiatry referrals 6. Special Populations Elderly/Frail: Relax glycemic targets (HbA1c ≤58–64 mmol/mol or 7.5–8.0%). Pregnancy: Tight glycemic control (fasting <5.3 mmol/L, postprandial <7.8 mmol/L) Mental health: Screen for diabetes distress, depression, and anxiety 7. Technology & Monitoring Flash glucose monitoring (Freestyle Libre) for: Type 1 diabetes. Type 2 diabetes on insulin with recurrent hypoglycemia Closed-loop systems (artificial pancreas) for type 1 diabetes GLP-1 RAs now prioritized for heart & kidney protection CGM expanded for non-insulin type 2 diabetes Weight-loss drugs (e.g., semaglutide) integrated into diabetes-obesity management Implementation Challenges Medication shortages: NICE advises alternatives (e.g., switching GLP-1 RAs if unavailable) Health inequalities: Tailor care for ethnic minorities (higher T2DM risk)

Answer 71

1. Acute Diabetic Emergencies (Medical Emergencies) A. Hypoglycemia Definition: Blood glucose <4.0 mmol/L (or <3.5 mmol/L if on insulin). Severe hypoglycemia: If patient cannot self-treat (needs glucagon/IV glucose). Causes: Excess insulin/sulfonylureas. Missed meals, alcohol, exercise. Symptoms: Mild: Sweating, tremor, hunger, irritability. Moderate: Confusion, drowsiness, slurred speech. Severe: Seizures, unconsciousness. Management (NICE NG17, NG28): Conscious patient: 15-20g fast-acting carbs (glucose tablets, sugary drink). Recheck glucose in 15 mins; repeat if still <4.0 mmol/L. Unconscious/severe: IM glucagon (1mg) or IV dextrose (10-20g, 20% or 50% solution). Hospital admission if prolonged/recurrent. Prevention: Structured education (e.g., DAFNE for type 1 diabetes). CGM (continuous glucose monitoring) for high-risk patients. B. Diabetic Ketoacidosis (DKA) Definition: Blood glucose >11 mmol/L + ketones ≥3.0 mmol/L (or significant ketonuria) + pH <7.3/HCO₃ <15 mmol/L. Causes: Infection, missed insulin, new-onset type 1 diabetes. Symptoms: Polyuria, polydipsia, nausea/vomiting, abdominal pain, Kussmaul breathing, confusion. Management (NICE NG18): Hospital admission (critical emergency!). IV fluids: 0.9% NaCl (1L over 1h, then adjust based on clinical status). Fixed-rate IV insulin (0.1 units/kg/hr): Do NOT stop insulin even if glucose normalizes (switch to glucose + insulin). Monitor K+: If K+ <5.5 mmol/L, add KCl to fluids (prevents hypokalemia). Treat underlying cause (e.g., infection). Prevention: Sick-day rules: Monitor ketones if glucose >14 mmol/L, never stop insulin. C. Hyperosmolar Hyperglycemic State (HHS) Definition: Blood glucose >30 mmol/L, osmolality >320 mOsm/kg, no significant ketosis, pH >7.3. Causes: Type 2 diabetes, infection, dehydration. Symptoms: Severe dehydration, confusion, seizures, coma. Management (NICE NG18): IV fluids (0.9% NaCl): Correct dehydration slowly (risk of cerebral edema). Insulin infusion (after fluids if glucose not falling): Lower dose than DKA (e.g., 0.05 units/kg/hr). Monitor electrolytes (K+, Na+). Diabetic Neuropathy: Peripheral: Pain management (e.g., duloxetine, pregabalin). Autonomic: Gastroparesis, orthostatic hypotension. B. Macrovascular Complications Cardiovascular disease: Statins (e.g., atorvastatin 20-80mg). Peripheral arterial disease: Foot checks, smoking cessation. C. Hypoglycemia Unawareness CGM recommended (NG17). Relax glycemic targets (e.g., HbA1c ≤58 mmol/mol instead of ≤48).

Answer 72

1. Insulin Common Side Effects Hypoglycemia (most serious, especially with long-acting insulins). Weight gain (due to anabolic effects). Lipodystrophy (fat thickening or atrophy at injection sites). Allergic reactions (rare: rash, swelling at injection site). Serious Complications Severe hypoglycemia (seizures, coma, death if untreated). Hypokalemia (insulin shifts K⁺ into cells). Management ✔ Rotate injection sites to prevent lipodystrophy. ✔ Use CGM (Continuous Glucose Monitoring) to detect hypoglycemia early. 2. Metformin (First-line for Type 2 Diabetes) Common Side Effects GI upset (diarrhea, nausea, abdominal pain – 20-30% of users). Metallic taste. Serious Complications Lactic acidosis (rare but life-threatening; risk factors: renal impairment, liver disease, alcohol abuse). Vitamin B12 deficiency (long-term use). Management ✔ Start low dose & titrate up to reduce GI effects. ✔ Monitor renal function (eGFR <30 → contraindicated). ✔ Check B12 levels annually. 3. SGLT2 Inhibitors (e.g., Empagliflozin, Dapagliflozin) Common Side Effects Genital mycotic infections (yeast infections – 10-15% of users). UTIs (increased risk). Polyuria & dehydration. Serious Complications Euglycemic DKA (rare but dangerous – normal glucose with ketosis). Fournier’s gangrene (necrotizing fasciitis of perineum – FDA warning). Increased risk of amputations (canagliflozin – mainly in high-risk patients). Volume depletion & hypotension. Management ✔ Hydrate well to prevent UTIs/dehydration. ✔ Monitor ketones if symptoms of DKA (nausea, fatigue). ✔ Avoid in recurrent genital infections. 4. GLP-1 Receptor Agonists (e.g., Liraglutide, Semaglutide) Common Side Effects GI effects (nausea, vomiting, diarrhea – up to 50% early on). Weight loss (desired effect but can be excessive). Injection-site reactions. Serious Complications Pancreatitis (rare but FDA warning). Thyroid C-cell tumors (seen in rodents; contraindicated in personal/family history of medullary thyroid cancer). Gallbladder disease (increased risk of cholelithiasis). Management ✔ Start low & escalate slowly to reduce nausea. ✔ Discontinue if severe abdominal pain (pancreatitis risk).

Answer 73

5. Sulfonylureas (e.g., Glimepiride, Gliclazide) Common Side Effects Hypoglycemia (higher risk than other oral agents). Weight gain. Serious Complications Severe hypoglycemia (elderly at highest risk). Cardiovascular concerns (some studies suggest increased CV risk). Management ✔ Avoid in elderly & renal impairment (higher hypoglycemia risk). ✔ Prefer short-acting sulfonylureas (gliclazide) over long-acting (glibenclamide). 6. Thiazolidinediones (TZDs, e.g., Pioglitazone) Common Side Effects Weight gain & fluid retention (worsens heart failure). Edema. Serious Complications Fractures (increased risk in women). Bladder cancer risk (pioglitazone – controversial). Heart failure exacerbation. Management ✔ Avoid in NYHA Class III/IV heart failure. ✔ Monitor for bone density loss in long-term use. 7. DPP-4 Inhibitors (e.g., Sitagliptin, Saxagliptin) Common Side Effects Generally well tolerated (minimal hypoglycemia risk). Nasopharyngitis, headache. Serious Complications Acute pancreatitis (rare). Heart failure exacerbation (saxagliptin – FDA warning). Management ✔ Discontinue if pancreatitis suspected. 8. Meglitinides (e.g., Repaglinide, Nateglinide) Common Side Effects Hypoglycemia (less than sulfonylureas but still a risk). Weight gain. Management ✔ Take before meals (short-acting, flexible dosing). Summary Table: Key Risks by Drug Class Drug Class Most Common Side Effects Serious Complications Insulin Hypoglycemia, weight gain Severe hypoglycemia, lipodystrophy Metformin GI upset Lactic acidosis, B12 deficiency SGLT2i Yeast infections, UTIs Euglycemic DKA, amputations GLP-1 RA Nausea, vomiting Pancreatitis, thyroid tumors Sulfonylureas Hypoglycemia, weight gain Severe hypoglycemia TZDs Edema, weight gain Heart failure, fractures DPP-4i Mild, well-tolerated Pancreatitis (rare) General Recommendations ✅ Individualize therapy (consider comorbidities like CKD, heart failure). ✅ Monitor for side effects (e.g., hypoglycemia, infections). ✅ Educate patients on recognizing complications (e.g., DKA symptoms with SGLT2i).

Answer 74

Gardner’s syndrome is a variant of Familial Adenomatous Polyposis (FAP), an autosomal dominant condition caused by mutations in the APC (Adenomatous Polyposis Coli) gene. It is characterized by colorectal polyps, osteomas, and soft tissue tumors. Key Features 1. Clinical Manifestations A. Gastrointestinal (GI) Polyps Hundreds to thousands of adenomatous polyps in the colon and rectum. Nearly 100% risk of colorectal cancer by age 40 if untreated. May also involve duodenal/ampullary polyps (risk of periampullary cancer). B. Extra-Colonic Tumors & Abnormalities Osteomas (benign bone growths, commonly in the skull, mandible, and long bones). Desmoid tumors (aggressive fibromatosis, often in the abdomen). Dental abnormalities (supernumerary teeth, odontomas). Epidermoid cysts (skin cysts, often on the face and scalp). Congenital Hypertrophy of the Retinal Pigment Epithelium (CHRPE) (seen on eye exam). 2. Genetics & Inheritance Autosomal dominant (mutation in APC gene on chromosome 5q21). De novo mutations occur in ~25% of cases (no family history). Genetic testing confirms diagnosis in at-risk individuals. 3. Diagnosis Clinical criteria: ≥100 colorectal adenomas + osteomas/desmoid tumors/other FAP features. Imaging: Colonoscopy (gold standard for polyp detection). CT/MRI for desmoid tumors & osteomas. Upper endoscopy (for duodenal polyps). Genetic testing (APC gene mutation). 4. Management A. Cancer Prevention Prophylactic colectomy (usually recommended in late teens/early 20s due to near-certain cancer risk). Options: Total colectomy with ileorectal anastomosis (IRA). Proctocolectomy with ileal pouch-anal anastomosis (IPAA). Regular surveillance: Upper endoscopy every 1-3 years (for duodenal/ampullary polyps). Thyroid ultrasound (increased risk of thyroid cancer). B. Desmoid Tumor Treatment Surgery (if resectable, but high recurrence risk). Medical therapy: NSAIDs (sulindac) + anti-estrogens (tamoxifen). Chemotherapy (doxorubicin, dacarbazine) for aggressive cases. Tyrosine kinase inhibitors (sorafenib, pazopanib). C. Osteomas & Dental Management Surgical removal if symptomatic (e.g., facial deformity, pain). Regular dental exams for odontomas/supernumerary teeth. 5. Prognosis Without colectomy, nearly all patients develop colorectal cancer by age 40-50. Post-colectomy, survival improves, but duodenal cancer & desmoids remain leading causes of death. Differential Diagnosis Condition Key Differences Classic FAP No osteomas/desmoids Turcot Syndrome Brain tumors (medulloblastoma/GBM) Peutz-Jeghers Syndrome Hamartomatous (not adenomatous) polyps + mucocutaneous pigmentation Key Takeaways ✔ Gardner’s = FAP + osteomas/desmoids/soft tissue tumors. ✔ APC gene mutation → 100% colorectal cancer risk without colectomy. ✔ Lifelong surveillance needed (colon, duodenum, thyroid). ✔ Desmoid tumors are a major cause of morbidity/mortality.

Answer 75

Psychogenic polydipsia is a condition characterized by excessive water intake (often >5–10 L/day) due to psychological factors, leading to hyponatremia and water intoxication. It is common in patients with psychiatric disorders, particularly schizophrenia. Drug side effects: Antipsychotics (e.g., clozapine, risperidone) → dry mouth → increased thirst. SSRIs (rarely). Habitual behavior (e.g., compulsive water drinking in health fads). 2. Pathophysiology Excessive water intake → dilutional hyponatremia (Na⁺ <135 mmol/L). Kidneys cannot excrete free water fast enough → water intoxication. Unlike SIADH, urine is dilute (low urine osmolality). ✔ Common in schizophrenia patients (up to 20% prevalence). ✔ Diagnosis: Dilute urine + low Na⁺ (vs. SIADH, which has concentrated urine). ✔ Treatment: Fluid restriction + psychiatric care (adjust meds if needed). ✔ Emergency: Hypertonic saline for severe hyponatremia.

Endocrine Flashcards

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