- Complement levels in glomerular diseases
Normal serum complement
PAN*, granulomatosis with polyangiitis (GPA), hypersensitivity vasculitis, Henoch-Schonlein purpura, Goodpasture’s syndrome, IgA or IgG nephropathy, anti-GBM disease
Low serum complement
Acute post-streptococcal glomerulonephritis and HUS (both show low C3 with normal C4), membranoproliferative glomerulonephritis, SABE**, cryoglobulinemia (low C4 with normal C3), SLE
*PAN polyarteritis nodosa
**SABE subacute bacterial endocarditis
- Drugs associated with glomerular diseases
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Conditions
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Associated drugs
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| Minimal change disease
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NSAIDS, interferons
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| Membranous glomerulonephritis
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NSAIDS, penicillamine, mercury
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| Focal segmental glomerulosclerosis
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Heroin, pamidronate
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| HUS
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Cyclosporine, tacrolimus, OC pills, mitomycin C
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Azotemia: Azotemia is characterized by elevated levels of nitrogenous compounds (such as creatinine and BUN) in the blood. It can be seen with prerenal, intrinsic renal, and postrenal causes, such as hypotension, obstructive uropathy, and glomerulonephritis.
Uremia: Uremia refers to elevation of blood urea levels. Azotemia can progress to uremia. Uremia is clinically symptomatic and may present with anorexia, nausea, vomiting, edema, and changes in the level of consciousness. It is seen in ESRD.
Indications for dialysis in AKI
- Refractory hyperkalemia
- Refractory volume overload, pulmonary edema
- Uremic pericarditis
- Uremic pleuritis
- Intractable acidosis
- Lithium or ethylene glycol poisoning
- Uremic encephalopathy
- Types of radiopaque and radiolucent stones
Radiopaque
- Calcium oxalate
- Calcium phosphate
- Calcium carbonate
- Struvite
Radiolucent
- Calcium phosphate and struvite stones form in alkaline urine. They may be seen after acetazolamide intake due to increased urine calcium and pH. Distal RTA is associated with calcium phosphate stones.
- Calcium oxalate, uric acid, and cystine stones form in acidic urine.
- Increased urinary calcium predisposes to calcium stones and may be seen with increased salt intake, low or high vitamin D levels, and increased dietary acid load (such as cheese, meats, dairy, etc.).
- Antibiotics can increase formation of calcium oxalate stones by increasing oxalate levels in the gut.
- Uric acid stones may be seen in metabolic syndrome, gout, diabetes, obesity, high-protein diet, myeloproliferative disorders, diarrhea, and probenecid.
Paraneoplastic syndrome associated with RCC
- Polycythemia from erythropoietin production
- Hypercalcemia from PTH production
- Hypertension from renin production
- Cushing’s syndrome from glucocorticoid production
- Feminization or masculinization from gonadotropin production
- Simple renal cysts: Simple renal cysts are fluid-filled cysts seen in one or both kidneys. They may be single or multiple. They are benign and do not interfere with renal function. They may range in size from a pea to a golf ball. They are common, especially after age 50 years.
Most simple cysts are found incidentally on imaging done for other reasons. Some cases may present with abdominal or back discomfort, urinary retention, UTI, fever, hypertension, and hematuria.
Asymptomatic cysts do not need treatment and are monitored with serial ultrasound. Symptomatic cysts can be drained by sclerotherapy with alcohol or removed surgically.
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Hydronephrosis is dilation of the renal pelvis and calyces due to urine buildup from obstruction to urine outflow. It may be unilateral or bilateral. Congenital PUJ (pelvi-ureteric junction) obstruction is the most common cause of hydronephrosis in the neonatal period.
Causes of hydronephrosis
Unilateral hydronephrosis
- Calculi in ureter or renal pelvis
- PUJ obstruction shows unilateral hydronephrosis without hydroureter
- Unilateral hydronephrosis with hydroureter may be seen in ureterovesical junction obstruction
- VUR
- Ureteral fibrosis
- Trauma to ureter
- Extrinsic ureteral obstruction from cancer cervix, colon, prostate, rectum, or cecum
- Retroperitoneal fibrosis
Bilateral hydronephrosis
- All causes of unilateral obstruction involving both sides at the same time
- Posterior urethral valves
- VUR
- Bladder neck stenosis
- Urethral stricture
- Cancer prostate
- BPH
Indications for retrograde urethrography and cystography in trauma patients
- Blood at the urethral meatus
- Gross hematuria after pelvic trauma
- High-riding or freely mobile prostate
- Pelvic hematoma
- Displaced fracture of the pubic rami
- Butterfly-pattern of perineal bruising, scrotal or penile hematoma
Criteria for the diagnosis of gestational diabetes*
Cut-off values following oral glucose tolerance test with 75 gm glucose
- Fasting >= 92 mg/dl
- 1 hour >= 180 mg/dl
- 2 hours >= 153 mg/dl
* Screening for GDM is done at 24-28 weeks of gestation.
- Hypoglycemia (insulin shock): Hypoglycemia is low blood glucose, typically < 70 mg/dl. Some people develop symptoms at blood glucose levels higher than 70 mg/dl, while others (especially diabetics) may be asymptomatic even at lower levels.
It may present with jitteriness, sweating, headache, tiredness, dizziness, pallor, confusion, irregular heart rate, and (in severe cases) seizures or loss of consciousness.
Most people recover with oral glucose tablets, sugar, candy, or fruit juice. Some cases may require glucagon.
Causes of hypoglycemia
- Insulin and antidiabetic medications
- Insulinoma
- Postprandial or reactive hypoglycemia, seen in gastric bypass due to excess insulin secretion
- Quinine, pentamidine
- Growth hormone deficiency
- Chronic liver and/or kidney disease
- Glycogen storage disorders
- Surreptitious use of insulin (C peptide will be low or undetectable, but insulin levels will be elevated), factitious disorder or Munchausen syndrome
- Differentials for common neck masses
Acute
- Sialadenitis: local edema, pain, erythema; seen in dehydration and following dental procedures
- Lymphadenopathy from CMV, EBV, toxoplasmosis, viral URTI, Bartonella henselae, HIV, tuberculosis (fixed, firm nodes); Staphylococcal and Streptococcal infections
- Hematoma: follows trauma; monitor if small, surgery if large or expanding
- Pseudoaneurysm or AV fistula: soft, pulsatile mass; thrill or bruit
Subacute
- Squamous cell carcinoma of upper GIT and upper respiratory tract (HPV, oral sex, smoking, alcoholism, betel nut chewers, non-healing ulcers)
- Amyloidosis
- Lymphoma (painless, enlarging node)
- Metastases (melanoma, lung, breast, colon, genitourinary cancers), matted, fixed nodes
- Parotid masses (slow growing, VII nerve involvement)
- Sjogren syndrome
- Sarcoidosis
- Chronic sialadenitis: pain after meals
Chronic
- Goitre: Grave’s disease, Hashimoto’s thyroiditis, iodine deficiency, lithium toxicity, toxic multinodular goitre
- Thyroid nodule: solitary benign nodules, thyroid cancer, toxic adenoma
- Thyroglossal duct cyst: in children, slow growing, more prominent after URTI, midline, close to hyoid bone, moves with swallowing, evaluate with CT, treat with antibiotics and excision (Sistrunk procedure)
- Branchial cleft cyst: in children, below angle of mandible, anterior to sternocleidomastoid; prominent after URTI, treat with antibiotics and excision
- Dermoid cyst: in children and young adults, submental triangle, soft, doughy mass, treat by excision
- Carotid body tumor: upper neck, pulsatile, hypertension, flushing, bruit or thrill
- Glomus jugulare tumors: similar to carotid body tumors
- Lipoma: soft, mobile, monitor or elective excision
- Laryngocele: midline, above thyroid cartilage, sensation of lump in throat; caused by repetitive blowing into a musical instrument, coughing
- Parathyroid masses: located in anterior cervical triangle, monitor PTH and serum calcium
- Euthyroid sick syndrome: Euthyroid sick syndrome refers to abnormal thyroid function tests in the absence of intrinsic thyroid disease. It shows increased reverse T3 and low T3; TSH and T4 are variable.
It is seen in gastrointestinal, pulmonary, renal, cardiovascular, and metabolic disorders, and in sepsis, burns, trauma, starvation, and malignancy. Thyroid function returns to normal after recovery from the underlying condition.
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Untreated hypothyroidism during pregnancy is associated with miscarriages, preterm delivery, fetal death, PPH, and mental retardation in newborns.
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Cretinism: Cretinism is untreated congenital hypothyroidism. Causes include thyroid gland dysgenesis, iodine-deficient diet (endemic cretinism), defects in thyroid hormone synthesis, and transplacental passage of maternal blocking antibodies in autoimmune thyroiditis.
It presents with delayed milestones, mental retardation, goitre, and failure to thrive. Treatment with oral thyroxine should be started immediately (within the first 15 days of life) to preserve neurological function.
- Amiodarone can cause type 1 thyrotoxicosis due to the drug’s high iodine content, or type 2 thyrotoxicosis due to thyroid gland damage with release of thyroid hormones.
Type 1 results in increased production and release of thyroid hormones, while type 2 causes increased release of preformed thyroid hormone. Drugs such as interferon alpha, lithium, and interleukin 2 also cause type 2 thyrotoxicosis.
Type 1 is treated with antithyroid drugs such as PTU and methimazole, along with potassium perchlorate (which inhibits iodine uptake by the sodium-iodide symporter, NIS). Type 2 is treated with glucocorticoids.
- Estrogen increases thyroid-binding globulin (TBG). As a result, in pregnancy and estrogen therapy, total T4 and T3 rise while TSH and free T4 remain normal. Because free hormone levels do not rise, this does not cause hyperthyroidism.
Androgens, cirrhosis, and protein malnutrition decrease TBG levels. The amount of TBG can be estimated by T3 resin uptake: the higher the resin uptake, the lower the TBG level (and vice versa).
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Dopamine and glucocorticoids decrease TSH, while total T4, total T3, and free T4 remain the same.
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Thyroid storm: Thyroid storm is a life-threatening event seen in patients with hyperthyroidism, typically after non-compliance with or discontinuation of antithyroid medications, combined with triggers such as infection, surgery, acute illness, trauma, or pregnancy.
It presents with hyperthermia, delirium, altered sensorium, seizures, coma, diarrhea, nausea, vomiting, jaundice, tachycardia, CCF, and atrial fibrillation.
Treatment is multi-pronged and includes PTU (preferred) or methimazole, inorganic iodine, cholestyramine, propranolol, intravenous hydrocortisone or dexamethasone, oral prednisone, paracetamol, and management of the precipitating illness. Plasmapheresis may help in severe cases. Diltiazem can be used as a substitute for beta blockers in patients with contraindications to beta blocker therapy (such as asthma).
Roles of drugs used to treat thyroid storm
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Drug
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Role
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| PTU and methimazole
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Block the synthesis of thyroid hormones; PTU also blocks the peripheral conversion of T4 to T3
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| Inorganic iodine, potassium iodide
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Decreases release of preformed T4 and T3; given 1 hour after antithyroid drugs, as iodine can increase hormone production
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| Beta blockers oral or iv (propranolol preferred)
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Control peripheral effects of thyroid hormones (such as tachycardia); decrease T4 to T3 conversion
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| Glucocorticoids
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Decrease the peripheral conversion of T4 to T3; manage accompanying adrenal insufficiency
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| Cholestyramine
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Decreases enterohepatic circulation of thyroid hormones, decreases serum levels, increases excretion in stool
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- Familial hypocalciuric hypercalcemia: It is an inherited, AD disorder caused by mutation in the calcium-sensing receptor, which makes the receptor insensitive to serum calcium levels. This interferes with feedback inhibition of PTH secretion, resulting in hyperparathyroidism.
Laboratory findings include hypercalcemia, and the calcium/creatinine ratio is < 0.01. Most patients are asymptomatic, but some may present with fatigue, weakness, excessive thirst, constipation, low concentration, chondrocalcinosis, and pancreatitis. No treatment is needed. Patients are at increased risk of MEN I.
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Causes of hypercalcemia with increased PTH include primary and tertiary hyperparathyroidism, lithium-induced hypercalcemia, and familial hypocalciuric hypercalcemia.
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Causes of hypercalcemia and hypocalcemia
Hypercalcemia
- Hyperparathyroidism
- Malignancy induced hypercalcemia
- Paraneoplastic syndromes due to excess PTHrP
- MEN 1
- Familial hypocalciuric hypercalcemia
- Sarcoidosis, tuberculosis
- AIDS
- Williams syndrome
- Drugs like thiazides, lithium, Vit D, A, aluminium toxicity, milkalklai syndrome, estrogens, theophylline
- Immobilization
Hypocalcemia
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Hypoparathyroidism
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Vit D deficiency or receptor defects
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Renal failure, chronic kidney disease
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Chronic liver disease
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Hungry bone syndrome
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Malnutrition
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Pseudohypothyroidism
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Hypomagnesemia and hypermagnesemia
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Massive blood transfusion with citrated blood
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Pancreatitis
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Hyperphosphatemia
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Osteomalacia
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Drugs like imatinib, bisphosphonates, calcitonin, denosumab
Malignancy-induced hypercalcemia is usually associated with a low PTH but possibly a high PTHrP.
- Autoimmune polyendocrinopathy syndrome: This is an autoimmune condition characterized by adrenal insufficiency, chronic mucocutaneous candidiasis, hypoparathyroidism, hypoplasia of the dental enamel and nail dystrophy, type 1 DM, Hashimoto’s thyroiditis or Grave’s disease, celiac disease, myasthenia gravis, atrophic gastritis, and pernicious anemia.