Uworld Step 3 Synopsis

PREPARED BY SANTOSH DHUNGANA UWORLD SYNOPSIS FIRST: step 3 usmleworld.com Cardiology 1. Decreasing LDL is more imp to prevent CAD than stopping smoking, DM control, HTN control or exercise. DM is the second most important. 2. Pt with CHF on amiodarone comes with desaturation and basal cracklesprobably chronic interstitial pneumonitis, or organizing pneumonia due to amiodarone. It’s a cumulative dose effect, and not dependent on blood levels. Other adrs are liver, lungs, thyroid, BM toxicity and skin changes including Photosensitivity. Steroids can be used for severe pul disease. 3. Young patient with sec HTN, most common finding is abdominal bruit( 50%). Tachycardia if pheochromocytoma, but is less common. 4. In a patient with HTN, in absence of any known CAD, baby aspirin is useless. 5. All pts with stable angina should undergo stress EKG for risk stratification. High risk patients, ie those with failure to inc BP with exercise, inability to complete stage I of Bruce protocol,, or appearance of downsloping or horizontal ST segment during exercise >1mm, should undergo cor angiography, and thallium scan to see viable salvageable myocardium before PTCA or CABG. 6. Pt on warfarin is started on amiodarone- dec the warfarin dose by 25% 7. In a pt with h/o angioedema with ACEI, ARB are not the choice drugs- B blockers are, because ARB still have low risk of causing angioedema. Especially if the pt has no compelling indication to use ACEI, like Diabetic Nephropathy. 8. Stress Echo is always more sensitive than stress ECG, and can show wall motion abnormalities, but stress ECG is still the first choice for risk stratification in pts with stable angina. In patients who cannot exercise, eg due to OA, use dopamine stress EKG or Echo. Probably can use adenosine and dipyridamole stress EKG/Echo too. 9. Adenosine thallium/sestamibi scan, Dipyridamole thallium perfusion/viability scan both are c/I if the pt has COPD or asthma. These are used to see hypoperfused myocardium during stress. 10. Pharmacological stress testing (and probably radionuclide scan) are done in those who cant exercise eg due to OA or MI or unstable angina, and in those with abnormal baseline ECGs like LBBB, LVH, baseline ST changes, WPW, externally paced heart, etc. 11. Aortic sclerosis and ESM are normal finding in old patients. 12. Pt with CHF is given ACEI even in asymptomatic stage, ie if Echo shows low EF; B blockers and diuretics are added only if symptomatic. Isosorbide Dinitrate if evidence of pul edema. Low sodium diet and diuretics if pt has some fluid retention. 13. Orthostatic hypotension means fall of 20 mm in systolic and 10 mm in diastolic 14. Verapamil, quinidine, amiodarone and spironolactone can cause digoxin toxicity, so for eg a pt on digoxin comes with nausea, vomiting, confusion after starting verapamil.

15. In a pt with high LDL and TG, the first step is always targeting LDL with statin, then add fibrates if statin doesn’t decrease the TG. Cholestyramine can increase TG so is contraindicated. 16. Post CABG angina, with permanent ECG changes- do radionuclide perfusion imaging and not stress EKG or even stress Echo, as we cant interpret the Echo with previous wall motion abnormality due to previous MI or ischemic cardiomyopathy. 17. Inc fibrinogen >2.7 7 puts patient at high risk of MI; and lovastatin and atorva both increase fibrinogen. So if the patient has elevated levels of fibrinogen, change to either prava or simvastatin, as they have no effect on fibrinogen. 18. Wt loss is the single most imp measure to dec BP, more than stopping smoking, or dec salt or alcohol consumption or exercise 19. Preop cardiovascular risk assessment; age above 70 yrs 5 points, MI6 mo 5 points; angina on walking 1-2 blocks 10 points, angina at rest 20 points, and critical aortic stenosis 20 points 20. Drug lupus with hydralazine, mdopa, CPZ, IFN a, diltiazem, minocycline, penicillamine, procainamide, INH- starts with flu like symptoms, fever, malaise, arthralgia and facial rash. 21. Asymptomatic hypoNa in CHF patients- water restriction is the TOC, even if NA 1mm in 2 contiguous leads, after nitroglycerine is given to rule out coronary spasm. Also in pts with new LBBB. No benefit in NSTEMI. C/I with BP>180, recent surgery or ischemic stroke. ST depression occurs with ischemia, strain, digitalis, hypokalemia and hypomagnesemia, so is not an indication, unless it is due to posterior MI. 40. Poor R wave progression- if the R remains same through V1 to V4. Seen in COPD, RVH, LVH, ant infarction, blocks and cardiomyopathy. 41. Prolonged QT means more than half of RR, seen in antiarrythmic

drugs, TCA, hypokalemia, seizure and stroke. 42. Metformin should be stopped before coronary angio or other dye related procedures that can harm kidney and cause lactic acidosis. Also in renal or hepatic failure, CCf, sepsis and alcoholics. 43. Aspirin should be stopped 7 d before most procedures, but needn’t be stopped for coronary angio or cath. 44. TCA overdose is treated with sod bicarb. Lidocaine is the DOC for any vent arythmia that occurs. Procainamide, disopyramide and quinidine are membrane stabilizer, hence increase TCA toxicity re. Also ppnl is contraindicated, as it dec conduction and inc arythmogenic potential of TCA re. 45. Pt can resume sexual activity 6 weeks after uncomplicated MI- ie if he recovers without any post MI chest pain, CCF or arythmia. 46. Severe symptomatic AS (area 10. 3. Immobility is a common cause of hypercalcemia, esp in adolescent and those with paget’s disease, who have high bone turnover, due to uncoupling of bone turnover, ie more resorption and less formation. Subsequent hypercalcemia will suppress PTH, and low PTH in turn suppresses D3 levels. Biphosphonates can be used in these patients to prevent this. 4. For every 1 g/dl decrease below 4 of serum albumin, add 0.8 mg to the total calcium level. 5. Paraproteinemia can increase the bound calcium, hence the total calcium in the serum. 6. Hypoglycemia with high C peptide can be both due to insulinoma and sulfonylurea overdose. History and context is imp. To differentiate, measure serum proinsulin levels. Also checking for sulfonylurea level in urine and plasma can be helpful. 7. Autoimmune hypoglycemia due to insulin antibodies which bind to insulin receptors, or release excess insulin into circulation 8. Diabetic for planned CS section- don’t stop regular dose of insulin night before, to prevent ketoacidosis, even if she is npo. Then start insulin infusion during the surgery, with D5,1/2NS and KCL. Insulin requirement will drop following delivery of the placenta. Switch to scheduled sc dosage as soon as the patient starts tolerating food. 9. DKA management- continue NS and insulin till blood glucose is 250, then change to DNS with KCL, and decrease the insulin infusion dose. Dextrose infusion is very imp to decrease ketone levels. Start KCL regardless of serum level. Switch to oral feed and sc insulin only after the anion gap has corrected, HCO3>10m and precipitating factor like infection is corrected. But always start sc insulin 1 hr before discontinuing iv insulin, as sc insulin needs time to act, so otherwise it might precipitate DKA again if we don’t overlap the insulin. 10. Pt with hyperthyroidism with chief complaints of palpitationtreatment is ppnl and not PTU 11. Preop patient for emergency surgery like CABG for unstable angina is found to have hypothyroidism- its not a contraindication for surgery, tho there is higher risk of ileus, hyponatremia and oversedation with narcotic. Only after the surgery, start with low dose T4 as the patient has CAD. 12. DM pt on metformin develops anion gap acidosis, and there is no leukocytosis or hyperamylasemia- implies its probably lactic acidosis and not DKA- so do ABG and blood lactate level, instead of ketone level and urinalysis, or

instead of starting DKA treatment. 13. In patients with thyroid cancer in remission, T4 supplementation should be used to suppress TSH below normal range (ie between 0.1-0.3). If distant mets, even lower, to undetectable levels, tho that increases the risk of AF and bone loss. T3 is only used short term and never used for long term management of hypothyroidism. Hormone supplement should be taken on empty stomach. 14. Mental state change in elderly- always do TFT for diagnosing apathetic hyperthyroidism. 15. A pt on prednisone for RA develops infection and then hypotension- acute adrenal insufficiency. Administer fluid and dexamet, as it is long acting and doesn’t interfere with measurement of serum cortisols. Then do cosyntropin test. Mineralocorticoids aren’t used, because, one- they are not deficient, two- they take a longer time then just simply infusing saline. 16. Amiodarone- monitor patient’s TFT 6mthly; if it causes hypothyroid, no need to stop amiodarone. Just give larger dose of T4, as amiodarone prevents peripheral conversion of T4 into T3. But check TSH first. If hyperthyroid, it can be either due to induction of Graves disease, which is treated with PTU or methimazole, or it is due to induction of destructive thryoiditis, in which case the treatment is steroids. 17. Female on HRT for hot flashes develops DVT- should stop HRT, then give warfarin for 3 mo as this DVT has a precipitating cause and is the first episode. DVT without precipitating cause, or subsequent episode should get warfarin for 6 months. Increasing anticoagulation for continuing HRT is not justified, neither does tamoxifen help with postmenopausal symptoms. 18. Urinary metanephrines and catecholamines are better test then VMA for pheochromocytoma. Alpha blockade should be started only after the test, as it can falsely increase the level of the CA. Only after biochemical confirmation we do CT/MRI to confirm location. Both have equal sensitivity, but MRI is useful for extraadrenal foci, and also to differentiate benign from malignant ones. MIBG scan can be used if either of the above three tests are equivocal and we still suspect pheo, or one test shows pheo but the other doesn’t. Treatment is with alpha blockade, only then start beta blockade. Long acting phenoxybenzamine is used before surgery, along with liberal salt and fluid intake to increase the intravascular volume. The common complication after surgery is hypotension- use normal saline bolus and infusion. Dopamine doesn’t help as the alpha blockade will blunt the response to vasoconstrictors. 19. Pt with Hashimoto develops rapidly enlarging thyroid and SVCO- probably thyroid lymphoma. Treatment is RT. 20. Long acting sulfonylurea induced hypoglycemia- treat with D50 bolus, then D5 infusion is required to prevent rebound hypo due to the D50 induced insulin release. If refractory to this treatment, start octreotide sc. Somatostatin is iv and is short lived so not used. Giving D10 or D50 infusion for long time is not recommended as they can cause thrombophlebitis. Glucagon is also not recommended as it is short acting, plus increases insulin release causing reboud hypo. Glucagon is hence only used in acute mgmt of hypo with mental

obtundation, and the patient is given readily absorbed carbo after gaining consciousness. 21. Pt on amiodarone can have inc T4 and low T3 due to decrease in conversion from T4 to T3. Ppnl also does that, but not atenolol. Aspirin displaces T4 from albumin, so don’t use it as an antipyretic in the treatment of thryotoxic storm. 22. AF due to Grave disease is treated like any other AF- with b blockers and anticoagulation. So antithyroid drug or RI ablation is not the answer. 23. Effect of tight glycemic control on microvascular complications is proved, but not macrovascular. It reduces the incidence of neuropathy, but there are conflicting evidence for reversing previous neuropathy. 24. Fahr syndrome: pseudohypoparathyroidism, with Albright hereditary osteodystrophy (short stature, round facies, short metacarpals and short neck); they have hypocalcemia with hyperphosphatemia, latter causing basal ganglia calcification and cataract. Their PTH is also elevated. Patients with hypopara will have low ca, high phosphorus and also low PTH. Vit D deficiency causes low ca and phosphorus both, and inc PTH. Acute hyperphosphatemia like with rhabdomyolysis, seizures, ARF can cause decrease in calcium, but no basal ganglia calcification and cataract like in chronic hyperphosphatemia. 25. Hypercalcemia due to sarcoidosis- , due to 1a hydroxylase enzyme, vit D increases, PTH is suppressed, hence urinary calcium is increased. Treatment is glucocorticoid and not pamidronate. 26. Exercise increases non insulin mediated glucose uptake by muscles, so can cause hypoglycemia in a patient on insulin. Avoid insulin injection to the exercising limb, and lower the dose of insulin. 27. Medullary Ca thyroid, post surgery rise in calcitonin level indicates residual metastatic disease- first step is HRCT of neck and chest with HRUSG of neck, with surgical resection if possible. If these don’t show any lesion, HRCT abdomen and bone scan, or iodine 111-octreotide scan and PET may be required. Total body iodine scan is for follicular and not medullary cancer, as the parafollicular cells don’t take iodine. Thallium scintiscan is also nonspecific. 28. Don’t take thyroxin with calcium or iron over the counter supplements. 29. Pt with amenorrhea, low FSH and LH with high alpha subunit, high prolactin and a pituitary mass- probably has gonadotroph adenoma, with lack of functioning beta subunit. Increase in prolactin is probably due to compression effect. Treatment is surgery as bromocriptine works only with GH or prolactin secreting tumor. RT is never the first choice due to delayed risk of hypopituitarism. Octreotide is also not much effective. 30. Pituitary incidentaloma with no symptoms shouldn’t be treated, only followed up with regular MRI. 31. To diagnose spurious hyperthryroidism due to external intake and to differentiate it from primary thyrotoxicosis, do the thyroglobulin level. It is decreased in external thyrotoxicosis. RAIU study doesn’t help, as the intake is decreased also in different thyroiditis, iodine or amiodarone induced thyrotoxicosis.

32. Subclinical hypothyroidism- treat if TPO AB present, as they have high rate of conversion to overt hypothyroidism. Also treat if symptomatic subclinical (ie inc TSH but normal T4). 33. HTN with hypokalemia- do aldosterone to renin ratio to differentiate hypo and hyperreninemic hyperaldosteronism. In Conn’s syndrome, the ratio is >30, with high aldosterone level also needed for diagnosis, as essential HTN can also suppress renin. Patients present with polyuria and polydipsia due to hypokalemia induced DI. If hyperreninemic, then do MR angio of renal arteries, with fibromuscular dysplasia giving a beaded appearance, and is the most common cause of RAS in young patients. Suppression of both renin and aldosterone in a pt with hypokal and HTN is probably due to apparent mineralocorticoid excess (AME), so obtain a serum cortisol level. 34. Pt with DM, NASH due to hyperTG, and obesity- TOC is metformin, as it causes wt loss,, and helpful in hyper TG and NASH. Glitazones are contraindicated as they cause wt gain, partly due to fluid retention, as well as they are hepatotoxic. 35. Subacute thyroiditis- thyrotoxicosis with painful thyroid enlargement. Tt is NSAID and beta blocker, and steroid rarely if severe. Since preformed thyroid hormones are the cause of the problem, antithyroid drugs and RI are not effective. Its not difficult to differentiate from bacterial suppurative thryoiditis, as in the latter case, people aren’t usually thyrotoxic as it involves the center of the gland, as well as USG will show multiple abscesses. 36. Hyperthyroidism in pregnancy- PTU is the TOC, as methimazole is teratogenic. If PTU doesn’t work, or cause neutropenia, surgery is indicated, else she can have thyroid storm during the stress of childbirth. 37. Asymptomatic thyroid nodules: first step is to, do TSH- if normal, and if 1cm need FNAC. If TSH is decreased, then RAIU study- if hot nodule, only observation. If symptomatic, then antithyroid drugs….. RAIU is seldom used in management of thyroid nodule, as most of cold nodules are benign, though most of malignant nodules are also cold. Since most of the nodules are benign, all nodules don’t need surgery, only FNAC is enough. Still, if we have done RAIU, then all cold nodules must be biopsied. IF the nodule is toxic or if there is carcinoma on FNAC, then the patient needs surgery. 38. CT of neck is less sensitive than USG for nodular thyroid diseases. 39. If pt has papillary cancer on FNAC, then he needs NTT- near total thyroidectomy, and then RI ablation therapy for residual tissue and mets, then RAIU study to see for remaining mets, then lifelong Thyroxine to suppress TSH. Also thyroglobulin can be followed up as a tumor marker. TSH should be suppressed below the normal range, tho this can risk AF and bone loss. Doing only subtotal thyroidectomy is ineffective, as it is difficult to ablate the remaining gland with RI, and we cant also use thyroglobulin as a marker when lot of thyroid tissue is still left in the body. 40. If medullary cancer, first test for RET to see for MENII syndrome, or do urine metanephrine/CA or abdominal CT to diagnose any

concomitant pheochromo. Then start the pt on alpha blockade for a few weeks before surgery then beta blockade only after alpha blockade (else there will be vasomotor crisis), then do surgery- total thyroidectomy with central neck dissection. 41. DM with autonomic dysfunction, gastroparesis- its difficult to adjust insulin because due to delayed gastric emptying, pt will be hypoglycemic just after meal. Plus problems of postprandial bloating and constipation. Treatment is metoclopramide, or cisapride or erythromycin, and small frequent, low fat meals. Cisapride is especially shown to be beneficial, tho it is not freely available due to incidence of QT prolongation and Torsades. Last resort is feeding jejunostomy. Metoclopramide cant be used for long due to side effects and tachyphylaxis, so cisapride is the TOC re. High fiber diet will increase the constipation. 42. Octreotide can be given in intractable diarrhea in DM gastroparesis patient. 43. DM neuropathy- amitryptiline is the DOC, but since most patients have heart disease also, beware- use gabapentin instead. 44. Erectile dysfunction with normal morning erection- its psychological impotence. Erectile dysfunction is never a normal part of aging, so don’t tick that. 45. Pt of hypoparathyroidism- Tt is high dose of vit D( calciferol) and calcium; high dose because conversion to calcipotriol is defective. We don’t use calcipotriol as it is expensive. Calcipotriol has a rapid OOA, and can be used in hypercalcemic crisis, or if pt is refractory to calciferol. Pts thus treated with vit D and Ca for hypoPTH usually develop high urinary excretion of Ca, due to lack of PTH, which can lead to nephrocalcinosis. So adding THIAZIDE not only helps reduce urinary calcium, but also increases the serum calcium effectively. 46. Hypercalcemia with high PTH- can be either primary hyperPTH, lithium toxicity or familial hypocalciuric hypocalcemia. If hyperPTH, surgery is indicated if Bone mineral density is less than 2.5 SD (ie T score below -2.5), overt bone disease or fracture, kidney stone, reduced creatinine clearance, Ca level more than normal by 1, urinary calcium >400 mg/d, or if young than 50 years. For eg a postmenopausal woman with T score of -3 comes with hypercalcemia and high PTH, then she probably needs surgery. Alendronate is not as effective as surgery in preserving the BMD. 47. Those with hyperPTH who don’t need surgery are managed with periodic msmt of ca, Cr, and BMD. Pt can continue their vit D and Ca supplement, as research hasn’t shown any aggravation on calcium level with those. 48. Acromegaly: COD is cardiac- LV dysfunction, asymmetric septal hypertrophy, CAD, HTN and myocardial fibrosis; these changes may be reversible with treatment. Also increased risk of colon cancer. 49. Offspring of mother with DM I has 3% risk, if father then 6% risk of having

DM I. 50. A patient with unknown goiter undergoes cardiac cath, then develops thyrotoxicosis- its iodine induced thyrotoxicosis. Treatment is b blocker, or Antithyroid drugs or KCLO4, but RAIU doesn’t help, as the iodine uptake is reduced in the gland. 51. Pt with inc TSH following say, pneumonia, with normal T4 but dec T3, its not subclinical hypothyroidism, its EUTHYROID SICK SYNDROME (low T3 syndrome). Just followup with TFT in a few weeks. No treatment needed, and no investigations for antibodies too. 52. T score in DEXA is calculated in comparison to healthy adult of age 25, while Z score is calculated in comparison with similar aged adults. WHO classifies T between -1 to -2.5 as osteopenia, and below that as osteoporosis. In a pt with osteoporosis, do CBC/Ca and PO4 levels for secondary causes; can do urinary calcium, SPEP, PTH, TSH, N telopeptide for bone resorption and AlP for bone formation. Pts with T score< -2, with low wt, smoking patient, or with fragility factures irrespective of T score, need antiresorptive therapy with alendronate or risedronate, in addition to vit D and Ca. Etidronate is old and not used, Pamidronate iv is used if pt cannot tolerate oral alendronate due to esophagitis. Calcitonin is not very effective, teriparatide (PTH) is very effective but needs daily injection and is expensive. HRT has fallen out of favor since 2002 due to report of inc MI, DVT, Stroke, and breast cancer. Pt who doesn’t respond with biphosphonates, has constitutional symptoms and pallor should be strongly suspected to have myeloma. Myeloma cells release OAF( osteoclast activating factor). 53. Medical therapy is the TOC in prolactinoma even if large and has effect on vision. 54. Pt with Addison’s disease develops diabetes I- its autoimmune polyglandular failure type II (Schmidt’s syndrome), which also has Graves, pernicious anemia, premature ovarian failure, vitiligo and celiac disease. 55. Postpartum patient on heparin for DVT comes with osteoporosis – discontinuing breastfeeding can help re, increasing dose of vit D and Ca isnot as much helpful. 56.

Old male comes with hip pain- XR shows thick outer cortex with sclerosis, and Tm scan shows increased uptake- its Paget’s disease. Biphosphonates are indicated if intolerable pain, involve wt bearing bones, hypercalcemia, or CCF. Calcitonin and steroids are not useful. HAEM/ONC 1. Pt of NHL comes with epidural spinal cord compression( radicular pain)- give high dose steroid, obtain an MRI to confirm diagnosis, then start RT. If only back pain due to vertebral mets, only RT. If saddle anesthesia or bowel bladder involvement, immediate decompressive surgery. 2. Patient comes with metastatic ER/PR + cancer with occult primary in breast- no need for multiple core biopsy of breast or RM- only do chemo and hormonal therapy. Tamoxifen is preferred, with fulvestrant in those not responding to tamoxifen. Trastuzumab (HERceptin) in Her + ones. 3. Pt with AML gets multiple platelet transfusion, still the platelet count doesn’t increase- its called platelet refractoriness, due to alloimmunisation (formation of anti-platelet antibodies). If initial increase in platelet and then decrease within 24 hrs, think DIC or sepsis or active bleeding or antiplatelet drugs. 4. Pt with lung tumor with FEV1 and contribution of each lung giventhe best next thing to do is still to do CT staging. PET/ bone scan can be used too. CT is best as it gives mediastinal and chest wall invasion, mets to adrenal and liver, and can also help in CT guided biopsy. 5. SVCO: dyspnea, persistent cough, hoarseness, dysphagia, syncope, chest and neck pain, cyanosis, collateral veins in thorax, ocular proptosis, lingual edema- best thing is CT with contrast. MRI only if dye cant be used. 6. If imatinib is not in the choices, then BMT is the TOC for CML, aka HCT( hematopoietic cell transplantation.) IFNa will lead to cytogenetic and not molecular remission. CPS is used to prepare for BMT to prevent GVHD. 7. HIT usually presents as thrombosis- very tricky- type I is less severe and occurs early, type II more severe and occurs after 4-10 days, due to heparin-platelet factor 4 complex antibody, decreases platelet upto 30,000, can lead to limb gangrene, mesenteric ischemia, cerebral sinus thrombosis. Prevention of HIT is by using LMWH or danaparoid, or using heparin for less than 5 days; while treatment is using DTI like lepirudin or argatroban. LMWH are not the treatment of HIT, as they can also rarely cross react with the antibodies and increase the problem. 8. Prostate cancer post treatment- f/u with PSA. If rising PSA or if skeletal complaints, do bone scan. 9. Pts on tamoxifen should be screened for endometrial hyperplasia with annual Pap and detailed history. TVS has a lot of false +ve leading to unnecessary endom biopsy, so not recommended. 10. Plt transfusion are useless in ITP, as they will also be rapidly destroyed. Only use in life threatening emergencies as intracerebral and massive GI hemorrhage. Steroid are the TOC in most cases, with IVIG in

severe cases ( IVIG is not the first answer). Plasmapheresis is for HUS and TTP. 11. Alcohol and colon cancer are strongly linked than remote smoking history, so beware if the pt is smoking currently. NSAID and hormone replacement are protective. Alcohol probably causes the risk by interfering with folate absorption. 12. Among inherited thrombophilia, factor V leiden is the most common, don’t tick antiphospholipid syndrome, that is not inherited. Methyl tetrahydrofolate reductase gene mutation is related to homocystinemia, and is another risk factor. Any patient with inherited thrombophilia and spontaneous thrombosis should be on lifelong warfarin. Also those with life threatening VTE like massive PE, or unusual site like mesenteric or cerebral venous thrombosis should also be on lifelong warfarin. 13. Primary vs secondary polycythemia- WBC and platelet count will also increase in the former. If secondary cause is suspected, eg in a pt with COPD, first test is pulse oximetry after minimal exertion, and sleep study to determine nocturnal desaturation. 14. Pt with RA has pneumonia and found to have anemia- ferritin is high ( can be due to both infection or due to ACD), transferring and TIBC are low (can be due to both IDA and ACD). In these patients, do BM biopsy to differentiate ACD and IDA. 15. Pts requiring frequent transfusion might develop antibodies to RH, Kelly and other antigens, causing acute transfusion reaction. Rx is hydration, stopping transfusion. Dopamine and osmotic diuresis can be used. 16. Of all the features of Pancoast syndrome, chest movement asymmetry with asymmetric lower leg DTR is the most dangerous, as it signifies phrenic nv involvement with possible iv foramina invasion and imminent cord compression. 17. Pt of CRF comes with esophagitis and massive bleedingDesmopressin is the TOC as it releases VIII/VWF from the endothelium, after that dialysis. Cryoppt can be used but associated with infections. Estrogen can be used too. 18. Pt with prostate cancer comes with back pain due to mets- TOC is hormonal therapy- LHRH analogue with flutamide to counter the initial flare, if back pain is unresponsive to this, then EBRT followed by chemotherapy. Radionuclide bone scan is the most effective diagnostic modality. DES reduces LHRH release from the hypothalamus too, but increases MI, PE and stroke. 19. SCC skin- surgery first line, RT if pt refuses surgery, and 5FU is the third line treatment. 20. Pancoast: RT with surgical resection is the TOC, but if there is evidence of distant mets, or brachial plexus involvement, or positive bone scan, then RT alone. 21. AIDS with PCNSL- best therapy is HAART itself, tho RT and corticosteroid help, they don’t increase life expectancy. The most important prognostic factor is the increase in CD4 count. 22. CholangioCa, even if Klatskin- if with mets, is inoperable, so the

treatment is ERCP and stenting for the pruritus and jaundice. PTC only if ERCP fails. Ursodeoxycholic acid doesn’t help as it doesn’t relieve the obstruction. 23. Pt comes with diarrhea, sclerotic bone lesions, eosinophilia and peptic ulcer- Systemic mastocytosis. 24. Lobular CIS of breast- it is multicentric and bilateral, so the best treatment is close observation, annual mammogram and tamoxifen which has shown dec risk of progression to overt carcinoma. Surgery, If at all, has to be bilateral prophylactic mastectomy. Local excision is useless. 25. Pt with ACD- low iron, high ferritin, normal or low transferring and transferrin saturation. BM is diagnostic, and shows normal or increased iron in macrophages, and decreased no of sideroblasts. Do EPO level, if it is low, EPO is the treatment. If EPO is already high, then periodic blood transfusion is the treatment. Plus treatment of the underlying disease with close f/u might be the right answer. 26. Pt with ESRD and ACD, doesn’t respond to EPO- first thing is to do iron study to rule out iron deficiency. Then see for folate deficiency, systemic inflammation and Al toxicity. Avoid BT in them, as that can risk causing allogenic graft rejection after kidney transplant. 27. Advanced gallbladder Ca with neuropathic pain in right thigh- for sharp pain, DOC is carbamazepine, second line being valproate or gabapentin. For dull pain, desipramine is the DOC. Not narcotics. 28. Pt treated for SCLC comes with features of acoustic neuroma, its probably not neuroma but mets. Contrast MRI showing the multiple well circumscribed mass with local edema is the investigation of choice. 29. A pt with normocytic anemia- first thing to do is retic count- if high, its hemolysis, if low its hypoproliferative Electrophoresis and Coombs for earlier, BM for the latter. 30. Myaesthenic syndrome means Lambert Eaton- treatment is plasmapheresis and immunosuppressive therapy. Electrophysiological studies confirm incremental response with repetitive stimulation. DTR are lost unlike in myasthenia gravis or polymyositis re. 31. Breast cancer metastasis to brain- stereotactic surgery if single, EBRT if multiple. Chemo don’t penetrate, steroid help, and prophylactic anticonvulsant are not indicated. 32. Sickling crisis- during mens, alcohol, nocturnal hypoxemia- mainstay of treatment is hydration. Morphine or iv ketorolac for pain. 33. Sickling crisis with splenomegaly- beware of splenic sequestrationdramatic fall in hemoglobin causing hypovolemic shock. So CBC should be monitored in these pts. CXR, blood and urine culture are followed by iv antibiotics esp if the pt wasn’t on prophylactic penicillin. Avoid contact sports. GASTRO 1. If polyps are found in sigmoidoscopy, next thing to do is colonoscopy to see for synchronous lesions and remove them. Double contrast enema is inferior, plus doesn’t allow intervention also.

2. TPN: average need is 30Kcal/d and protein 1g.kg.d, but in malnourished or critically ill patients, its 35-40 and 1.5 respectively. Overfeeding leads to hyperglycemia, hyperinsulinemia, inc TNF. PEG (percut gastrostomy) should be considered if pts need TPN for a long time. 3. LGIB: urgent colonoscopy is the procedure of choice due to diagnostic and therapeutic advantage. IF there is poor visualization due to bleeding, then do Tm tagged RBC scan, which is better than angio to localize the site. Vasopressin is inferior as bleeding recurs after stopping, and it can cause ischemic damage to organs and arythmia. Octreotide works only in variceal bleeding. Urgent colectomy might be needed, but only after localization of the site of bleeding. 4. Chronic pancreatitis: low fat diet is the most effective method to stop steatorrhea, while enzyme supplement is inferior. 5. Mallory Weiss tear that has stopped bleeding needs no intervention. Hiatal hernia is a very frequent predisposing factor for the tear, and can occur during blunt abd trauma, CPR and endoscopy too. 6. Mesentric angina- duplex USG is the screening test done first, as it has a high negative predictive value. Angiography is the gold standard, but is done only after duplex. 7. Mild pancreatitis- manage with pain control and iv fluid, npo, ng aspiration to prevent further pancreatic stimulation. Hypoechoic mass in pancreas doesn’t mean abscess unless there are systemic signs. Antibiotics have been shown to be useful prophylactically only in severe pancreatitis (Ranson criteria), or necrotizing pancreatitis or large peripancreatic fluid collection. Imipenem or cefuroxime penetrate pancreas well. No indication of daily CT scan or CT aspiration unless features suggestive of infected necrosis. Surgical debridement if severe necrosis, biliary pancreatitis, lack of response to therapy or complications. ERCP if concurrent dilatation of biliary system or elevated LFT. 8. If the patient with pancreatitis develops fever, then take blood culture and start imipenem, piperacillin, quinolones. IF pt fails to improve after 1 week of antibiotic therapy, a CT guided aspiration of the tissue for C/s is done. 9. Acute HepB needs only supportive treatment, as most resolve on their own. Only chronic active hepatitis needs lamivudine and adefovir. Conversion to chronic stage depends on age- 90% if perinatal, 20-50% if below 5 and 7, ie class B or C in child pugh classification. Class A is you can call this metabolic acidosis + respiratory alkalosis. eg : Salicylate Toxicity If Hc03 - is 16, the expected PCo2 as per Winter;s formula should range between 30 to 34 ( see the above formula). However, let us say your patients Pco2 on the arterial blood gas is 44 --> you can call this metabolic acidosis + respiratory acidosis. eg : Cardiac arrest NOTE, normal anion gap is 12, and normal bicarb is 24. Normal ph is 7.35 to 7.45 A. Identifying benign hematuria and its approach B. Correct interpretation of "Dipstick" Hematuria C. Evaluation of Asymptomatic Microscopic Hematuria in normal patient population vs. those at high risk for urological malignancy. D. Test of choice for symptomatic hematuria ( Urolithiasis, Cystitis etc) E. Evaluation of Asymptomatic Hematuria F. If upper tract imaging for Asymptomatic Hematuria is chosen, what is the initial test of choice? - Many get confused about the initial test for upper tract imaging becauses several sources state several different things. Students are stuck between the choices CT urogram vs. Traditional Intravenos Pyelogram. The guidelines have been updated recently and there is an increasing trend towards CT Urogram even in asymptomatic hematuria ( please check the explaination below). Here is a summary on how to approach Hematuria on your exam as well as in your office. All the recommendations are taken from AUA, American college of radiology guidelines on appropriate imaging choice. Hematuria: The following Q and A aaproach will help you understand the principal concepts of Hematuria. How do you test for Hematuria?

The initial office test that we use to detect hematuria is "Dipstick". Dipstick is highly sensitive but not specific. False negatives are very rare but false positives are common. Dipstick detects "BLOOD" but it does not say whether this "blood" is an RBC or a Pigment. Remember that pigments such as myoglobin ( as in rhabdomyolysis) or Hemoglobin ( as in hemoglobinuria, Black water fever) can stain as "Blood" on dipstick. So, please do not automatically assume that everything that stains as "blood" on a dipstick is an RBC. In order to know if there is true hematuria, the next step is to do urine microscopy. If the urine reveals RBCs then there is true hematuria. However, if the dipstick reads "blood" and if the urine did not reveal RBCs on microscopy then you are dealing with a pigment - either myoglobinuria ( rhabdomyolysis) or hemoglobinuria. At this point, if the CPK is also elevated it suggests that the etiology of blood on the dipstick is Rhabdomyolysis. So, a dipstick hematuria should always be confirmed with urine microscopy! If dipstick is negative for blood, it excludes abnormal hematuria ( false-negative results are unusual with dipstick testing). Benign causes of "Red" urine but negative dipstick test - In some conditions, you may see a red urine resembling "Gross hematuria" but dipstick is negative for blood. This should not be called hematuria. This is just reddish discoloration of urine. Occurs in : a) Ingestion of red pigmented foods ( eg: beets, berries, rhubarbs, paprika) b) Drugs like Rifampin or Phenazopyridine derivatives ( remember these drugs only cause reddish urine but NOT a positive dipstick). c) Diseases such as "Porphyria" Causes of a Positive Dipstick but no true Hematuria: Here Dipstick stains positive for blood but no RBCs in the urine a) Myoglobinuria ( Rhabdomyolysis, vigorous exercise) b) Hemoglobinuria ( Intravascular hemolysis) Is the Hematuria associated with pain? - Understand the causes of painless hematuria are different from painful hematuria. Painless hematuria is often from tumors of the urinary tract, bladder cancer or glomerulonephritis. Painful hematuria is often associated with urolithiasis ( renal calculi) or inflammation/ infection of the bladder ( Cystitis). What will be the approach to identify the source of Hematuria? - The work up for hematuria may involve invasive and expensive approaches. So, it is important to determine the nature of hematuria so that you can limit investigations to the real and pathological hematurias. Gross Hematuria: Reddish or Tea colored urine, dipstick positive for blood and urine microscopy shows RBCs. Any patient with gross hematuria should

always be referred for urological evaluation unless this is secondary to an infection. If a woman has gross hematuria but the urine dipstick also reveals leucoesterase or nitrite or if the woman has symptoms of UTI ( dysuria etc) or if the cultures are growing bacteria, this can be treated as UTI ( cystitis) with antibiotics with out referring for further evaluation. Even in this setting of infection, if there are risk factors for urological malignancy the patient should still be referred for further evaluation ( since hematuria from cancer can also be intermittent). Runner's hematuria or March hematuria is another benign condition that presents as gross hematuria after a severe physical activity. In such cases, patients may be observed for resolution however, if the hematuria is persistent or if the patient has any risk factors for having a urological malignancy, must be referred to a urologist Microscopic Hematuria: Grossly, urine looks normal. Dipstick positive for blood and urine microscopy reveals RBCs. Microscopic Hematuria is often intermittent and most causes are usually benign. So, it is important to define a significant microscopic hematuria that requires further investigations. Microhematuria is defined as three or more red blood cells per high-power microscopic field (RBCs/HPF) in two out of three properly collected and prepared specimens. Repeat urinalyses to establish whether significant hematuria is present must be done within 3 to 6 months of the initial test. Minimal microhematuria ( i.e; one or 2 rbcs per HPF ) in asymptomatic young adults does not require any evaluation. ( many studies have indicated that small amounts of blood may be released into the urine of persons with no detectable pathology in the urinary tracts) In patients with risk factors for having a urological malignancy, a microhematuria even in one or more samples must be considered significant and be evaluated. Some benign causes of Microhematuria : A) Exercise B) Sexual activity C) Menstruation D) UTI If UTI is present ( symptoms and dipstick for leucoesterase are clues that point towards infection) - treat it with antibiotics and repeat urinalysis after the infection has cleared. E) Benign Prostatic Hypertrophy F) Prostatitis

Now, carefully look for other charecterestics of urinalysis - Presence of other findings on the microscopic urinalysis such as RBC casts or Dysmorphic RBCs or proteinuria or the labs revealing elevated serum creatinine suggests a the hematuria is originating from the kidney/ glomerulus itself ( eg: Glomerulonephritis, IgA nephropathy). In such cases, the next step in evaluating hematuria is referral to a nephrologist ( not urologist) and a renal biopsy. Further Approach to Microscopic Hematuria Symptomatic Hematuria: In painful hematuria --> first rule out infection and renal colic. If infection is absent or if there is a pain similar to renal colic ( classic flank pain) - consider renal stones as the cause of Hematuria. The best initial step in evaluating the cause of painful hematuria that is not explained by UTI is Non-Contrast CT scan (Spiral CT) ( test of choice for imaging renal calculi). In pregnant women, ultrasound can be performed to avoid radiation exposure. Asymptomatic MicroHematuria : Patients without the classic flank pain of urolithiasis should be evaluated extensively. Once benign causes such as infection and the kidney ( glomerular) origin are ruled out, further approach should be defined based on the patient's risk profile. A) For patients with low risk of urological disease, a less extensive work-up may be appropriate ( First do upper tract imaging and if this is negative, add urine cytology+cystoscopy). B) If the patient is a high risk of having a urological malignancy, extensive work-up is needed ( see the risk factors below) --> Upper tract imaging + cystoscopy+ urine cytology all are needed. Urine cytology should be obtained in all patients with asymptomatic hematuria since it is an easy and non invasive step. Sensitivity of urine cytology is only 48% but remember that if it is positive it is highly specific for urological cancer ( 94% specificity) Risk factors for urological cancer ( bladder ca): 1. Heavy somkers 2. Occupational exposure to aniline dyes 3. History of Gross hematuria 4. History of pelvic irradiation 5. Age > 40 years 6. Analgesic abuse 7. Presence of irritative voiding symptoms 8. Previous use of Cyclophosphamide ( increases the risk of bladder cancer where as ongoing use often causes hemorrhagic cystitis as a adverse effect) What imaging studies should be done as initial step in evaluating

Asymptomatic Hematuria? For both high risk and low risk patients, upper tract imaging must be performed as an initial step. For upper tract imaging, CT urography ( i.e; non-contrast CT followed by contrast CT imaging from kidney to bladder) is best recommended initial test now to evaluate asymptomatic hematuria. CT urography is less affected by overlying bowel gas and is more sensitive for detecting small tumors and calculi than the IVP. Students often confuse this with other choices such as ultrasound and Intravenos pyelogram. IVP used to be the best preferred test for upper tract imaging in hematuria evaluation but now CT urogram is becoming the preferred method. IVP and ultrasound are good to image the urinary tract but they do not completely assess the renal parenchyma. If you order an IVP, you may eventually need to order a CT urogram again to image the parenchyma better - so, in order to avoid ordering multiple studies, CT urogram is recommended as the best initial test.