Post-void residual volume Determined by bladder scan Interpreted in context of clinical scenario & status of patient No absolute value

at which catheter must be inserted Many pts have long-standing urinary sx & incomplete emptying of bladder, leading to large capacity bladder over time; these pts w/chronic urinary retention may still present as acute urinary retention when they can no longer void Pt in discomfort who cant void w/any volume on bladder scan may need catheter Bladder scan can be inaccurate: body habitus, tissue edema, prior surgery & scarring If uncertain about dx of urinary retention, can place urethral catheter & vol of urine drained in 1st 10-15 mins noted & recorded o If vol > 400 cc, catheter is left in place o If vol 200-400 cc, decision to leave catheter in place is guided by clinical scenario o If vol < 200, catheter is removed

CKD Definition: either decreased kidney fn (GFR < 60) or kidney damage (structural or fnal abnormalities) for at least 3 months Causes: DM (MC), HTN, chronic GN, interstitial nephritis, PCKD, obstructive uropathy, causes of AKI if prolonged and/or if tx is delayed Pathophys o Plasma Cr varies inversely w/GFR o Cr clearance is MC clinical measure of GFR o Increase in plasma Cr disease progression o Decrease in plasma Cr recovery of renal fn More common in blacks than whites Clinical features o CV HTN: secondary to salt & water retention; decreased GFR stimulates RAAS & aldosterone secretion to increase increase in BP Renal failure is MCC of secondary HTN CHF: due to volume overload, HTN, anemia Pericarditis (uremic) o GI (usually due to uremia): N/V, loss of appetite (anorexia) o Neuro Sx: lethargy, somnolence, confusion, peripheral neuropathy, uremic seizures Signs: weakness, asterixis, hyperreflexia, restless legs (neuropathic pain in legs only relieved w/movement), hypocalcemia (lethargy, confusion, tetany) o Hematologic Normocytic normochromic anemia: secondary to EPO def

o Dx o o

Bleeding secondary to platelet dysfn (due to uremia): platelets do not degranulate in uremic environment Endocrine/metabolic Ca-PO4 disturbances: hypocalcemia, hyperphosphatemia Decreased renal clearance of phosphate hyperphosphatemia decreased renal production of 1,25-dihydroxy vitamin D hypocalcemia secondary hyperparathyroidism renal osteodystrophy weakening of bones & possibly fractures Hypercalcemia can be seen due to long-standing secondary hyperparathyroidism & Ca-based phosphate binders Hyperphosphatemia Ca & PO4 precipitates vascular calcifications that may result in necrotic skin lesions = calciphylaxis Sexual/reproductive sx: due to hypothalamic-pit disturbances & gonadal response to sex hormones (decreased testosterone in M; amenorrhea, infertility & hyperprolactinemia in F) Pruritus: multifactorial causes, common, hard to tx; dialysis & UV light Fluid & electrolyte problems Volume overload: watch for pulm edema Hyperkalemia: due to decreased urinary secretion Hypermagnesemia: secondary to reduced urinary loss Hyperphosphatemia: decreased renal clearance Metabolic acidosis: due to loss of renal mass (and thus decreased ammonia production) & kidneys inability to excrete H+ Immunologic: uremia inhibits cellular & humoral immunity UA, CBC (anemia, thrombocytopenia), serum electrolytes GFR Stage 1: > 90 Stage 2: 60-90 Stage 3: 30-60 Stage 4: 15-30 Stage 5: < 15 Renal US (evaluate size of kidneys, R/O obstruction) Small kidneys suggestive of chronic renal insufficiency w/little chance of recovery Presence of normal-sized or large kidneys does not exclude CKD Renal bx if needed to determine specific etiology Diet

Tx o Low protein; low-salt if HTN, CHF or oliguria present Restrict K, PO4, Mg intake

o o o

o o o o o

ACEIs: dilate afferent arteriole of glomerulus If used soon enough, reduce risk of progression to ESRD b/c they slow progression of proteinuria Can cause hyperkalemia BP control Decreases rate of disease progression ACEIs are preferred; diuretics may also be needed Glycemic control if pt is diabetic prevents worsening of proteinuria Smoking cessation Correction of electrolyte abnormalities Correct hyperphosphatemia w/Ca citrate (phosphate binder) Tx w/long-term oral Ca & vit D to prevent secondary hyperparathyroidism & uremic osteodystrophy Acidosis: tx underlying cause (renal failure); may require oral bicarb replacement Anemia: tx w/EPO Pulm edema: arrange for dialysis if condition is unresponsive to diuresis Pruritus: try capsaicin cream or cholestyramine & UV light Dialysis Transplant is only cure

Herpes zoster (shingles) Due to reactivation of VZV (stays dormant in DRG & is reactivated in stress, infection or illness; only in those who have had chickenpox before) In pts > 50 yo; if younger, suspect immunosuppressed state Contagious when open vesicles present & only for those whove never had chickenpox, immunocompromised or newborns; not as contagious as chickenpox Severe pain (before rash) & rash in dermatomal distribution Rash is of grouped vesicles on erythematous base; if severe, low-grade fever & malaise MC sites are thorax & trigeminal distribution (esp ophthalmic division), also other CN, arms & legs Not life-threatening even if dissemination occurs; more severe in immunocompromised Keep lesions clean & dry Analgesic for pain relief, if severe inject triamcinolone in lidocaine Antiviral agents (acyclovir) to reduce pain, decrease length of illness & reduce risk of postherpetic neuralgia; giving corticosteroids to reduce incidence of post-herpetic neuralgia is controversial Live vaccine is effective in reducing # cases of shingles > 60 yo & reduces severity & duration of post-herpetic neuralgia in pts who do end up w/shingles; give vacc to all pts > 60 yo who do not have C/I

Transplant rejection

Hyperacute o W/in minutes o Ab-mediated (type II): presence of preformed anti-donor Abs in transplant recipient o Occludes graft vessels ischemia & necrosis Acute o Weeks later o Cell-mediated due to CTL & reacting against foreign MHCs o Reversible w/immunouppressants (i.e. cyclosporine, muromonab-CD3) o Vasculitis of graft vessels w/dense interstitial lymphocytic infiltrate Chronic o Months to years later o Class I MHC non-self is perceived by CTLs as class I MHC self presenting non-self Ag o Irreversible o T cell & Ab-mediated vascular damage (obliterative vascular fibrosis) o Fibrosis of graft tissue & BVs GVHD o Time varies o Grafted immunocompetent T cells proliferate in irradiated immunocompromised disease host & reject cells w/foreign proteins severe organ dysfn o Maculopapular rash, jaundice, hepatosplenomegaly, diarrhea o Usually in BM & liver transplant (organs rich in lymphocytes) o Potentially beneficial in BM transplant

Malaria regimens Chloroquine phosphate unless resistant If chloroquine-resistant quinine sulfate & tetracycline OR atovaquone-proguanil & meflaquine P. falciparum IV quinidine & doxycycline Relapses can occur in P. vivax & P. ovale infection due to dormant hypnozoites in liver add 2 week regimen of primaquine phosphate Prophylaxis: chloroquine or mefloquine in chloroquine-resistant areas

Travelers diarrhea Primaquine & G6PD Acne vulgaris Inflamm condition of skin most prevalent during adolescence Severe acne more common in M due to more circulating androgens Pathogenesis o Obstruction of sebaceous follicles by sebum proliferation of P. acnes in sebum non-inflamm comedones or inflamm papules or pustules

o RFs: M, puberty, Cushings syndrome, oily complexion, androgens, meds Obstructive type: closed comedones (whiteheads) or open comedones (blackheads) Inflammatory type: lesions progress from papules/pustules to nodules to cysts to scars Tx o Mild to moderate acne Start w/topical benzoyl peroxide Add topical retinoids if benzoyl peroxide fails Add topical erythromycin or topical clindamycin o Moderate to severe nodular pustular acne Systemic abx: tetracycline, minocycline, doxycycline, erythromycin, clindamycin, TMP-SMX Add oral retinoids (isoretinoin) for severe recalcitrant nodular acne not response to systemic abx Extremely teratogenic so all F must have 2 neg pregnancy tests before starting F pts should also use 2 forms of birth control for 1 month prior to starting med through 1 month after stopping med

Indication for surgery in mucormycosis: as soon as dx is suspected HIV vs AIDS infections Guillain-Barre syndrome Inflamm demyelinating polyneuropathy that affects motor nerves Preceded by viral or mycoplasmal infection of upper resp or GIT (Campylobacter, CMV, hepatitis, HIV) Can also occur in Hodgkins disease, lupus, after surgery or after HIV seroconversion Abrupt onset w/rapidly ascending weakness/paralysis of all 4 extremities; progresses to involve respiratory, facial & bulbar mm Usually symmetric Weakness can be mild or severe, progresses from distal to central mm Extremities may be painful but sensory loss is NOT typical Sphincter control & mentation spared Autonomic features (arrhythmias, tachycardia, postural hypotension) dangerous complications Dx by CSF analysis (elevated protein, normal cell count) & electrodx studies (decreased motor nerve conduction velocity) Carefully monitor pulm fn; mech vent may be necessary Administer IVIG if pt has significant weakness; if progression continues, plasmapheresis may reduce severity of disease Do NOT give steroids; usually harmful & never helpful in GBS

Albumin-cytologic dissociation

CLL MC leukemia after age 50 Monoclonal proliferation of lymphocytes that are morphologically mature but functionally defective (do not differentiate into Ab-manufacturing plasma cells) Least aggressive type of leukemia; these patients survive longer than those w/acute leukemias or CML Course is variable: may follow prolonged indolent course; many patients die of other causes Same as indolent NHL B-cell neoplasm small lymphocytic leukemia; considered same disease at different stages Asx at time of dx, discovered on routine CBC (lymphocytosis) Generalized painless lymphadenopathy, spenomegaly Frequent respiratory or skin infections due to immune deficiency More advanced: fatigue, weight loss, pallor, skin rashes, easy bruising, bone tenderness, abd pain Dx o CBC: WBC 50,000-200,000 o Anemia, thrombocytopenia, neutropenia o PBS: absolute lymphocytosis (almost all WBCs are mature, small lymphocytes), smudge cells (fragile leukemic cells that are broken when placed on glass slide) o Flow cytometry shows clonal population of B cells o BM bx: presence of infiltrating leukemic cells in BM Tx o Chemo has little effect on overall survival but is given for sx relief & reduction of infection; pts observed until sx develop o Px is variable depending on # LN sites involved & presence/absence of anemia/thrombocytopenia

Alport dx & tx Trigeminal neuralgia DOC Diabetes & pre-diabetes dx Diabetes meds Metabolic syndrome Ekgs: pericarditis vs anteroseptal vs lateral vs inferior MI Pericarditis ddx Constrictive pericarditis Pericardial tamponade

Kayexelate, how to tx hyperkalemia Jnc Young pts which bp meds first Hearing loss Pericardial effusion Syphilis, rpr or vdrl +, stages PCI How to tx acute STEMI What thrombolytic therapy if cant do cath Pancreatic pseudocyst vs abscess PFT values in OLD & RLD Cervical spine involvement in RA Sleep apnea & GH in kids Disseminated gonococcal infection Blood cultures need to specify media