Renal/Pulm/Acid-Base Flashcards

Question

urine dip

Answer 1

can only detect macroalbuminuria >300 mg/24hrs

Answer 2

TYPES: 75-90% of stones are Ca oxalate - radio-opaque, enveloped-shaped - risk factors - small bowel disease (Crohns), surgical resection, chronic diarrhea --> malabsorption of fat --> Ca starts to bind fat instead of oxalate --> oxalate is absorbed more Ca phos stones - in primary hyperparathyroidism, RTA struvite stones/staghorn calculi - Proteus, urease-producing orgs cystinura - impaired amino acid transport (COLA) - radio-opaque stones, hexagonal crystals - pos urinary cyanide nitroprusside test - used as a screening test, detects homozyotes uric acid - needle shaped crystals, low urine pH, radiolucent stones - tx - hydration, alkalinization of urine (with K citrate), low purine diet, allopurinol xanthine stones are also radiolucent ********************************************* stones < 1 cm will pass spontaneously can get vagal reaction reaction with ureteral colic --> can cause ileus obstructive ureterolithiasis (or anything obstruction of hollow viscus) - colicky, poorly localized referred pain - to dx stone - US or non-con spiral CT - non-con CT due to risks associated with contrast administration - allergy, AKI, (clinically, concern for obscuration of stone by contrast dye) tx - NSAIDs > narcotics - narcotics can exacerbate N&V - 2L or more water/day - tamsulosin - a1 antagonist --> relaxes ureteral muscle, decreases intraureteral pressure --> facilitates stone passage recurrent renal stones - 24hr urine to id underlying metabolic disorder - increase fluids, reduce Na (because Ca is reabsorbed passively with active Na absorption., intake more Na --> more is excreted) , reduce protein, normal Ca intake, increase citrate, reduce oxalate - drugs: thiazide, urine alkalinization, allopurinol

Answer 3

hyponatremia, hypoK, hypoMg hyperCa decreased renal uric acid excretion - gout impairs insulin release and glucose utilization in peripheral tissues = hyperglycemia - worse with chlorthalidone (but is the preferred agent because of results of ALLHAT, showed decrease in CV mortality) increase LDL and triglycerides

Answer 4

oliguria < 500/24hrs (or less than 0.5 mL/kg/hr) H&P --> bedside bladder scan to assess for urinary RT - if bladder scan is inconclusive (obesity) --> cath no urine RT --> serum and urine chem and imaging - pre-renal - hypovolemia, sepsis, low CO --> give fluids - renal - ATN, interstitial nephritis, glomerular disease urine RT --> urethral catheter --> serum and urine biochem and imaging - >50 mL postvoid residual bladder volume is diagnostic for urinary RT/bladder outlet obstruction - treat underlying cause (BPH, malignancy aka extrinsic compression) with uro consultation - meds can cause this - amitriptyline, first gen H1 blockers (diphenhydramine, chlorpheniramine, hydroxyzine, have anticholinergic effects) constipation and urinary sxs can be linked

Answer 5

most common from of drug-induced chronic renal failure (3-5% of ESRD in USA) - seen in 50s females who use combined analgesics (ASA and naproxen) chronic tubulointerstitial nephritis - focal glomerulosclerosis, papillary necrosis - polyuria and sterile *pyuria* are early manifestations - microscopic hematuria and renal colic may occur following sloughing of renal papilla - HTN, mild proteinuria, impaired urinary concentration - CT can show small kidneys with bilateral renal papillary calcifications pt with chronic analgesic abuse - more likely to develop premature aging, atherosclerotic vascular disease, urinary tract cancer

Answer 6

hematuria in general - neoplasms, infections, trauma, nephrolithiasis, glomerulonephritis, prostatic disease (BPH) glomerular - microscopic (but gross hematuria can be present) - glomerulonephritis, Alport syndrome - sxs - non-specific - UA - blood AND protein, RBC casts, dysmorphic RBCs nonglomerular - gross - causes - nephrolithiasis, cancer, PKD, infection, papillary necrosis - px - dysuria, urinary obstruction - UA - blood (NO protein)

Answer 7

most often due to decreased urinary K excretion - most common causes - CKD, meds that impair RAAS acute hyperkalemia - ascending muscle weakness and flaccid paralysis, peak T waves --> short QT --> wide QRS --> disappearance of P --> sine wave, v fib - emergent treatment if serum K is rapidly rising, > 6.5, or pt has ECG changes chronic hypokalemia is more insidious - no sxs until > 7.0 1) med review 2) work-up for hypoaldosteronism EMERGENT TX: 1) cardiac membrane stabilization - calcium gluconate infusion rapid acting tx - insulin with glucose, b2-agonists (albuterol), sodium bicarb - dont use b2-agonists in pts with CAD - can cause tachy and precipitate angina ``` removing K (slow-acting) - diuretics (30 min), K-exylate (remove via GI tract), hemodialysis (prep time) - diuretics are contraindicated in dehydrated patients) ``` all else fails - cardioversion for v fib, transvenous pacemaker for symptomatic bradycardia, IV amiodarone for v. arrhythmias MEDS: nonselective b-blockers - inhibit b2-mediated intracellular K uptake ACEi, ARBs ... decreased aldosterone secretion K sparing diuretics, trimethoprim (blocks ENaC) - inhibit ENaC or aldosterone receptor cardiac glycosides (digoxin) - inhibit Na/K pump NSAIDs - inhibit local PG synthesis --> decreased renin and aldosterone secretion cyclosporine - blocks aldosterone activity heparin - blocks aldosterone production sux - causes extracellular leakage of K through AchR

Answer 8

HTN is the second leading cause of ESRD in the US (behind diabetes) benign nephrosclerosis --> glomerulosclerosis 1) arteriosclerotic lesions, glomerular capillary tufts 2) decrease in RBF and GFR - nephrosclerosis - hypertrophy and intimal medial fibrosis of renal arterioles - glomerulosclerosis - loss of glomerular capillary surface area with glomerular and peritubular fibrosis, microscopic hematuria, proteinuria, kidneys decrease in size

Answer 9

CV - tachy, impaired exercise tolerance, orthostasis peripheral nerves - dry skin, pruritis, callus formation - foot ulcers and poor wound healing - charcot arthorpathy (neurogenic arthropathy) - increased fracture risk with resultant secondary ulceration gastrointestinal - gastroparesis - esophageal dysmotility with dyspepsia - intestinal involvement with diarrhea, constipation, or fecal incontinence GU - ED, decreased libido and dyspareunia in F - neurogenic bladder = decreased ability to sense full bladder --> incomplete emptying, decreased urination - eventually recurrent UTIs or overflow incontinence

Answer 10

increased K entry into cells, renal K wasting, GI fluid loss adrenergic agents - stimulate Na/K ATPase and release of insulin hypoMg - cause of refractory hypoK - intracellular Mg inhibits K secretion in the collecting tubules of the kidney - causes: chronic alcoholism - malnutrition, associated with a number of electrolyte abnormalities, hypoMg is the most common - -> acute alcohol withdrawal -increase SNS activity --> K shifts into cells --> hypokalemia increased hematopoiesis, GCSF - increased K uptake by cells

Answer 11

sudden-onset pleuritic CP, dyspnea, tachycardia - hemoptysis - due to pulm infarct - pts will also develop small pleural effusions (exudative, grossly bloody) RFs - ... HIV, hemoconcentration (dehydrated) wedge shaped infarct on CT EKG - S1Q3T3 occurs in minority of pts indicators of poor prognosis - afib and low O2 sat approach: 1) stabilize with O2 and IVFs 2) evaluate for abs contraindications to anticoag --> if yes --> get CT angio and place IVC filter - if no - get D-dimer if PE is unlikely (Wells) and CT angio if PE is likely - early effective anti-coag reduces mortality risk of PE - so if pt likely has PE and presents with concerning hx --> start anti-coag while you are waiting for CT angio Wells score - 4 is cutoff - most important (3 pts each) - signs of DVT and PE is most likely dx - other things - hx of PE/DVT, tach, recent surgery/immobilization (flights DONT count), hemoptysis, cancer massive PE with cardiogenic shock - syncope - will see R heart strain - JVD, RBBB on EKG - tx - fibrinolysis (surgery within the preceding 10 ds is a contraindication) - survival is poor - death often occurs within an hr of sxs - distinguishing this from an MI - CVD risk factors, EKG signs (ST elevation, T wave inversion, Q waves)

Answer 12

remaining nephrons maintain the kidney's ability to excrete acid (by producing more NH3 buffer --> H+ NH3 excreted as NH4) - metabolic acidosis is not seen until there is advanced kidney dysfunction (GFR < 20 mL/min) RTA - metabolic acidosis that occurs with normal/preserved kidney function - type 1 - hypOkalemia - type 2 - hypOkalemia and low bicarb - hyperkalemic RTA (type 4) - occurs in poorly controlled diabetics --> damage to JG apparatus --> hyporeninemic hypoaldosteronism --> acidosis, hyperkalemic

Answer 13

flank pain, poor urine output - can have intermittent episodes of high volume urination when obstruction is overcome by large volume of retained urine (post-obstructive diuresis) excessive diuresis may lead to K wasting --> weakness

Answer 14

ADH secreted with high serum osm and hypovolemia aldosterone escape - escape from sodium-retaining effects of excess aldosterone - by volume and/or pressure natriuresis

Answer 15

most often due to preceding respiratory illness (viral) px - cough for 5d-3wks - can have purulent, *blood-tinged* sputum - sputum is due to epithelial sloughing (not bacterial infection) - no systemic findings - can have wheezing or rhonchi, crackles that are cleared with cough - secretions are easily mobilized clinical dx - get CXR if you are concerned about pna - otherwise symptomatic tx with bronchodilators and NSAIDs - abx NOT recommended

Answer 16

low - anemia, PE, pulm HTN high - pulm hemorrhage, polycythemia nl - bronchitis, asthma, MSK disease

Answer 17

progressive fibrosis of interstitium, alveoli, and conducting airways - restrictive disease - DLCO is decreased (increased thickness of alveolar membrane) px - progressive dyspnea over mo causes - asbestos (navy, shipyard, insulation), Be, silicon dioxide, HS pneumonitis - amiodarone, bleomycin, nitrofurantoin - infections - PNA, fungal, TB - radiation - RA, scleroderma, vasculitis, SLE exam - fine crackles during mid-late inspiration, clubbing CXR - reticular or nodular opacities - HRCT - fibrosis, honeycombing, traction bronchiectasis - PFTs - normal-inc FEV1/FVC, decreased DLCO (and increased Aa gradient), decreased TLC and RV (increased elastic recoil) - resting ABG may be normal or show mild hypoxemia - hypoxemia becomes significant with exertion (V/Q mismatch) ************************************** NOTES: silicosis increases the risk of developing Tb

Answer 18

aka bird fancier's lung/farmers lung - occurs due to repeated inhalation of antigen --> alveolar inflammation acute episode - cough, breathlessness, fever, malaise 4-6hrs after exposure chronic exposure --> pulmonary fibrosis and restrictive lung disease - noncaseating granulomas tx - avoid antigen exposure (will produce remission in most pts) - for acute/severe episodes - SYSTEMIC corticosteroids speed recovery

Answer 19

disorder that produces excess bicarb (generation phase) + process that prevents renal bicarb excretion (maintenance phase) RESPONDS to saline administration = volume depletion - vomiting, gastric suctioning, diuretics, laxative abuse, decreased oral fluid intake - will have generally have low urine Cl (unless pt is currently using diuretics, current diuretic use will increase urine Cl) - because RAAS is activated --> increased renal Na and Cl reabsorption, increased urinary H+ and K+ secretion - urine Cl < 20 does NOT respond to saline administration = mineralocorticoid excess - hyperaldosteronism, Cushing disease, ectopic ACTH production, severe hypokalemia (<2 meQ/L) - will have hypervolemia - because of excess mineralocorticoid --> Na and volume RT... - Cl usu > 20 (aldosterone has nothing to do with Cl reabsorption) - Bartter and Gitelman syndromes - hypo/euvolemic - need to treat underlying cause

Answer 20

PRERENAL due to decreased renal perfusion - true volume depletion - decreased arterial blood volume (HF, cirrhosis) - displacement of intravascular fluid (sepsis, pancreatitis) - renal artery stenosis - afferent arteriole vasoconstriction - NSAIDs decreased GFR - increased Cr, decreased urine output, BUN/Cr > 20, FeNa 1%, bland urine sed - can see metabolic acidosis - this would occur in uremia - if hypoperfusion persists --> renal ischemia --> ATN treat with IVFs - NS ***************************** AKI - AG metabolic acidosis, hyperkalemia

Answer 21

panacinar (panlobular) emphysema - lower lobe emphysema (vs emphysema due to smoking, which would be in the upper lung lobes) liver - asx until endstage disease - LFTs will be normal tx - AAT supplementation - bronchodilators and corticosteroids as needed

Answer 22

triad: flank pain, hematuria, mass - *scrotal varicoceles* - left-sided (gonadal vein enters renal vein on the left side, mass obstruction) - paraneoplastic syndromes - anemia (advanced tumors) OR erythrocytosis, thrombocytosis, fever, hyperCa, cachexia hematuria - tumor invasion into the collecting system dx - CT abd

Answer 23

Na - bicarb - Cl normal = 8 - 12 (sometimes Uworld says 6-12) elevated AG - means presence of non-Cl containing acids AG metabolic acidosis M - methanol (risk is blindness), formaldehyde U - uremia (ESRD, impaired excretion H+) D - dka P - paraldehyde I - inh, iron L - lactic acidosis (postictal, sepsis, hypoperfusion and shock, ESLD) E - ethylene glycol (urinary ca oxalate crystals, envelope shaped crystals) S - salicylate osmolar gap = measured - calculated serum osmolality - useful when ethanol, methanol, or ethylene glycol tox is suspected ``` **************************************** causes of non-AG metabolic acidosis - diarrhea - RTA - fistulas - pancreatic, ileocutaneous - acetazolamide - causes decreased reabsorption of bicarb, Na, Cl - ureteral diversion (ileal loop) - iatrogenic ``` can calculate urine AG to distinguish between renal and intestinal bicarb losses *************************************** give bicarb if pH < 7.1 - bicarb can cause myocardial depression and increased lactic acid production - so not recommended for high pHs

Answer 24

asx or can present with fatigue, weight loss, cough, dyspnea, or chest pain CXR - bilateral hilar LAD

Answer 25

subacute - chronic (8+ wks) cough for: - ACEis - stop ACEi - upper airway cough syndrome (PND, worse at night) - first gen H1 blocker - asthma (can present with white sputum) - PFTs (alternatively, can treat with 2-4 wks of inhaled glucocorticoids (?), response suggests asthma) - GERD - empiric PPI - -> if no improvement after 2-3 wks above - CXR for: parenchymal disease, purulent sputum/immunocompromised, no specific etiology - -> straight to CXR

Answer 26

EXUDATIVE - occurs when fluid moves into pleural space due to *increased permeability* of membranes = leakage of fluid for an exudative effusion: - pleural protein/serum protein ratio >0.5 - pleural/serum LDH > 0.6 - pleural LDH > 2/3 ULN for serum LDH etiologies of exudative effusion - empyema, chylothorax, malignancy, Tb (acid fast bac) - malignant effusion - will be subacute in onset; lung, breast, and lymphoma are the 3 most common causes TRANSUDATIVE effusions - oncotic or hydrostatic pressure differentials **************************************** 1) thoracentesis --> 2) bronch if pt has lung mass and pleural fluid cytology is non-diagnostic - if cytology shows cancer - no need for bronch

Answer 27

most common - bronchitis, lung cancer, bronchiectasis - bronchitis - cough (white sputum) for 3+ mo in 2 successive yrs, prominent bronchovascular markings - bronchiectasis - chronic cough, inadequate mucus clearance, associated with recurrent respiratory tract infections, daily copious mucopurulent sputum mitral stenosis, acute pulm edema tb, lung abscess, bac pna, aspergillosis coaguloapthy PE, AV malformation Wegners, Goodpastures trauma, cocaine use

Answer 28

increased water intake or decreased water excretion px - headache, N&V, AMS --> cerebral edema and brain herniation risk factors for iatrogenic causes - hypotonic fluid hydration, hypoxia, CNS disorders; children, premenopausal women, elderly - pain and morphine - associated with SIADH A) serum osm low (<275) 1) assess volume status a) hypovolemic --> UNa - UNa <40 - nonrenal loss (GI, dehydration) - UNa > 40 - renal loss (diuretics, p adrenal insufficiency) - can give isotonic fluids to these pts for volume resus (NS, LR) b) euvolemic --> Uosm - <100 - psychogenic polydipsia (takes a LOT of water, eventually capacity of kidneys to excrete water becomes overwhelmed and pt develops euvolemic hyponatremia), Beer potomania - >100 (and UNa >40) - SIADH (rule out hypothyroidism, secondary adrenal insufficiency) c) hypervolemia - CHF, hepatic failure, nephrotic syndrome B) serum osm nl-high - urine findings will be variable (so dont carE) - nl - pseudohyponatremia (due to proteins, lipids) - high (>295) - hyperglycemia, mannitol serum osm = 2*Na + glu/18 + BUN/2.8 ********************************************* SPECIFIC FEATURES: serum osm > 290 -- marked hyperglycemia, advanced renal failure urine osm <100 - primary/psychogenic polydipsia, malnutrition (beer drinkers potomania) urine sodium <25 - no - SIADH, adrenal insufficiency, hypothyroidism - yes - volume depletion, CHF, cirrhosis general tx - 3% saline, serial measurements of electrolytes - serum sodium 6-8 meq/L in first 24hrs (or 0.5 meq/L/hr) - if you correct too quickly - risk of osmotic demyelination (water quickly moves out of the brain --> disruption of cellular metabolic activity --> subsequent cell damage) ********************************************** SIADH (euvolemic hyponatremia) - small cell lung cancer/pneumonia, carbamazepine, cyclophosphamide, SSRIs, CNS disturbance, pain/nausea - *euvolemic* - so urine Na will be elevated (>40 meq/L), urine will be concentrated - also low serum uric acid, serum K is normal, normal acid-base status - risk is cerebral edema - tx - fluid restriction and salt tablets for mild symptoms --> 3% saline for severe hyponatremia - less than 8 meq/L increase over first 24hrs (note - need fluid infusion to be greater than urine osm) --> NS (0.9%) = 300 mosm/kg H2O

Answer 29

1) CVD - general population and esp in dialysis pts | - ESRD is an independent risk factor for CVD

Answer 30

airway inflammation and bronchospasm --> wheezing or cough

Answer 31

signs/sxs typically develop at BUN of >100 but BUN level is not used to dx - signs/sxs are used to dx uremic encephalopathy is indication for urgent HD (lactulose is used to treat hepatic encephalopathy) uremic coagulopathy - plt dysfunction, bleeding time prolonged, aPTT and PT will be normal - ecchymoses, epistaxis, more severe complications can occur (but dont occur as often due to advent of dialysis) note - GI bleed can cause elevated BUN - metabolism of blood proteins --> urea

Answer 32

infection + impaired bacterial clearance - causes - CF (pseudomonas infection, upper lung lobe involvement), A1AT (lower lobe emphysema), airway obstruction (cancer), rheumatic disease (RA, Sjogren), toxic inhalation, chronic prior infection (aspergillosis, mycobacteria), immunodeficiency (hypogammaglobulinemia) dyspnea, cough, rhinosinusitis, hemoptypsis, crackles, wheezing - obstructive lung disease airway thickening - tram-track and ring signs on CXR evaluation - initial dx - HRCT scan chest - Ig quantification - test for CF and sputum culture - PFTs

Answer 33

preceding URI IgA nephropathy - usu within 5d of URI, more common in young adult men - recurrent gross hematuria - NL serum complements - bx - mesangial IgA deposits - benign, possible RPGN or nephrotic syndrome PSGN - delayed - 10-21 d after URI, more common in kids, adults can be asymptomatic or develop acute nephritic syndrome - gross hematuria - LOW C3, elevated anti-streptolysin O/anti-DNAse B - bx - subepithelial humps (C3 complement) - good prognosis, possible CKD in adults

Answer 34

painless hematuria RFs - age, cigarette smoking, exposure to industrial chemicals, cyclophosphamide, FHx USPSTF recommends against screening for bladder cancer due to low incidence and poor PPV of current screening tests

Answer 35

CAP - majority bacterial, viral, fungal - orgs - S pneumo, H flu, Legionella, M pneumo - physical exam has <50% sensitivity - if you suspect, get CXR (dx requires CXR with infiltrate) - flu - would present with fever and URI sxs - CURB-65- 65+, confusion, BUN > 20, RR > 30, BP < 90/60 (0 outpatient, 1-4 floor, >4 ICU) - outpatient, healthy - macrolide or doxy - inpatient floor - cef + azithro or FQ - inpatient ICU - cef + azitrho or cef + FQ - high risk pts should be discharged with flu and pneumococcal vaccinations ATYPICALS - Mycoplasma pna - cold agglutinins (though these are not used for dx) ASPIRATION predisposing conditions - altered consciousness impairing cough reflex (dementia, drug intoxication), dysphagia (stroke, neurodegen), GERD - NG, ET tubes - protracted vomiting - large-volume tube feeds in recumbent position occurs days after aspiration event location - posterior segments of R upper lobes and superior segments of lower lobes tx - anaerobic (oropharyngeal bac) coverage = clinda, augmentin compare to pneumonitis - which is due to direct lung injury from gastric acid and will present few hours after event - supportive tx ``` OTHER eosinophilic PNA - gradual onset - pts will present with asthma-like sxs - exam - diffuse wheezes and inspiratory crackles - peripheral eosinophilia ``` PCP - CD4 < 200 cryptogenic organizing PNA - bilateral ground glass infiltrates ********************************************** OTHER FEATURES: in PNA - there is V/Q mismatch - in consolidative process - shunting occurs (V = 0, alveoli are filled with inflammatory exudate but are still perfused), increasing FiO2 will NOT correct hypoxemia after a single episode of PNA - in pts >50, get CXR in 6-12 wks to assess for malignancy parapneumonic effusion - exudative effusions (require more investigation than transudative) - protein ratio > 0.5, LDH ratio > 0.6, LDH >2/3 ULN - if you have low glucose in an effusion - means there is a high level of bacteria/leukocytes (RA, empyema, malignancy, TB, lupus, esophageal rupture) - sterile exudate in the setting of pna - glucose >60, WBC < 50K, tx with abx - bacterial invasion of pleural space - glucose < 60, WBC >50L, negative gram stain and culture (due to low bacterial counts), abx and drain - empyema - will have pos gram stain and culture, abx and drainage ********************************************** RECURRENT same region of lung: - local airway obstruction - extrinsic bronchial compression (neoplasm, adenopathy), instrinsic bronchial compression (foreign body, bronchiectasis) - recurrent aspiration - seizures, alcohol/drug use, GERD, dysphagia different region of lung: due to immunodeficiency, sinopulmonary disease, non-infectious (vasculitis, BOOP) work-up: 1) CT, 2) bronch and bx

Answer 36

restrictive lung disease patterns OSA - daytime sleepiness, impaired concentration, and morning headaches, sexual dysfunction - relaxation of pharyngeal muscles --> closure of airway - factors are tonsillar hypertrophy, excessive soft tissue, short mandible - loud snoring with periods of apnea - sequela include systemic HTN (which will improve with tx of OSA), pulm HTN, and RHF - dx - get nocturnal polysomnography - -> apnea - cessation of breathing >10 sec - -> hypopnea - drop in SaO2 by >4% - -> 5 events are diagnostic - note - PFTs will NOT aid in dx because the obstruction is transient OSH - fatigue, DOE in pts with morbid obesity - BMI > 30 - chronic (daytime and nighttime) hypoxia and hypercapnia --> increased bicarb RT (and Cl excretion) --> decreased ventilatory response to increased CO2... (cant breathe, wont breathe) - chronic hypoxia --> pulm HTN and cor pulmonale (because lung vasculature constricts when there is low O2 tension, hypoxic vasoconstriction) - work-up includes TSH, sleep study - tx - PPV (first-line), weight loss, avoidance of sedative meds, respiratory stimulants (acetazolamide, last resort)

Answer 37

tinnitus, fever, tachypnea, GI upset 1) respiratory alkalosis - stimulates the respiratory center in the medulla 2) AG metabolic acidosis - increased production and decreased renal excretion - uncouples oxidative phosphorylation - lactic acidosis, low bicarb - Winter's formula for resp compensation of met acidosis: PaCO2 = 1.5*HCO3 + 8 +/- 2 end result - pH is usu in normal range - start tx early - because pt will reach a point where acidosis >> ability to blow off CO2 note - if pt only had metabolic acidosis and appropriate resp compensation --> pH would be acidic (compensatory processes dont perfectly correct the pH to normal)

Answer 38

thin basement nephropathy - familial, isolated microscopic hematuria

Answer 39

PE, PNA, pulm edema hypoxemia with elevated A-a gradient dead space - ventilated but not perfused

Answer 40

5-yr survival of non-diabetics on dialysis - 30-40% | - 20% in diabetics

Answer 41

renovascular HTN should be treated with ACEis or ARBs (+ additional agents prn) unilateral renal artery stenosis - ACEI --> dilates the glomerular efferent arterioles - no rise in Cr bilateral renal artery stenosis - fall in GFR --> rise in Cr (acceptable is <30%) - ACEIs are sometimes contraindicated but can still be used with close renal function monitoring - due to their long term renoprotective effects revascularization - has NOT been proven superior to medical managment - reserved for pts refractory to medical therapy, HF, or recurrent flash pulmonary edema

Answer 42

risk factors - immobilization, cocaine abuse (vasoconstriction --> diffuse ischemia, seizures, hyperpyrexia, toxic effect on myocytes) causes ATN - due to excessive filtered myoglobin other hint - urine dipstick positive for blood but no blood on microscopy tc - aggressive hydration, mannitol, urine alkalinization

Answer 43

intermittent asthma - albuterol prn - attacks <2d/wk and nighttime awakenings <2x/mo persistent asthma - treated based on mild-mod-severe - frequency of daytime sxs and nighttime awakenings - albuterol prn AND 1) low dose ICS (beclomethasone, fluticasone) 2) low dose ICS + LABA (salmeterol), or medium dose ICS or theophylline (PDEi) 3) medium-dose ICS + LABA 4) high dose ICS + LABA (add omalizumab for pts with allergies) 5) high dose ICS + LABA + short course oral corticosteroid (add omalizumab for pts with allergies) - summary - start with ICS, add LABA, for most severe disease add oral corticosteroids - high dose ICS for long times can cause the same systemic effects as oral corticosteroids patients whose condition is well controlled for 3 mo should be considered for step-down ****************************************** asthma exacerbation - trigger - viral infection (will have leukocytosis due to stress and not infection) - decreased breath sounds, prolonged expiration, diffuse wheezing, lung hyperinflation - mild-mod - inhaled SABAs (reverses airflow obstruction) --> may need to escalate to systemic corticosteroids - severe asthma exacerbations - SABA + ipratroprium (potentiates bronchodilation) + systemic corticosteroids --> give 1x mag sulfate if pt shows no improvement - increased respiratory drive and hyperventilation - when you seen a nl-elevated PaCO2 --> that means that pt has respiratory muscle fatigue and is unable to blow off the necessary CO2 - signs of impending resp failure - elevated PaCO2, decreased breath sounds, absent wheezing, decreased MS, hypoxia with cyanosis --> intubate - severe hypoxemia (PaO2 < 60) - rare in acute asthma exacerbation ASA-exacerbated asthma - cough, asthma, refractory chronic rhinosinusitis and nasal polyposis in a pt with NSAID use - termed a pseudo-allergic reaction to NSAIDs - another sign - facial flushing within 30 min-3hrs after NSAID ingestion - briefly: ASA and NSAIDs block COX1 and 2 (blocks production of pro and anti-inflammatory PGs), shunts metabolites to LOX and LT pathway (LTS are all pro-inflammatory) - tx - manage underlying asthma and chronic rhinosinusitis, avoid NSAIDs, LT inhibitors pts can have comorbid GERD and asthma - px - sore throat, morning hoarseness, worsening cough at night, need for albuterol inhaler *after meals* - trial of PPI LABA monotherapy has been shown to increase asthma-related mortality inhaled cromolyn (mast cell stabilizer), zafilukast - asthma only

Answer 44

AD- due to mutation of Ca-sensing receptor - highER calcium concentrations are required to suppress PTH release - increased reabsorption of Ca in renal tubules asymptomatic hypercalcemia - high-nl PTH - low urine Ca v.s. primary hyperparathyroidism - which will also have high PTH, but urine Ca will also be high

Answer 45

other sxs - enthesitis (pain over bony prominences), acute anterior uveitis (unilateral), IBD, aortic regurg restrictive PFTs - FRC and RV are nl/increased due to fixed rib cage - if there is overlying pulmonary fibrosis - FRC, LC, and RV are reduced

Answer 46

broad casts - occur in dilated tubules of enlarged nephrons (undergone compensatory hypertrophy in response to reduced renal mass) waxy casts - also in chronic renal disease

Answer 47

HTN, palpable bilateral abdominal masses, microhematuria - NO proteinuria note - R kidney is easier to palpate because it lies lower than the L complications - intracranial berry aneurysms, hepatic cysts, valvular disease, colonic diverticula, abd wall and inguinal hernia

Answer 48

muddy brown, granular casts BUN/Cr < 20:1, urine Na > 20 mEq/L and FeNa > 2% causes - AGs, iodinated contrast dye, hypotension

Answer 49

fever, respiratory distress, hypoxemia, bilateral opacities associated with infections, trauma, massive transfusion, pancreatitis - lung injury --> release of proteins, inflammatory cytokines, neutrophils into alveolar space --> alveolar collapse and diffuse alveolar damage --> shunting, increased physiologic dead space, impaired gas exchange, decreased lung compliance - PaO2/FiO2 <300 mm Hg - increased A-a gradient will also have increased pulmonary arterial pressure - hypoxic vasoconstriction, destruction of lung parenchyma, and compression of vascular structures (PAP in mechanically ventilated pts) PaO2 goal - 55-80 mm Hg (88-95%) ways to improve low PaO2 - increase FiO2 or *PEEP* - high PEEP approaches may improve mortality in pts with severe ARDS - want FiO2 <60% - higher increases the risk of O2 tox (generation of pulmonary free radicals) - permissive hypercapnia - avoid overdistending alveoli (LTVV, 6 mL/kg ideal body weight) - improves mortality note - ways to change PaCO2 is TV and RR - increasing TV increases peak inspiratory pressure (and risk of barotrauma)

Answer 50

bones, groans, moans, psych overtones pts are typically volume depleted - due to hypercalcemia-induced nephrogenic DI and decreased oral intake severe >14, or symptomatic - immediate - NS hydration + calcitonin (avoid loops unless pt is volume overloaded) - long-term - bisphosphonate (onset takes 2-4 days) moderate - 12-14 - usu no tx asx or mild < 12 - no tx - avoid thiazides, Li, volume depletion, and prolonged bed rest causes - squamous cell cancer of lung - BUT have to correct electrolyte abnormalities before contrast imaging - MM - pancytopenia, get bone marrow bx - hypercalcemia of malignancy gets worse with time - start on bisphosphonates other tx - glucocorticoids inhibit 1,25-vitamin D to be activated by mononuclear cells in lungs and LNs - can be used to treat excessive vitamin D intake, granulomatous disease, lymphomas

Answer 51

intraalveolar hemorrhage --> hypoxia --> hyperventilation --> resp alkalosis

Answer 52

pH = pK + log(c. base/acid) pH = 6.1 + log(bicarb/0.03*PaCO2)

Answer 53

simple - thin smooth wall, homogenous, no contrast enhancement, asx - reassurance - other notes - infection is rare malignant cystic mass - thick, irregular wall - multilocular, septae, heterogenous - contrast enhancement - sxs - f/u imaging and referral to urology

Answer 54

obstructive FEV1 < 80% FEV1/FVC <70% FVC - nl-decreased restrictive FEV1 > 80% FEV1/FVC >70% FVC < 80% * *FEV1/FVC** - low = obstructive disease --> get DLCO --> nl or increased in asthma, decreased in COPD - nl-high (and low VC) = restrictive disease --> get DLCO --> normal in chest wall dysfunction (OHS, myasthenia, ALS), decreased in ILD pos bronchodilator response (>12% in FEV1) = asthma - this means there was complete reversibility of the obstruction with bronchodilators - DLCO in asthma is nl-increased (severe asthma) - it is nl-low in COPD

Answer 55

elderly post-op pt with agitation and lower abdominal (suprapubic) tenderness - risk factors - male, old, BPH, hx of neuro dz, surgery - opioids, anesthetics, and anticholinergics can precipitate AIUR 1) bladder ultrasound >300 mL of urine --> foley and UA - if you cant do bladder ultrasound --> directly to foley

Answer 56

anterior mediastinum - thymoma, teratoma, thyroid, thoracic aorta, terrible lymphoma - hoarseness, horners, facial and UE edema - get CT middle mediastinum - bronchogenic cyst, tracheal tumors, percardial cyst, lymphoma, LN enlargement, aortic enlargement of arch - get CT posterior mediastinum - neurogenic tumors (meningocele, enteric cysts, lymphoma, diaphragmatic hernias, esophageal tumors, aortic aneurysms) - get MRI

Answer 57

A - acidosis <7.1 (refractory to medical therapy) E - electrolytes - hyperkalemia with EKG changes - K > 6.5 refractory to medical therapy Ingestion - toxic alcohols, salicylate, Li, sodium valproate, carbamazepine - Li >4 OR L > 2.5 + tox sxs (seizures, depressed mental status) or inability to excrete (renal dz, decompensated HF) O - volume overload refractory to diuretics U - symptomatic encephalopathy, pericarditis, bleeding - asterixis is seen in hepatic encephalopathy, uremic encephalopathy (advanced renal failure), and CO2 retention

Answer 58

= net loss of free water - less common than hyponatremia - occurs in debilitated or inds with altered levels of consciousness (NM disorder pts, these pts will also have dysphagia) sxs - lethargy, AMS, irritability, seizures, muscle cramps and weakness, decreased DTRs * **ASSESS VOLUME STATUS*** - etiologies overlap HYPOvolemic hypernatremia - dehydration, renal losses, GI upset, excess sweating tx 1) isotonic (0.9% NS saline, LR) IVFs (to return Na slowly back to normal) 2) can switch to 5% dextrose preferred (or 1/2 NS) once volume deficit has been restored - rate of correction - 0.5 meQ/L/h - 1/2 NS and 5% dextrose are hypotonic - DONT use because they will lower Na too rapidly (risk is cerebral edema) ************************************** HYPERvolemic hypernatremia - due to exogenous Na intake and mineralocorticoid excess - tx - 5% dextrose in water (D5W) ************************************* EUvolemic hypernatremia - DI - complete v.s. partial - complete is urine osm < 300 mOsm/kg (often less than 100 mOsm/kg), partial is a higher urine osm - central - nephrogenic - hypercalcemia, severe hypokalemia, tubulointerstitial renal disease, meds (Li, demeclocycline, foscarnet, cidofovir, ampho B) - correct with free water supplementation

Answer 59

digital clubbing is accompanied by sudden-onset arthopathy (of hand and wrists) but issue is in lungs - get CXR to evaluate for underlying lung disease (cancer, TB, bronchiectasis, emphysema) associated with adenocarcinoma

Answer 60

cause - combustion of wool or silk, metal extraction in mining, and sodium nitroprusside CN - inhibits oxidative phosphorylation flushing (cherry-red color), cyanosis occurs later CNS - headache, AMS, hyperreflexia (CN accumulation) CV - arrhythmias Respiratory - tachypnea followed by respiratory depression, pulm edema GI - upset renal - metabolic acidosis (from lactic acidosis), renal failure tx - sodium thiosulfate

Answer 61

for increased intracranial pressure

Answer 62

kidney rapidly excretes drug into renal tubules but drug has low solubility in tubules - easily precipitates in renal tubules --> intratubular obstruction --> direct renal tubular tox causes - acyclovir, sulfonamides, methotrexate, ethylene glycol, protease inhibitors, uric acid (needle shaped crystals, tumor lysis syndrome) px - usu asx or nonspecific sxs, AKI < 7d of starting drug - UA will show hematuria, pyuria, crystals - increased risk with volume depletion and CKD d/c drug, volume repletion, loop

Answer 63

drugs - b-lactams, cephalosporins, cipro, PPIs, sulfonamides - usu 5d after starting drug less commonly due to infection occurs 7-10 d after drug exposure - can also have skin rash (maculopapular rash), arthralgias, eosinophilia, eosinophiluria, and pyuria d/c the offending drug - dont give steroids because they may hasten the recovery but may aggravate the underlying infection

Answer 64

distant heart sounds due to hyperinflated lungs acute exacerbation - increased dyspnea, increased cough, sputum production - exam - wheezing, JVD during expiration (due to increased thoracic pressure) - URI is the most common trigger, 50% of exacerbations are due to bacterial pathogen - sputum cultures NOT recommended - difficulty isolating a single pathogen - tx - O2 (88-92%, PaO2 60-70mm Hg), inhaled bronchodilators, systemic glucocorticoids (improves outcomes), abx (for 2+ sxs or if needing mechanical vent), oseltamivir (if flu), --> if ventilatory failure - try CPaP/BiPaP (preferred to intubation in mild-mod exacerbation, pts with COPD are harder to extubate, if all else fails then intubate) - empiric abx - azithro, FQs, or augmentin for 3-7d - roflumilast - PDEi, has anti-inflam properties, used as maintenance tx in pts with hx of COPD exacerbations O2-induced CO2 RT in COPD - pts with COPD are chronic CO2 retainers - have hypoxic vasoconstriction, high affinity for CO2 (Haldane effect), and increased RR - -> hypoxic vasoconstriction = destruction of alveoli --> hypoxia and hypercapnia --> hypoxic vasoconstriction and blood flow is redirected to alveoli with better SA - when O2 is administered --> vasodilation in lungs (V/Q mismatch because dead space is being perfused), decreased CO2 uptake from tissues (due to now decreased CO2 affinity), and decreased RR --> CO2 RT - AMS and seizures due to CO2 RT ipratropium inhalers + b-agonists - added bronchodilator effect LABA = maintenance therapy decreased mortality - smoking cessation and long-term supplemental O2 therapy

Answer 65

small and medium vessel vasculitis ENT + pulm + renal insufficiency - chronic sinusitis and otitis - ulcerations - lower respiratory tract involvement with tracheal narrowing and ulcerations and cavitations - active urine sediment, rapidly progressive GN - skin - livedo reticularis, non-healing ulcers - systemic sxs dx - first ANCA (this is a serum autoantibody, c-ANCA is usu pos) - HIV can increase the chance of getting a false positive ANCA - test for HIV first - confirm with bx - skin (leukocytoclastic vasculitis), kidney (pauci-immune GN), lung (granulomatous vasculitits) tx - corticosteroids and immunomodulators (MTX, cyclophosphamide)

Answer 66

140-180 mg/dL (in practice, it is below 180) SSI

Answer 67

solitary nodule - <3cm nodule, no associated LN enlargement - most incidentally discovered SPN are benign - high risk features - age, size, smoking cessation and quit date, irregular contour - 1) usu found on CXR --> 2) look for previous CXR and stability --> if no previous imaging or growth --> CT --> work-up accordingly high malignancy risk - surgical excision low-intermediate risk - proceed by nodule size - greater than 8 mm --> FDG-PET or bx --> excise if suspicious for malignancy or serial CTs if not suspicious - less than 5-8 mm - serial CTs - less than 4mm and low malignancy risk - no follow-up infectious granulomas are responsible for the majority of benign solitary pulm nodules - BUT important to rule out cancer if nodule has been stable over 2-3 yrs --> reassurance, no further work-up - nodule with ground-glass appearance - more likely to be malignant, repeat assessment annually *********************************************** small cell - rapid growth, will present with metastatic disease - SIADH, ACTH production squamous cell - hypercalcemia - vs sarcoid - bilar LAD, erythema nodosum bronchogenic carcinoma - asbestos exposure - asbestos = pleural plaques - bronchogenic carcinoma more common than pleural mesothelioma - bronchogenic carcinoma and asbestosis can present similarly - progressive dyspnea, bibasilar, end-inspiratory crackles, clubbing - -> asbestosis presents 20-30yrs after the exposure, honeycombing, bilateral pleural thickening pancoast tumor - squamous cell, lung adeno - inferior brachial plexus involvement - ulnar nerve dist - Horners (sympathetic chain, hoarseness, SVC, weight loss multiple nodules - mets

Answer 68

initial eval - UA, PSA - get Cr if patient has significant sxs or additional risk factors - hypertension, diabetes acutely elevated Cr --> renal ultrasound to assess for obstruction - cath pts with hydronephrosis

Answer 69

increased capillary hydrostatic pressure - heart failure - primary renal Na retention - renal disease (acute nephritic syndrome) and drugs - venous obstruction - cirrhosis, venous insufficiency with renal disease: primary glomerular damage --> decreased GFR --> volume overload --> fluid RT and increased BP ********************************************* decreased capillary oncotic P - protein loss - nephrotic syndrome, protein-losing enteropathy - decreased albumin synthesis - cirrhosis, malnutrition increased capillary permeability - burns, trauma, sepsis - allergic reactions - ARDS - malignant ascites lymphatic obstruction/increased interstitial oncotic pressure - malignant ascites, hypothyroidism, LN dissection

Answer 70

causes - autoimmune, infections (Tb, HIV, disseminated fungal), hemorrhagic infarct, metastatic cancer (lung), granulomatous disease acute - shock, N&V - hypoNa, hyperKa, hyperCa, normal AG acidosis (H + retention) - eosinophilia chronic - fatigue, weakness, anorexia and weight loss - GI sxs - hyperpigmentation or vitilgo - hypotension, hyponatremia, hyperkalemia, normal AG acidosis, hyperCa - anemia, eosinophilia dx - measure ACTH and serum cortisol with high dose ACTH stim test - primary adrenal insufficiency - secondary - brain issue

Answer 71

indications - COPD exacerbation, cardiogenic pulm edema, acute respiratory failure, to facilitate early extubation contraindications - medically unstable - CP arrest, pH < 7.10, ARDS, non-respiratory organ failure - inability to protect airway - uncooperative or agitate, inability to clear secretions/high aspiration risk - mechanical issues - recent esophageal anastomosis, facial or neuro surg/trauma, upper airway obstruction

Answer 72

hydralazine, procainamide, isoniazid anti-histone abx are sensitive

Answer 73

cause - pts with cirrhosis and ESLD develop splanchnic arterial dilation and decrease in vascular resistance (due to portal HTN) --> RAAS --> renal vasoconstriction, decreased perfusion, and GFR risk factors - advanced cirrhosis with portal HTN and edema precipitating factors - most common causes - GI bleed, SBP - reduced renal perfusion, vomiting, sepsis, excessive diuretic use - reduced glomerular pressure and GFR - NSAID use (constricts afferent arterioles) dx - renal hypoperfusion - FeNA < 1% (or urine Na < 10 mEq/L) - no tubular injury, RBCs, protein, or casts in urine - no improvement in renal function with fluids tx - hepatic recovery - splanchnic vasoconstrictors (midodrine, octreotide, norepi) and albumin can be used in the interim - dialysis is of limited benefit - but may be used as a bridge to liver transplantation - note - pts who are unlikely to have a quick recovery will not be candidates for liver transplant

Answer 74

tox - theophylline has narrow therapeutic index - metabolized by liver - affected by liver disease or drugs (abx like cipro) - CNS stimulation (headache, insomnia, seizures), GI upset, arrhythmias

Answer 75

severe electrolyte abnormalities - elevated phos, K, and uric acid (released from lysed cells) - decreased Ca - because phosphate binds Ca AKI - due to uric acid/Ca- phosphate px - N&V, muscle cramps, seizures, tetany tx - continuous tele (risk of arrhythmias) - aggressive electrolyte monitoring/tx ppx - IV fluids, allopurinol

Answer 76

peak airway pressure = resistive pressure + plateau pressure - plateau pressure = elastic pressure + PEEP increases in resistive pressure can occur due to - bronchospasm, mucus plug, ET obstruction decreased pulm compliance - pulm edema, atelectasis, PNA, right mainstem intubation, atelectasis, pneumothorax intrinsic or auto PEEP - normally end-expiratory pressure should be = Patm - in pts with COPD, alveoli cant empty completely so there will be an "auto PEEP"

Answer 77

obstructive lung disease - progressive narrowing of medium and small bronchioles wheezing

Renal/Pulm/Acid-Base Flashcards

(101 cards)