Week 1 Flashcards

1
Q

Stress Incontinence Tx

A
  • kegel exercises: 3-6 weeks of daily exercises, 200/day
  • vaginal estrogens
  • pessary
    • SEs: vaginal irritation, foul-smelling discharge, UTIs
  • surgery → mid-urethral sling
  • weight loss
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2
Q

Prostate Cancer Etiology, S/sxs, PE, Dx, Tx

A
  • most are adenocarcinomas
  • associated with the BRCA1 gene
  • Risk factors: african american, old age, family hx
  • S/sxs: urinary retention (more likely sign of BPH), decrease in urine stream strength
    • back pain (metastatic disease)
    • painful ejaculation
  • PE: DRE: hard, nodular, enlarged, and asymmetrical prostate
  • Dx:
    • indications for transrectal biopsy with normal rectal exam → PSA > 10 or abnormal transrectal U/S
    • PSA > 4: U/s with needle biopsy
    • PSA >10: bone scan to r/o metastases
  • Tx;
    • radical prostatectomy → complication = erectile dysfunction & urinary incontinence
    • with metastases: need androgen deprivation therapy (leuprolide) → type of medical castration, but can be reversible
      *
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3
Q

Calcium Nephrolithiasis Risk factors and Prevention

A
  • calcium oxalate = most common
  • Radiopaque
  • Risk factors: decreased fluid intake, high urinary calcium or pH, high animal protein intake, hypercalcemia, males, medications (loop diuretics, acetazolamide, antacids)
  • Prevention: increased fluid intake, thiazide diuretics, citrate, low sodium diet, decreased animal protein diet
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4
Q

When to screen for PSA

A

DISCUSS WITH PATIENT

  • men age 55-69 yo
  • 50 years old if first degree family hx
  • 45-50 if african american
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5
Q

BPH S/sxs, PE, Dx, & Tx

A

Benign Prostatic Hyperplasia

  • 50% of men have BPH by age 60, >90% by age 85
  • S/sxs: difficulty starting stream, post-void dribbling, hesitancy (start and stop)
    • nocturia
    • weak urinary stream
  • PE: digital rectal exam → uniformly enlarged firm and rubber prostate
  • Dx:
    • DRE +PSA
    • PSA < 4 = normal
    • PSA > 4 → BPH, prostate cancer, prostatitis
    • UA to r/o other causes
  • Tx:
    • if mild → watchful waiting
    • alpha blockers can provide the most rapid relief (smooth muscle relaxation of porstate and bladder neck
      • tamsulosin, prazosin, terazosin (shrink size of prostate)
        • finasteride & dutasteride
    • TURP (transurethral resection of the prostate) if unresponsive to meds
    • 5-alpha reductase inhibitors
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6
Q

UTI prevention

A
  • drink adequate amount of water
  • avoid delay in voiding
  • personal hygiene
  • cranberry juice/tablets
  • abx prophylaxis for 3 UTIs/12 months
    • Bactrim/Cipro
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7
Q

Major Risk Factors of Coronary Artery Disease (CAD)

A
  • Diabetes Mellitus (Worst risk factor, considered a CAD equivalent)
  • Smoking (Most important modifiable risk factor)
  • Hyperlipidemia, HTN
  • Men >45yo, Women >55yo
  • Fam Hx of CAD: (first degree relative – father or brother before age 55, mother or sister before age 65)
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8
Q

Post MI Complications

A
  • Pericarditis: 1-3 weeks post MI (Dressler Syndrome)
  • VSD (ventricular septal defect: 1-5 days post MI: shock, new murmur, pulmonary edema
  • Acute Mitral Regurg: shock, apical murmur, pulmonary edema
  • new or recurrent MI: chest pain, new ECG changes possible, new bump in troponins
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9
Q

Acute vs. Chronic Heart Failure

A
  • S/sxs:
    • Chronic Heart Failure (compensated):
      • congestion
      • laterally displaced apical impulse
    • Acute Heart Failure:
      • breathlessness
      • rapid weight gain
      • fluid build-up in the lungs and around the body
      • inadequate time for compensation: largely systolic (HTN crisis, acute MI, papillary muscle rupture); often fatal
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10
Q

Systolic Heart Failure

A
  • Definition: heart failure with decreased ejection fraction
    • impaired contractility
    • thin ventricular walls (DILATED)
    • S3 gallop (sys-tol-ic)
  • Etiology:
    • ischemic heart disease, rapid HTN, dilated cardiomyopathy (LEADING CAUSE), myocarditis, congenital, post-surgical, PE, sepsis
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11
Q

Diastolic Heart Failure

A
  • Definition: Heart failure with preserved ejection fraction
    • impaired filling/relaxation
    • thick ventricular walls (**Hypertrophied**)
    • S4 gallop (Di-a-stol-ic)
  • Etiology:
    • HTN, aortic stenosis, restrictive & hypertrophic cardiomyopathy, fibrosis, amyloidosis, sarcoidosis, constrictive pericarditis, normal aging, CAD scarring
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12
Q

Tx of Heart Failure

A
  • **initial management usually consists of an ACEI & (maybe a beta blocker) + diuretic (for sxs)**
  • Long Term Tx (Afterload reduction:
    • ACE Inhibitors (Captopril, Enalapril, Lisinopril): reduce afterload by vasodilation & BP reduction, useful in pts with EF <35%,mainstay of tx, (adverse effects: hyperkalemia, cough, angioedema, & elevated creatinine)
    • Angiotensin II Receptor Blockers (Losartan, Valsartan): blocks effects of angiotensin II, indicated in pts who cannot tolerate ACEI (cough)
    • Angiotensin Receptor Neprilysin Inhibitor (Sacubitril/Valsartan): inhibits breakdown of BNP so BNP no longer becomes a reliable marker in pts taking this
    • Beta-Blockers (Carvedilol, Metoprolol, Bisprolol): usually added after ACEI or AR
  • Long Term Tx (Preload Reduction)
    • Loop Diuretics (furosemide, bumetanide, torsemide): inhibit water transport across the Loop of Henle, effective for sx tx.
    • potassium sparing diuretics (spironolactone, eplerenone): aldosterone antagonist, decreased mortality
    • Thiazides (hydrochlorothiazide, Metolazone): inhibits DCT reabsorption of Na+
  • Long Term Tx (Positive Inotropes):
    • Digoxin: positive inotrope; 2nd line for pts in CHF with sinus rhythm, 1st line for pts with afib + CHF
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13
Q

Primary Prevention of ASCVD in Age 40-75 and LDL-C ≥ 70 to <190 mg/dL without diabetes mellitus

A

10-year ASCVD risk percent begins risk discussion:

  • <5%: “low risk”
    • emphasize lifestyle to reduce risk factors
  • 5-<7.5%: “borderline risk”:
    • If risk enhancers present then risk discussion regarding moderate-intensity statin therapy
  • ≥7.5-<20%: “Intermediate Risk”
    • Risk discussion:
      • if risk estimate + risk enhancers favor statin, initiate moderate-intensity statin to reduce LDL-C by 30-49%
      • if unsure, can use CAC score
  • ≥ 20%: “high risk”:
    • initiate statin to reduce LDL-C ≥ 50%
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14
Q

At what LDL-C level do you initiate high intensity statin with no risk assessment?

A

LDL-C ≥ 190 mg/dL

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15
Q

Best meds to lower elevated LDL

A
  • Statins (Rosuvastatin, atorvastatin, etc) → inhibit HMG Co-A reductase
    • impair production of cholesterol in the liver → upregulation of LDL receptors
  • Bile Acid Sequestrants (Cholestyramine, colesevelam, colestipol) & Cholesterol absorption inhibitors (Ezetimibe)
    • impair enterohepatic recirculation and gut absorption → less hepatic cholesterol → upregulation of LDL receptors
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16
Q

Best Meds to Lower Triglycerides

A
  • Fibrates (fenofibrate, gemfibrozil): inhibit triglyceride synthesis = Drug of Choice;gemfibrozil should NOT be given with statins
  • Niacin
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17
Q

Best Meds to Increase HDL

A
  • Niacin
  • Fibrates (fenofibrate, gemfibrozil): inhibit triglyceride synthesis = Drug of Choice;gemfibrozil should NOT be given with statins
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18
Q

Abnormal Lipid Values

A
  • Low HDL <40 mg/dL
  • High LDL > 190 mg/dL
    • high LDL in diabetic >70 mg/dL
  • high total cholesterol >250 mg/dL
  • high fasting triglyceride >150 mg/dL
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19
Q

Secondary HTN Definition and Causes

A
  • Definition: SBP ≥130 and/or DBP ≥80 WITH identifiable cause
  • Causes:
    • Primary aldosteronism = MOST COMMON
    • renal vascular disease
    • pheochromocytoma
      • adrenal tumor that secretes catecholamines (ie norepi and epi)
    • Cushing’s Syndrome
      • activation of the renin-angiotensin system
    • Congenital Adrenal Hyperplasia
    • Hyperthyroidism
    • Myxedema
      • associated with hypothyroidism
    • Coarctation of the Aorta
    • Excessive alcohol intake
    • Use of Oral Contraceptives
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20
Q

Secondary HTN Red Flags, Dx, & Tx

A
  • Red Flags:
    • HTN at an early age <25 without a family hx
    • HTN first develops >50 yo
    • previously controlled now refractor
    • Pt is refractory on antihypertensive medications or has severe BP
  • Dx:
    • when HTN is newly diagnosed consider ordering:
      • urinalysis
      • spot urine albumin: creatinine ratio → albuminuria ratio = >30mg/day
        • indicative of CKD
      • Blood tests
        • creatinine, K, Na, fasting glucose = BMP
        • lipid panel
        • TSH
      • EKG
  • Tx:
    • tx the underlying condition and aim for BP <130/80
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21
Q

Acute Bacterial Endocarditis Definition and organism

A
  • Definition: infection of a normal valve with a virulent organism (usually S. Aureus).
  • Rapidly destructive (fatal < 6 weeks if untreated)
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22
Q

Beck’s Triad

A

Associated with Cardiac Tamponade

  1. elevated JVP
  2. muffled heart sounds
  3. systemic hypotension
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23
Q

Mnemonic to Remember Medical Tx of STEMI

A

MOAN & BASH

Morphine, oxygen if O2 <90%, Aspirin 162 mg, Nitro q 5 min (don’t give to pts with systolic <90, or to inferior MI with R ventricular involvement → dependent on preload and nitro decreases preload)

Beta blockers (Decrease remodeling, decrease oxygen demand of heart, decreases HR, improve L ventricular hemodynamic funx, reduce incidence of ventricular arrhythmias; Contraindication in Heart block, high risk for cardiogenic shock) , ACE-I/ARB (more for long term use → improve L ventricular EF, mortality rate), Statin, Heparin (antithrombotic therapy → impede progression of thrombus in coronary artery)

TPA if pt cannot have reperfusion from cath lab in <90minutes from door to lab

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24
Q

Dressler’s Syndrome

A

Post-MI pericarditis

tx = aspirin or colchicine

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25
Q

Triad of R Ventricular Infarction

A
  1. JVD
  2. Clear Lungs
  3. Positive Kussmaul Sign
    1. paradoxical rise of JVP with inspiration (blood backs up into vein during inspiration due to failure of R ventricle)
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26
Q

3 populations with atypical sxs for acute MI

A

elderly, women, diabetics

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27
Q
A

Heliotrope Sign (associated with Dermatomyositis**)

  • dermatomyositis = autoimmune disease that leads to degeneration of the skin and muscle
    • characterized by muscle weakness heliotrope sign and Gottron’s Papules
28
Q
A

Gottron’s Papules (indicative of Dermatomyositis**)

  • dermatomyositis = autoimmune disorder that leads to the degeneration of the skin and muscle
    • characterized by muscle weakness and Gottron’s papules and Heliotrope sign
  • Gottron’s papules = over the joints of the hands
29
Q
A

Butterfly/Malar Rash

  • indicative of Systemic Lupus Erythematosus
    • worsened when exposed to the sunlight
  • systemic lupus erythematosus also will show a rash on the hands that spares the knuckles
30
Q

Net Effect of Increased PTH

A

hypercalcemia, hypophosphatemia

31
Q

Causes of Pre-Renal Acute Renal Failure

A
  • due to volume loss, heart failure, or loss of peripheral vascular resistance → all lead to loss of perfusion in kidneys
    • NSAIDs also can cause this (vasoconstriction of the afferent arteriole)
    • ACEI and ARB block effect of angiotensin (vasodilation of the efferent arteriole)
    • Diuretics
  • ***Kidneys are working fine, the organs that perfuse the kidneys arent working properly***
32
Q

PreRenal Acute Renal Failure S/sxs, Dx, and Tx

A
  • S/sx: weak oliguria (decreased urine output), dizziness, sunken eyes, tachycardia, orthostatic BP changes
  • Dx: BUN:Cr > 20:1, urine osmolality > 500, FeNa <1%, FeUrea <35%, Urine Na <20 mEq/L
  • Tx: tx with fluids, cardiac support, and/or tx shock
33
Q

PostRenal AKI Etiology, S/sxs, dx, tx

A
  • Etiology: obstruction (most common = prostate), bilateral outlet obstruction or bilateral ureteral obstruction
  • S/sxs: oliguria or anuria +/- suprapubic pain
  • Dx: foley catheter placement to find source of obstruction
    • if large urine output after foley = bladder, urethra, BPH
    • if low urine output after foley = ureter obstruction or pathology
    • Renal U/S but CT is most specific!!
  • tx: removal of obstruction → if done rapidly = quick reversal of AKI
34
Q

Acute Tubular Necrosis Etiology

A
  • ***Type of Intrinsic AKI***
  • Etiology = kidney ischemia or toxins
  • prolonged pre-renal AKI = most common cause
  • Major Causes:
    • drugs and toxins: ampho B, cisplatin, sulfa drug, aminoglycosides, radiocontrast media, NSAIDs, ACEI, cocaine use
    • ischemic related ATN : dehydration, shock, sepsis, hypotension
    • endogenous toxins: heme from hemolysis, myoglobin from rhabdomyolysis (iron is myoglobin is toxic to renal epithelial cells), tumor lysis syndrome, muscle breakdown in a marathon runner
35
Q

Acute Tubular Necrosis S/sxs, Dx, Tx

A
  • S/sxs: Oliguria, increased SCr etc
  • Dx: urinalysis = muddy brown casts (renal tubule epithelial cells), myoglobinuria, hemoglobinuria
    • FeNa >2%, FeUrea >35%, Urine Osmolality <350
  • Tx: remove toxin or re-perfuse kidney via IV fluids
    • can use loop diuretics if pt is euvolemic and not urinating
    • ***most pts return to baseline within 7-21 days ***
36
Q

Etiology of Interstitial Nephritis

A
  • Etiology: immune-related response
  • due to:
    • drugs: PCN, sulfa (bactrim), NSAIDs, phenytoin, Diuretics, etc
    • immunologic & infx disease: strep (get an ASO antibody), SLE, CMV, Sjogren’s, sarcoidosis
37
Q

Interstitial Nephritis S/sxs, Dx, & Tx

A
  • ***type of intrinsic AKI***
  • S/sxs: oliguria, increased SCr
  • Dx: urinalysis = WBC cats, WBCs, and eosinophils
    • acute azotemia (accumulation of nitrogenous waste, BUN)
    • diagnosed with RENAL BIOPSY → interstitial inflammatory cell infiltrates
  • Tx: d/c offending drug, corticosteroids, dialysis PRN
    • → usually self-limiting if caught early
    • most people recover kidney function within 1 year
38
Q

Etiology of Nephrotic Syndrome

A
  • glomerular damage results in higher loss of proteins in the urine
  • Most common primary causes:
    • membranous nephropathy: most common in non-DM adults associated with malignancy
    • MINIMAL CHANGE DISEASE: most common cause in children, idiopathic nephrotic syndrome sxs improve after tx
    • focal segmental glomerulosclerosis: obese pts, heroin, and HIV (+) black males
  • Most common Secondary Cause:
    • lupus
    • DM
39
Q

Nephrotic Syndrome S/sxs, Dx, & Tx

A
  • S/sxs: peripheral or periorbital edema, ascites, weight gain, fatigue, and HTN, frothy urine
  • Dx: serologic testing and renal biopsy
    • proteinuria >3.5g/day = diagnostic ( 24h urine collection)
    • urinalysis: free lipid or oval fat bodies or fatty casts → lipiduria
    • Hypoalbuminemia < 3.5g/dL
    • hyperlipidemia LDL > 130mg/dL, Triglycerides > 150mg.dL
  • Tx:
    • tx the causative disorder, corticosteroids
40
Q

Etiology of Glomerulonephritis

A
  • inflammation of the glomeruli due to blockage from immune complexes → immune response causes this
  • Post-Infectious Group A strep → diagnosed with ASO titers and low serum complement
  • IgA Nephropathy (berger disease): Most common cause of acute glomerulonephritis
    • young males after URI or GI infx (within 24-48 hours) → IgA immune complexes are first line defense in respiratory/GI secretions so infx → overproduction which damages the kidneys
    • more common in asian population
  • Membranoproliferative Glomerulonephritis: caused by SLE, viral hepatitis (Hep C)
    • secondary to immune-complex deposition or complement mediated mechanism
41
Q

Glomerulonephritis S/sxs, Dx, & Tx

A
  • S/sxs: edema + HTN + hematuria + RBC casts, jaundice, HTN
  • Dx: urinalysis = hematuria >3 RBCs/HPF + RBC casts + proteinuria (1-3.5g/day)
    • ASO titer for post-strep
    • serum complement = decreased (not always
    • RENAL BIOPSY = GOLD STANDARD
  • Tx: steroids and immunosuppressive drugs to control inflammation due to immune response
    • dietary management = salt and fluid restrictions
    • Dialysis if symptomatic azotemia
    • ACEI/ARBs (enalapril or losartan) are renoprotective → BP goal <130/80
    • use meds to control hyperkalemia
42
Q

Definition of CKD

A

dx: GFR < 60mL/min/1.73m2 for 3 months or any of the following:

  • albuminuria: urine albumin: creatinine ratio >30mg/day
  • proteinuria: urine protein: creatinine ratio > 0.2
  • hematuria
  • structural renal abnormalities ( solitary kidney, hx of abnormal renal histology hx of renal transplant)
43
Q

Etiology of CKD

A
  • Diabetes = MOST COMMON CAUSE (30%)
  • HTN (25%)
  • chronic glomerulonephritis (15%)
  • interstitial nephritis, polycystic kidney disease, obstructive uropathy
44
Q

S/sxs of CKD

A
  • Pruritus = common, but difficult to tx
  • Cardio: HTN → caused by salt and water retention → decreased GFR = stimulation of RAAS → increased BP → CHF due to volume overload, HTN, anemia → pericarditis
  • GI: (usually due to uremia) nausea, vomiting, loss of appetite
  • Neuro: lethargy, confusion, tetany → (due to hypocalcemia), uremic seizures, peripheral neuropathy
  • Heme: normocytic, normochromic anemia (secondary to deficiency of erythropoietin)
    • bleeding secondary to platelet dysfunction→ platelets do not degranulate in uremic environment
  • Endo/Metabolic:
    • Ca2+/Phosphorus disturbances→ decreased renal secretion of phosphate leads to hyperphosphatemia → decreased production of 1,25-dihydroxy vitamin D → hypocalcemiahyperparathyroidism
  • hyperkalemia → decreased secretion and acidosis
  • Fluid & Electrolyte problems:
    • volume overload: watch for pulm edema
    • hyperkalemia: due to decreased urinary secretion
    • hypermagnesemia: secondary to reduced urine secretion
    • hyperphosphatemia: decreased clearance of phosphate
    • metabolic acidosis: due to loss of renal mass (& therefore decreased ammonia production) & kidneys’ inability to secrete H+
45
Q

Tx of CKD

A
  • Tx: ACEI and ARBs → slow progression of renal dysfunction
    • manage the comorbidities!! : control HTN, glycemic control (A1C 6.5-7.5%), cholestrol control, tobacco cessation
  • Maintain HGB at 11-12 g/dl → Do not want to bring pt up to normal hgb levels → pro-thrombotic b/c it thickens the blood & increases mortality
  • Dietary management: protein restriction, calcium and vitamin D supplements, limit water, sodium, and potassium and phosphorus
  • Need for hemodialysis or kidney transplant
  • PCV-23
  • Fluid overload management: dietary salt <2 gm/day
  • GFR > 30 → thiazide diuretics (hydrochlorothiazide, chlorthalidone)
  • GFR <30 → loop diuretics (furosemide, torsemide, bumetanide)
  • can use phosphorus binders to reduce hyperPTH → calcium carbonate, calcium acetate, sevelamer, lanthanum, iron
  • tx the acidosis: may reduce risk of CKD progression → NaHCO3- → goal bicarb level >22
46
Q

NSAIDs and Sodium

A

NSAIDs reduce renal prostaglandins

and prostaglandins inhibit the action of ADH

so NSAID use can increase action of ADH and cause increased water reabsorption

47
Q

Desmopressin (DDVAP)

A

synthetic analogue of ADH

Act on V2-receptors at the collecting duct → reabsorption of water

used to tx central diabetes insipidus → the underlying pathophys behind isovolemic hypernatremia

48
Q

Hypokalemia Tx

A

When to tx? <3.5 mEq/L and/or pt is symptomatic

  • treatment:
    • oral: K-chloride, KPO4, K-acetate, K-citrate, k-gluconate
      • IV: if >10 mEq/L should be monitored via telemetry
    • other: diuretic induced (spironolactone- K+ sparing diuretic)
      • correct hypomagnesemia
        • ****low magnesium makes body resistant to K+ replacement, so tx mg deficiency first or concurrently*****
      • correct acid-base imbalance
49
Q

Goodpasture’s Syndrome

A
  • causes rapidly progressive Glomerulonephritis (nephritic syndrome)
  • anti-glomerular basement membrane
  • presentation:
    • lungs/kidneys hemorrhage
    • teenagers & >50 years
    • rapidly progressive→ fatal
  • Pathology:
    • antibodies against the glomerular basement membranne
      • often associated with crescent formation
  • Tx:
    • cyclophosphamide + corticosteroids + plasmapheresis
      • due to high fatality → START RX while waiting for dx
50
Q

Hemolytic Uremic Syndrome

A
  • Presentation:
    • E.coli O157:H7 (foodborne), Salmonella, etc. → undercooked meat consumption
    • bloody diarrhea that has resolved
    • fever; low platelets; AKI
  • Dx:
    • often via serum assays
  • Treatment: symptomatic manage,ent
    • HUS may require dialysis, 10% death rate
51
Q

Pauci-Immune Vasculitis S/sxs & Tx

A
  • type of nephritic syndrome → cause of rapidly progressive glomerulonephritis
  • Presentation: hematuria + signs of necrotizing small vessel vasculitis (diffuse skin lesion, lung hemorrhage, sinusitis, etc.)
  • Tx: aggressive tx with steroids, cyclophosphamide or rituximab
  • plasmapheresis → severe disease
52
Q

Lupus Nephritis S/sxs & Tx

A
  • S/sxs: usually hx of lupus
    • SLE more common in female AA population
    • proteinuria, hematuria, + elevated creatinine
  • Tx: dependent on biopsy classifications
53
Q

Dipstick positive for hemoglobin and myoglobin but no RBCs?

A

Rhabdomyolysis

54
Q

Normal Urine protein/creatinine ratio

A

< 0.2 or 200

aka SPOT urine protein/SPOT urine creatinine

55
Q

Normal Urine 24 hour protein

A

<200mg/day

56
Q

Microalbuminuria

A

30-300mg/g

57
Q

Macroalbuminuria

A

>300mg/g

58
Q

Rapidly Progressive Glomerulonephritis (RPGN)

A

when the “nephritis” is causing an AKI that is rapidly progressive over days to weeks

  • Nephritis:
    • RBC casts
    • proteinuria <3.5g
59
Q

Non-Oliguria vs Oliguria vs Anuria

A

Non-oliguria: >400mL/day

Oliguria: 100-400 mL/day

Anuria: <50mL/day

60
Q

Indications for Acute Dialysis

A

A: severe metabolic Acidosis

E: Electrolyte Problems (Hyperkalemia)

I: Intoxication (Antifreeze)

O: Overload of fluids

U:Uremic symptoms (pericarditis, altered mental status)

61
Q

At what GFR should we refer to nephrology?

A

GFR <30 ml/min/1.73m2 *CKD stage 4-5)

62
Q

Winter’s Formula

A

to calculate expected pCO2

  • Expected pCO2 = (1.5 x bicarb) + 8 +/- 2
  • if pCO2 = higher than expected → additional respiratory acidosis
  • if PCO2 = lower than expected → additional respiratory alkalosis
63
Q

Albuminuria

A

urine albumin: creatinine ratio >30 mg/g (per day)

64
Q

Aldosterone

A

Causes K excretion in principal cells of renal Collecting Duct and K reabsorption in intercalated cells of CD

65
Q

ACEI/ARBs in CKD

A

1st line therapy for HTN in early CKD as they “tell kidneys to take a break & not filter so hard”

Will cause slight incr in SCr. Expected and ok as long as <30% and proteinuria is improving.

Watch K as ACEi/ARB can increase

Do not use ACEi & ARB together d/t incr risk of AKI, hyperkalemia, hypotension