Week 1

Question 1

Stress Incontinence Tx

Answer 1

• 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

Question 2

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

Answer 2

• 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
    *

Question 3

Calcium Nephrolithiasis Risk factors and Prevention

Answer 3

• 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

Question 4

When to screen for PSA

Answer 4

DISCUSS WITH PATIENT

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

Question 5

BPH S/sxs, PE, Dx, & Tx

Answer 5

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

Question 6

UTI prevention

Answer 6

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

Question 7

Major Risk Factors of Coronary Artery Disease (CAD)

Answer 7

• 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)

Question 8

Post MI Complications

Answer 8

• 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

Question 9

Acute vs. Chronic Heart Failure

Answer 9

• 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

Question 10

Systolic Heart Failure

Answer 10

• 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

Question 11

Diastolic Heart Failure

Answer 11

• 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

Question 12

Tx of Heart Failure

Answer 12

• **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

Question 13

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

Answer 13

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%

Question 14

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

Answer 14

LDL-C ≥ 190 mg/dL

Question 15

Best meds to lower elevated LDL

Answer 15

• 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

Question 16

Best Meds to Lower Triglycerides

Answer 16

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

Question 17

Best Meds to Increase HDL

Answer 17

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

Question 18

Abnormal Lipid Values

Answer 18

• 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

Question 19

Secondary HTN Definition and Causes

Answer 19

• 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

Question 20

Secondary HTN Red Flags, Dx, & Tx

Answer 20

• 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

Question 21

Acute Bacterial Endocarditis Definition and organism

Answer 21

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

Question 22

Beck’s Triad

Answer 22

Associated with Cardiac Tamponade

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

Question 23

Mnemonic to Remember Medical Tx of STEMI

Answer 23

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

Question 24

Dressler’s Syndrome

Answer 24

Post-MI pericarditis

tx = aspirin or colchicine

Question 25

Triad of R Ventricular Infarction

Answer 25

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)

Question 26

3 populations with atypical sxs for acute MI

Answer 26

elderly, women, diabetics

Question 27

Answer 27

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

Question 28

Answer 28

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

Question 29

Answer 29

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

Question 30

Net Effect of Increased PTH

Answer 30

hypercalcemia, hypophosphatemia

Question 31

Causes of Pre-Renal Acute Renal Failure

Answer 31

• 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***

Question 32

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

Answer 32

• 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

Question 33

PostRenal AKI Etiology, S/sxs, dx, tx

Answer 33

• 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

Question 34

Acute Tubular Necrosis Etiology

Answer 34

• ***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

Question 35

Acute Tubular Necrosis S/sxs, Dx, Tx

Answer 35

• 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 ***

Question 36

Etiology of Interstitial Nephritis

Answer 36

• 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

Question 37

Interstitial Nephritis S/sxs, Dx, & Tx

Answer 37

• ***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

Question 38

Etiology of Nephrotic Syndrome

Answer 38

• 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

Question 39

Nephrotic Syndrome S/sxs, Dx, & Tx

Answer 39

• 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

Question 40

Etiology of Glomerulonephritis

Answer 40

• 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

Question 41

Glomerulonephritis S/sxs, Dx, & Tx

Answer 41

• 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

Question 42

Definition of CKD

Answer 42

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)

Question 43

Etiology of CKD

Answer 43

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

Question 44

S/sxs of CKD

Answer 44

• 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 → hypocalcemia → hyperparathyroidism
• 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⁺

Question 45

Tx of CKD

Answer 45

• 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

Question 46

NSAIDs and Sodium

Answer 46

NSAIDs reduce renal prostaglandins

and prostaglandins inhibit the action of ADH

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

Question 47

Desmopressin (DDVAP)

Answer 47

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

Question 48

Hypokalemia Tx

Answer 48

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

Question 49

Goodpasture’s Syndrome

Answer 49

• 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

Question 50

Hemolytic Uremic Syndrome

Answer 50

• 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

Question 51

Pauci-Immune Vasculitis S/sxs & Tx

Answer 51

• 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

Question 52

Lupus Nephritis S/sxs & Tx

Answer 52

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

Question 53

Dipstick positive for hemoglobin and myoglobin but no RBCs?

Answer 53

Rhabdomyolysis

Question 54

Normal Urine protein/creatinine ratio

Answer 54

< 0.2 or 200

aka SPOT urine protein/SPOT urine creatinine

Question 55

Normal Urine 24 hour protein

Answer 55

<200mg/day

Question 56

Microalbuminuria

Answer 56

30-300mg/g

Question 57

Macroalbuminuria

Answer 57

>300mg/g

Question 58

Rapidly Progressive Glomerulonephritis (RPGN)

Answer 58

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

• Nephritis:
  
  • RBC casts
  • proteinuria <3.5g

Question 59

Non-Oliguria vs Oliguria vs Anuria

Answer 59

Non-oliguria: >400mL/day

Oliguria: 100-400 mL/day

Anuria: <50mL/day

Question 60

Indications for Acute Dialysis

Answer 60

A: severe metabolic Acidosis

E: Electrolyte Problems (Hyperkalemia)

I: Intoxication (Antifreeze)

O: Overload of fluids

U:Uremic symptoms (pericarditis, altered mental status)

Question 61

At what GFR should we refer to nephrology?

Answer 61

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

Question 62

Winter’s Formula

Answer 62

to calculate expected pCO₂

• Expected pCO₂ = (1.5 x bicarb) + 8 +/- 2
• if pCO_{2 = higher than expected → additional respiratory acidosis}
• if PCO_{2 = lower than expected → additional respiratory alkalosis}

Question 63

Albuminuria

Answer 63

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

Question 64

Aldosterone

Answer 64

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

Question 65

ACEI/ARBs in CKD

Answer 65

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