Renal Flashcards

Question 1

Q

Loop Diuretics

Answer

A

furosemide, bumetanide, torsemide

inhibits water, Na, K, Cl transport
inhibits Ca and Mg absorption across the thick ascending limb in the loop of henle
causes dilute urine
increased prostaglandin synthesis -→ improves renal blood flow
Indication:
- HTN, edema (pulmonary, peripheral edema due to CHF, nephrotic syndrome, and cirrhosis), hypercalcemia, hypermagnesemia-→does not cause hyponatremia -→ loose more water than salt
SEs:
- decreased electrolytes (hypoK, hypoCa, HypoMg, HypoCl)
- hyperglycemia, hyperuricemia (can precipitate gout)
- NSAIDs may decrease efficacy
- ContraIndicated in pt with sulfa allergy

Question 2

Q

Thiazide Diuretics

Answer

A

hydrochlorothiazide, chlorthalidone, chlorothiazide
MOA: block NaCl reabsorption at the early distal convoluted tubule (diluting segment)
- leads to diuresis and inability to produce a dilute urine
electrolyte imbalances caused by thiazide diuretics:
- hyponatremia
- hypokalemia
- hypercalcemia

Question 3

Q

Net effect of increased calcitriol

Answer

A

aka Vitamin D

increased absorption of calcium and phosphorous in gut

Question 4

Q

Net Effect of Increased PTH

Answer

A

hypercalcemia, hypophosphatemia

Question 5

Q

Net Effect of increased Calcitonin

Answer

A

hypocalcemia, hypophosphatemia

Question 6

Q

Hypophosphatemia causes, s/sxs, txs

Answer

A

Causes: renal losses-→ HyperPTH
- GI: severe malnutrition, malabsorption, alcoholism, phosphate binders
S/sxs: Muscle weakness, bone pain, rickets, osteomalacia
tx: mild or moderate: milk, sodium, or K-phosphate tablets
- SEVERE = <1mg/dL → IV phosphorus replacement

Question 7

Q

Hyperphosphatemia causes and tx

Answer

A

causes: CKD, AKI, hypoPTH, tissue breakdown: rhabdomyolysis, hemolysis, tumor lysis (these are problems that cause hypocalcemia as a result of hyper K)
tx: management in CKD: low phosphorus diet, phosphate binders, dialysis

Question 8

Q

Hypermagnesemia causes, sxs, and tx

Answer

A

causes: in CKD, Mg containing antacids, enemas, epsom salts, magnesium citrate, milk of magnesia
- iatrogenic: pre-eclampsia
Sxs: Mg = vasodilator
- levels > 4-6 mg/dL: hypotension, nausea, vomiting, facial flushing, urinary retention, and ileus
- levels > 8-12: flaccid paralysis, respiratory arrest, cardiac arrest
Tx: Mild: d/c mg supplements
- severe: IV calcium (to protect heart), saline diuresis (to flush excess Mg), furosemide
- Dialysis

Question 9

Q

Cisplatin

Answer

A

chemo drug

“punches holes” in renal tubules → hypoK and hypoMg

Question 10

Q

Hypomagnesemia causes, s/sxs, treatments

Answer

A

Causes: polyuria from osmotic diuresis, DKA, AKI, PPIs, diuretic use
- extracellular volume expansion: reduced Na and H20 reabsorption in PCT, so less passive Mg reabsorption
- Hypercalcemia = reduced Mg reabsorption
- Drugs: Cisplatin, aminoglycosides, amphotericin B
S/sxs:
- cardiac: repolarization abnormalities, ventricular arrhythmias
- Neuromuscular: tremor, twitching, tetany, seizures, migraine
- ***can cause unexplained hypocalcemia (due to impaired PTH secretion) and hypokalemia (due to released inhibition of ROMK channel so increased distal K secretion***
Tx:
- Severe: Mg levels <1mg/dL
  - 1-2 grams of Magnesium sulfate
    - can cause diarrhea
- minimal or no sxs:
  - oral repletion (diarrhea side effect)
    - preferred: sustained release Magnesium chloride
- Amiloride = prevents Mg wasting

Question 11

Q

Amiloride

Answer

A

prevents Mg wasting

reduces renal Mg excretion by increasing its reabsorption in the distal nephron

Mg repletion in CKD or AKI = half dosage with close monitoring

Question 12

Q

Causes of Pre-Renal Acute Renal Failure

Answer

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***

Question 13

Q

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

Answer

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

Question 14

Q

RIFLE criteria and AKI

Answer

A

Risk:
- GFR: increased SCr x 1.5 or GFR decrease greater than 25%
- UO (urine output): <0.5 ml/kg/h x 6 hours
Injury:
- GFR: increased SCr x 2 or GFR decrease greater than 50%
- UO: < 0.5mL/kg/h x 12 hours
Failure:
- GFR: increased SCr X 3, GFR decrease by 75%
  - OR SCR >4mg/dL
- UO: < 0.3mL/kg/h x 24 hours or anuria x 12 hours
LOSS: persistent AKI = complete loss of kidney function > 4 weeks
ESKD: greater than 3 months

Question 15

Q

AKIN Classification/Staging Classification & AKI

Answer

A

Stage 1: Absolute SCr: ≥ 0.3mg/dL
- % SCr: 150-200% (1.5-2x)
- UO: <0.5mL/kg/hr x 6 hours
- → no need for renal replacement therapy
Stage 2: % SCr: 200-300% (2-3x)
- UO: <0.5mL/kg/hour x 12+ hours
- → no need for renal replacement therapy
Stage 3: Absolute SCr: ≥ 4mg/dL with an acute increase of at least 0.5mg/dL
- %SCr: 300% + (≥ 3x)
- UO: <0.3mL/kg/hr x 24 hours or anuria x 12 hours
- → need for renal replacement therapy indicates stage 3 regardless of serum creatinine or UO

Question 16

Q

PostRenal AKI Etiology, S/sxs, dx, tx

Answer

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

Question 17

Q

Acute Tubular Necrosis Etiology

Answer

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

Question 18

Q

Acute Tubular Necrosis S/sxs, Dx, Tx

Answer

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 ***

Question 19

Q

Etiology of Interstitial Nephritis

Answer

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

Question 20

Q

Interstitial Nephritis S/sxs, Dx, & Tx

Answer

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

Question 21

Q

Etiology of Nephrotic Syndrome

Answer

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

Question 22

Q

Nephrotic Syndrome S/sxs, Dx, & Tx

Answer

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

Question 23

Q

Etiology of Glomerulonephritis

Answer

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

Question 24

Q

Glomerulonephritis S/sxs, Dx, & Tx

Answer

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

Question 25

Q

Staging of CKD

Answer

A

Chronic Kidney Disease

Stage 1: Normal GFR ≥ 90mL/min/1.73m2
- either persistent albuminuria or known structural or hereditary renal disease
Stage 2: Mild GFR 60-89 mL/min/1.73m2
Stage 3: Moderate GFR 30-59 mL/min/1.73m2
Stage 4: Severe GFR 15-29 mL/min/1.73m2
Stage 5: Kidney Failure GFR < 15mL/min/1.73

Question 26

Q

Definition of CKD

Answer

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)

Question 27

Q

Etiology of CKD

Answer

A

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

Question 28

Q

S/sxs of CKD

Answer

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 → 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 29

Q

Dx of CKD

Answer

A

Dx: GOLD STANDARD = GFR
- urinalysis: waxy casts, or granular casts → show dilation and hypertrophy of remaining nephrons
- Proteinuria
- elevated BUN & creatinine
- hyperphosphatemia & hypocalcemia
- low erythropoietin levels (due to loss of renal function)
- Tests to order: CBC, chem panel (CMP), iron studies, lipid profile, urinalysis

Question 30

Q

Tx of CKD

Answer

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

Question 31

Q

Renal Osteodystrophy

Answer

A

caused by secondary hyperPTH often as a result of CKD

increased phosphate due to decrease in secretion in kidneys → decreases production of 1,25-dihydroxy vitamin D (Calcitriol) → hypocalcemia → hyperparathyroidism
body then break down bones to increase serum calcium

Question 32

Q

Hydronephrosis

Answer

A

Urinary Tract obstruction that leads to the collecting system in one or both kidneys to dilate
Etiology: kidney stones (uretral), tumors, bladder outlet obstruction (BPH or prostate cancer) and sloughed off renal papillae
S/sxs:
- usually asymptomatic
  - can have change in urine output (Difficulty urinating/hesitancy), HTN, hematuria, and CVA tenderness, pain in the side, abdomen, or groin
Dx:
- UA→often benign but may show hematuria or elevated pH
- may have a palpable abdominal or flank mass caused by an enlarged kidney
- Labs: may have increased serum creatinine
- U/S: initial imaging that you should do → will show dilation of the collecting system in one or both kidneys
- CT Scan: indicated for those with flank pain and suspected nephrolithiasis or in pts whom visualization of the ureters is needed
Tx:
- Removal of obstruction → rapidly reversible if removed quickly, can lead to UTIs and possible ESRD

Question 33

Q

Polycystic Kidney Disease

Answer

A

Autosomal Dominant → mutations of PKD1 or PKD2 → causes 10% of ESRD

formation & enlargement of kidney cysts (cysts also common in the liver (most common), then spleen and pancreas
Pathophys:
- vasopressin (ADH) stimulates cytogenesis and eventually leads to ESRD over time
S/sxs: renal → abdominal pain & flank pain, nephrolithiasis, UTI and hematuria
- ~10% of pts have brain aneurysms (so be concerned about headache complains)
- abdominal fullness
- mitral valve prolapse and L ventricular hypertrophy
Dx: U/S → shows fluid filled cysts, CT scan will show large renal size and thin walled cysts
- need to U/s rest of direct family members
Tx: no cure, only supportive to ease sxs
- control HTN <130/80 with use of ACE-I & ARBs
- infx should be treated quickly/vigorously with abx
- dialysis or transplant should be considered when renal insufficiency becomes life threatening

Question 34

Q

Renal Vascular Disease

Answer

A

aka renovascular HTN

HTN caused by renal artery stenosis in one or both kidneys
***MOST COMMON cause of secondary HTN***
Pathophys: decreased renal blood flow leads to activation of RAAS
Etiologies: atherosclerosis = most common in elderly, fibromuscular dysplasia = most common cause in women <50
S/sxs:
- suspect in pts with headache & HTN <20 years
- or >50 years, severe HTN or HTN resistant to 3+ drugs
- or abdominal bruits
- or it pt develops AKI after the initiation of ACE-I therapy
Dx:
- non-invasive option: CT angiography, MR angiography, Duplex doppler (duplex doppler = less sensitive, specific)
- Renal Catheter Arteriography = GOLD STANDARD and definitive → revascularization can be performed during the same procedure if stenosis is found (not used in pts with renal failure)
Tx:
- Revascularization = definitive management
- angioplasty with stent → performed if creatinine >4.0, increased creatinine with ACE-I tx, or >80% renal stenosis
- Bypass if angioplasty is not successful
- Medical Management:
  - ACE-I or ARBs (BUT these are contraindicated in pts with bilateral stenosis or solitary kidney b/c can cause AKI due to ischemia

Question 35

Q

ESRD, Etiology, Dx, and Tx (NOT S/Sxs)

Answer

A

End Stage Renal Disease

Stage 5 CKD → GFR <15, complete loss of kidney function for more than 3 months
Most Common Cause = DM
Dx:
- GFR <15mL/min/1.73m2 for ≥3months
- low EPO levels
- metabolic acidosis
- increased potassium, phosphate, and PTH
- low calcium, sodium, bicarb
- “Waxy” cats with low urine flow
Tx:
- Dialysis & kidney transplant
- Manage co-morbidities:
  - bring HGB up to 11-12 (no higher or else possibility of clots)
  - dietary management: protein restrictiion, Calcium and Vitamin D supplements, limit water, sodium, potassium, and phosphorus
  - ACE-I & ARBs = slow progression of renal dysfunction
  - Loop diuretics: preferred addition to the management of edema associated with HTN due to ESRD
  - Pneumococcal vaccine

Question 36

Q

S/sxs of ESRD

Answer

A

End stage renal disease

S/sxs:
- pruritus
- HTN, may have A/B nicking, copper wire changes on retina
- S4 heart sound
- Kidneys affected by ESRD cannot regulate levels of electrolytes → sodium excess = retention of water
- potassium excess = abnormal heart rhythm, can lead to cardiac arrest
- magnesium deficit = can affect heartbeat and cause changes in mental state
Hormones: cannot absorb calcium and bones become weak and may break (renal osteodystrophy)
- erythropoietin production decrease = normochromic, normocytic anemia
Enzymes: kidneys affected by ESRD respond to lower GFR by making too much renin → keeps blood pressure levels high → difficult to tx

Question 37

Q

Hyperkalemia and EKGs

Answer

A

shortened QT
ST depression
Peaked T wave

Question 38

Q

Hypokalemia and EKGs

Answer

A

decreased T-wave amplitude
ST depression
increased U-wave amplitude

Question 39

Q

Hypokalemia Causes

Answer

A

Urine potassium < 20mmol/L
- metabolic acidosis: diarrhea, laxative
Urine potassium > 20 mmol/L
- metabolic acidosis:
  - proximal RTA, or distal RTA
- Metabolic Alkalosis + Normal or Low BP
  1. Low urine chloride (<20)
    1. vomiting
  2. High Urine Chloride (>20)
    1. Lasix
    2. thiazide
    3. Mg depletion
    4. Bartter’s
    5. Gitelman’s
- Metabolic Alkalosis + High BP
  - increased renin + increased aldosterone:
    - renal artery stenosis or renal tumors
  - decreased renin + increased aldosterone
    - primary aldosteronism
  - decreased renin + decreased aldosterone
    - Cushings
    - liddles
    - apparent mineralocorticoid excess (licorice, drugs)
    - MR mutation

Question 40

Q

Treatment of Metabolic Acidosis

Answer

A

identify and tx underlying causes

NaHCO₃^- indicated when:
- renal dysfunction→ not enough HCO3- is regenerated
- Severe acidemia: pG <7.10
- goal: increase HCO3- by 10mEq/L; and ph> 7.2
- ½ of the amount is given over 3-4 hours; then remainder given over 8-24 hours
- ****1mEq/kg/dose and monitor***

Question 41

Q

NaHCO₃ IV

Answer

A

used to treat metabolic acidosis

can be used with loop diuretics to avoid too much fluid (fluid overload)
indicated when:
- renal dysfunction → not enough HCO3- regenerated
- severe acidemia: pH<7.10
- ½ of the amount is given over 3-4 hours; then remainder given over 8-24 hours
one amp is 50mL (or 50mEq)
- can give up to 3 amps + 1L D5W

Question 42

Q

K-citrate

Answer

A

used to tx metabolic acidosis

helpful when the acidosis is coupled with hypoK+
- be cautious with renal impairment → needs to be avoided if pt has hyperK+ (can cause increased HyperK+)

Question 43

Q

Tx of Metabolic Alkalosis

Answer

A

pts rarely have symptoms due to alkalemia
- sxs often related to volume depletion
  - muscle cramps
  - dizziness depending on position
  - HypoK+ → muscle weakness, polyuria, polydipsia
Tx: tx the underlying cause
- i.e. meds, citrate containing products (K-citrate used to tx metabolic acidosis), or acetate in parenteral nutrition → causes HCO3- levels to rise
- alkalosis caused by vomiting, NG suction, or diarrhea +/- urinary Cl- (<25mEq/L) → saline infusion
- acetazolamide (carbonic anhydrase inhibitor) → reduces HCO3- concentration
- ******Hemodialysis or HCl infusion for life-threatening metabolic alkalosis******

Question 44

Q

Tx of Respiratory Acidosis

Answer

A

represents ventilation failure or impaired control of ventilation

hypoxemia + hypercapnia
severe, acute respiratory acidosis =
- HA, blurred vision, restlessness and anxiety, tremors, somnolence, and/or delirium
Tx = identify cause and tx that:
- opiate/opioids → naloxone
- acute bronchospasm/asthma → bronchodilators
- assisted ventilation and mod-severe acidosis → BiPAP
- NOTE: NaHCO3 may actually worsen acidemia due to increased CO2 generation so do NOT use this
Goals:
- careful monitoring of pH
- maintain oxygenation
- improve alveolar ventilation

Question 45

Q

Tx of Respiratory Alkalosis

Answer

A

represents hyperventilation

sxs: irritability of central and peripheral nervous system
- light headedness, altered consciousness, cramps, syncope
- severe cases: HypoPhos shifts from ECF to ICF
tx: identify cause and tx accordingly
- for mild-moderate severity in spontaneously breathing pts → no specific tx
- severe alkalosis:
  - rebreathing
    - rebreathing mask, or paper bag
    - mechanical ventilation
    - high level sedation or paralysis is a good option

Question 46

Q

Major Extracellular Ions

Answer

A

Na+, Cl-, HCO3-

Question 47

Q

Major Intracellular Ions

Answer

A

K+, Mg2+, PO₄^2-, SO₄^2-

Question 48

Q

General Tx strategy for severe volume depletion or hypovolemic shock

Answer

A

at least 1-2 L of NS as rapidly as possible (bolus)
- restores tissue perfusion
- fluid replacement is continued at rapid rate until clinical signs of hypovolemia improve

Question 49

Q

Types of Hyponatremia

Answer

A

Na+ <135
Hypertonic hyponatremia (Osmolarity >300 mOsm/L)
Hypotonic Hyponatremia (i.e. dilutional→ <275 mOsm/L)
- hypervolemic
  - gain of both water and sodium
    - water >>>>> sodium
- euvolemic
  - gain of water (ECF volume is normal)
    - total body water >>>>normal total Na+
- hypovolemic
  - loss of both water and sodium
    - sodium >>>>>water

Question 50

Q

Hypertonic Hyponatremia

Answer

A

osmolarity > 300 mOsm/L

associated with severe hyperglycemia

60mg/dL of Glc >200 = 1mEq/L reduction of Na+

tx: Tx the hyperglycemia → insulin

Question 51

Q

Hypervolemic Hyponatremia

Answer

A

Hypotonic hyponatremia (osmolarity <275 mOsm/L)

body gains excess Na+ and Water
- but Water >>>>>Na+
- Causes: HF, cirrhosis, nephrotic syndrome
tx: Fluid & Na+ restriction (i.e. 2 gm/day)
- optimize the underlying disease state
- diuretics
- increase the intravascular oncotic pressure (albumin)
  - pulls fluid of out intracellular compartment

Question 52

Q

Euvolemic Hyponatremia

Answer

A

aka isovolemic hyponatremia

hypotonic hyponatremia (osmolarity <275 mOsm/L)

ECF volume is normal

have excess water → total body water >>>>normal total Na+
- water intoxication
causes: SiADH (too much ADH secreted), Polydipsia, decreased water secretion
- carcinomas (small cell lung cancer)
- CNS disorders → stroke, meningitis, trauma
- medications: SSRIs, NSAIDs, antipsychotics, sulfonylureas
Tx:
- Non-acute (Na >115mEq/L and asymptomatic:
  - fluid restriction, possible chronic therapy
- Acute (Na <115 mEq/L and/or sxs):
  - 3% NaCl infusion
    - +/- diuretics to correct fluid accumulations
  - fluid restriction → 1000-1200mL/day
- ******no more than 12 mEq/L/24 hours (0.5mEq/hour)******
  - can cause osmotic demyelination syndrome → myelin cells swell/shrink and die

Question 53

Q

Hypovolemic Hyponatremia

Answer

A

hypotonic hyponatremia (osmolarity <275 mOsm/L)

decreased ECF volume

decrease in both Na+ and Water
- deficit of Na+ >>>>> deficit of water
Causes:
- diuretics (thiazides), diarrhea, vomiting, NG suction
Treatment: NS @ 300ml/hr until improvement in symptoms
*****DO NOT CORRECT SODIUM LEVELS >12mEQ/L/24 HOURS******

Question 54

Q

Types of Hypernatremia

Answer

A

Hypernatremia = >145 Na+
Hypovolemic Hypernatremia
- loss of water >>>>> sodium
Isovolemic Hypernatremia
- water loss only
Hypervolemic Hypernatremia
- body has excess sodium and water
  - sodium >>>>>>water

Question 55

Q

Hypernatremia General S/sxs and Causes

Answer

A

S/sxs: polyuria, polydipsia, confusion, obtundation, stupor, tremor, rigidity, coma
causes (free water deficit):
- dehydration
- incapable of obtaining water
- fever/infx/sweating/burn pts
- diabetes insipidus
- hyperglyuria/osmotic diuretics
- excessive sodium intake & cushing sx

Question 56

Q

Hypovolemic Hypernatremia

Answer

A

when water loss >>>sodium loss
- causes: diarrhea, sweating, diuretics
- tx: d/c diuretics or laxatives
  - if symptomatic: initially 200-300ml/hr with NS (to achieve hemodynamic stability)
    - replace free water deficit: D5W, ½ NS or a combo
  - asymptomatic: D52, ½ NS, or a combo

Question 57

Q

Isovolemic Hypernatremia

Answer

A

aka euvolemic hypernatremia

water loss only

causes:
- Diabetes insipidus:
  - central DI = decreased ADH production
  - Nephrogenic DI = decreased renal response to ADH
  - drug induced DI:
    - aminoglycosides, Ampho B, cochicine, demeclocycline (used to tx chronic euvolemic hyponatremia)
Tx:
- initially: D5W (replace free water)
- chronically:
  - for central DI: desmopressin (DDVAP) b/c it is a synthetic analog to ADH → act on the V2-receptors of collecting duct → water reabsorption
  - for nephrogenic DI: NSAIDs [can cause euvolemic hyponatremia] (indomethacin, IBU, naproxen, diclofenac, ketoprofen) and thiazides

Question 58

Q

NSAIDs and Sodium

Answer

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

Question 59

Q

Desmopressin (DDVAP)

Answer

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

Question 60

Q

Hypervolemic Hypernatremia

Answer

A

body has excess sodium and water

sodium >>>> water

causes:
- renal failure
Tx:
- replace intravascular deficit if necessary (use D5W, ½ NS or a combo)
- loop diuretics (if making urine) (increases sodium excretion)
- hemodialysis

Question 61

Q

Hypokalemia Tx

Answer

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

Question 62

Q

Hyperkalemia Tx

Answer

A

Symptomatic (urgent/emergent)
- IV calcium to stabilize the heart membrane
- insulin +/- glucose/dextrose to temporarily push K+ back into the cell
- albuterol to also temporarily push K+ back into the cell
- Sodium bicarb to be considered to tx acidosis
- Eliminate Source: IV, total parenteral nutrition (TPN), tube feeds, oral supplements, K sparing diuretics
Symptomatic:
- sodium polystyrene sulfonate (Kayexelate) → binds potassium, slower onset, but duration of 4-6 hours (constipation though…)
- Loop diuretics (lasix)
Asymptomatic;
- eliminate source
- kayexelate (sodium polystyrene sulfonate) → binds potassium
- loop diuretics

Question 63

Q

Hypokalemia Etiology, S/sxs, Dx, & Tx

Answer

A

potassium <3.5 mEq/L
Etiology:
- increased urinary/Gi losses
  - diuretic therapy, vomiting, diarrhea; renal tubule acidosis
- increased intracellular shifts
  - metabolic acidosis, beta-2 agonists, hypothermia, insulin, aldosterone
- hypomagnesemia
- decreased intake→ rare
S/sxs:
- neuromuscular: severe muscle weakness, rhabdomyolysis
- nephrogenic DI: polyuria (affects renal concentrating ability), cramps, n/v, ileus (obstruction of ileum
- cardiac: palpitations, arrhythmias
- no change in mental status
Dx:
- BMP: potassium <3.5mEq/L, magnesium, glucose, and bicarb should be ordered in work up
- Spot Urine K > 20 mmol/L (renal cause)
- Spot Urine K < 20mmol/L (non-renal cause)
- ECG findings: T-wave flattenedfollowed by a prominent u-wave
Tx: potassium replacement→ KCl oral if possible, IV KCl if rapid/severe tx needed
- potassium sparing diuretic (spironolactone, amiloride)
- check for hypomagnesemia (need to correct for this 1st or concurrently)
- ***Use non-dextrose IV solutions b/c dextrose will cause spike in insulin release which will cause more K to shift into the cells ***

Question 64

Q

Hyperkalemia Etiology, S/sxs, Dx, & Tx

Answer

A

serum potassium > 5-5.5mEq/L

Etiology:
- decreased renal excretion: acute/chronic renal failure
- decreased aldosterone → hypoaldosteronism, adrenal insufficiency
- Meds: K+ supplements, K+ sparing diuretics (thiazides, spironolactone, amiloride), ACEI/ARBs, digoxin, beta-blockers, NSAIDs, cyclosporin
- Cell lysis → rhabdomyolysis, hypovolemia, thrombocytosis, tumor lysis syndrome
- K redistribution → metabolic acidosis
S/sxs:
- neuromuscular: weakness (progressive ascending), fatigue, paresthesias (tingling), flaccid paralysis
- cardiac: palpitations and cardiac arrhythmias
- GI: abdominal distention, diarrhea
Dx:
- ECG: peaked T-waves, prolonged QRS, St depression
- BMP: potassium > 5.0 mEq/L, glucose and bicarb part of the workup +/- CBC (hemolysis)
Tx: repeat blood draw to ensure that increased K isnt from hemolysis (since venipuncture may cause this)
- IV Calcium Gluconate → stabilize the cardiac membrane → only for severe symptoms, K >6.5, + significant ECG findings
- → insulin with glucose/dextrose → insulin shifts K+ intracellularly
- Kayexalate (sodium polystyrene sulfonate) → enhances GI excretion of K+, lowers total K+
- SABA: albuterol (4-8x dosing for asthma)
- loop diuretics; dialysis if severe

Answer 65

A

serum sodium >145 mEq/L
- caused by increased free water loss, hypotonic fluid loss, or hypertonic sodium gain
Etiology: diabetes insipidus, diarrhea, sweating, burns, fever, insensible loss
- → infants, elderly, debilitated pts or impaired thirst mechanism → water intake decreased
S/sxs: PRIMARILY CAUSED BY SHRINKAGE OF BRAIN CELLS → dehydration
- thirst = most common initial sx
- confusion, lethargy, disorientation, fatigue, N/V, muscle weakness, seizures, coma, brain damage resp. arrest
PE: dry mouth, mucus membranes, decreased skin turgor, tachycardia, hypotension
Dx: serum studies → serum Na, urine osmolarity, serum osmolarity, assess volume status
Tx: hypotonic fluids: pure water oral, D5W, 0.45%NS,
- isotonic fluids if hypovolemic to replenish volume then hypotonic fluids
- if Central diabetes insipidus → desmopressin (synthetic analog to ADH)
- renal diabetes insipidus → NSAIDs (constrict afferent renal arteriole and reduce GFR)
- rapid correction (>0.5mEq/L.hr) → can results in Cerebral edema

Answer 66

A

serum sodium <135 mEq/L

due to increased free water
clincially significant → hypotonic hyponatremia
etiology:
- hypertonic hyponatremia → due to hyperglycemia or mannitol infusion
- Isotonic Hyponatremia → lab error due to hyperproteinemia or hypertrigliceridemia
- Hypotonic Hyponatremia →
  - hypovolemic → renal volume loss (diuretics, ACEI); extraneal volume loss → GI loss (diarrhea & vomiting), burns, fever
  - Isovolemic: SIADH, hypothyroidism, adrenal insufficiency water intoxication, MDMA, tea and toast syndrome
  - hypervolemic: edematous states → CHF, nephrotic syndrome, cirrhosis
- S/sxs: primary caused by cerebral edema → confusion, lethargy, disorientation, fatigue, N/V, cramps, Seizures, coma, respiratory arrest
- PE:
  - hypervolemia → edema, JVD, HTN; decreased HCT, serum protein, BUN:creatinine
  - hypovolemia→ poor skin turgor, dry mucus membranes, flat neck veins, hypotension; increased hct, serum protein, BUN:creatinine ratio >20:1
- Dx:
  - 3 steps:
    1. measure serum sodium
    2. serum osmolality (275-295 mOsm/kg)
    3. assess volume status (if hypotonic/decreased osmolality)

Answer 67

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

Answer 68

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

Answer 69

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

Answer 70

A

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

Answer 71

A

Rhabdomyolysis

Answer 72

A

albumin

can have a false negative if proteinuria composed of light chains
- → will be detected in protein precipitation test aka sulfosalicyclic Acid (SSA)

Answer 73

A

albumin

can have a false negative if proteinuria composed of light chains
- → will be detected in protein precipitation test aka sulfosalicyclic Acid (SSA) → Myeloma

Answer 74

A

< 0.2 or 200

aka SPOT urine protein/SPOT urine creatinine

Answer 75

A

<200mg/day

Answer 76

A

30-300mg/g

Answer 77

A

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

Nephritis:
- RBC casts
- proteinuria <3.5g

Answer 78

A

Non-oliguria: >400mL/day

Oliguria: 100-400 mL/day

Anuria: <50mL/day

Answer 79

A

A: severe metabolic Acidosis

E: Electrolyte Problems (Hyperkalemia)

I: Intoxication (Antifreeze)

O: Overload of fluids

U:Uremic symptoms (pericarditis, altered mental status)

Answer 80

A

3-4+ proteins, RBCs and RBC casts, granular & epithelial casts, oval fat bodies

Answer 81

A

4-5 years

Answer 82

A

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

Answer 83

A

Advantages:
- less sxs f
- continuous theraoy
- fewer dietary restrictions
- needleless
- home therapy
- flexibility with schedule
- easy night-time therapy
- easier travel
Disadvantages:
- daily (as opposed to 3 times a week)
- training required
- weight gain, sugar-load
- need for clean space in room for PD and supplies
- peritonitis risk (though balanced by bacteremia risk of HD)

Answer 84

A

15 years more

Answer 85

A

tacrolimus and cyclosporine (CSA)

tacrolimus can cause kidney injury

SE: DM, HTN, hypercholesterolemia

Answer 86

A

generally okay to keep going as long as:

K controlled
creatinine increases <20-30% within 6-8 weeks at start
no abrupt AKI
no other SEs (ACEi → cough, angioedema, etc. so can use an ARB instead)

Answer 87

A

Urine Na: >40mEq/L
urine osmolality: <350
BUN/Creatinine Ratio: 10:1
FeNa: >2%
FeUrea: >35%

Answer 88

A

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}

Answer 89

A

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

Answer 90

A

urine protein: creatinine ratio >0.2g/g

or >200mg/g

Answer 91

A

along afferent arteriole that detect blood pressure

if BP = low → secrete renin and activate RAAS system

Answer 92

A

Decr ADH in Central Diabetes Insipidus (neuro issue)
Urine osmo <300, corrects w/ ADH administration

Decr sensitivity to ADH in Nephrogenic Diabetes Insipidus (renal issue)
Urine osmo <300, does NOT correct w/ ADH

Hypernatremia will only occur if water intake is inadequate

Answer 93

A

Insensible losses
GI losses
Fluid shift into cells

Urine osmo >800
Urine Na <10

Hypernatremia will only occur if water intake is inadequate

Answer 94

A

Causes K excretion in principal cells of CD and K reabsorption in intercalated cells of CD

Answer 95

A

urine [K+] > 20 mmol/L = renal cause
urine [K+] < 20 mmol/L = nonrenal cause

Answer 96

A

GFR:
< 60 mL/min = CKD
< 30 mL/min = referral to nephrology
< 20 mL/min = eligible for transplant listing
< 10 mL/min = dialysis

Answer 97

A

Stage 1: Incr SCr by 0.3 mg/dL x 48 hrs or +50% x 7d, UOP <0.5 mL/kg x >6h

Stage 2: UOP <0.5 mL/kg x >12h

Stage 3: UOP <0.3 mL/kg x >24h or anuria >12h

Answer 98

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

Brainscape's Knowledge GenomeTM

Renal Flashcards

Brainscape's Knowledge Genome^TM