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Clinical Medicine 3 > Lecture 13 (Renal)-Exam 5 > Flashcards

Lecture 13 (Renal)-Exam 5 Flashcards

1
Q

Notes on Dr.S from Dr. Houstons

  • What makes hormones helps with RBC synthesis?
  • What is needed for calcium absorption?
  • What is needed fro aldosterone synthesis?
A

Erythropoetin (RBC synthesis)

1,25 Dihydroxycholcalciferol (Vitamin D)-> Needed for Calcium absorption

Renin->Needed for Aldosterone synthesis
* Na re-absorption=>Fluid retention

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2
Q

Hydronephrosis
* Not what?
* What is it?
* If allowed to persist, what will occur?

A
  • Not a disease
  • A result of urinary obstruction leading to dilatation of the collecting system in one or both kidneys leading to declines in glomerular filtration, tubular function
  • If allowed to persist, nephron loss will occur
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3
Q

Hydronephrosis
* What are some causes? (5)
* What is the clinical presentation?

A
  • Etiologies – renal calculi, BPH, neoplasm, congenital, pregnancy, strictures etc.
  • Clinical – usually asymptomatic, may have a triad of decreased urine output, HTN, hematuria
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4
Q

What are the types of hydronephrosis?

A
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5
Q

Hydronephrosis: Dx
* What is elevated?
* What is the study of choice?

A
  • Azotemia: elevation of BUN and serum creatinine
  • US is study of choice
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6
Q

Hydronephrosis
* What should always lead to a renal US?
* What is the first step? What happens if nothing happens?

A
  • Sudden or new onset of hypertension should always lead to a renal US (related to increased renin release with unilateral obstruction)
  • First step is to cath the bladder (or US scan bladder if available)-If diuresis occurs, the blockage is belows the bladder neck (urethra)
  • If no diuresis-then US of kidney

Normal amount in urine: 300 CC

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7
Q

Hydronephrosis-Clinical findings
* What motivates adults to come?
* How is the pain?
* What sxs of complete obstruction?

A
  • Pain motivates adults to seek attention
  • Pain is often severe, steady, radiates to lower abdomen, testicles or labia.
  • Oliguria and anuria are symptoms of complete obstruction
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8
Q

Hydronephrosis – Clinical Findings
* What is present from UTI associated?
* Exam may reveal what?
* Rectal exam may reveal what?
* Pelvix exam may reveal?

A
  • Fever and dysuria – if UTI associated
  • Exam may reveal distention of kidney or bladder.
  • Rectal exam may reveal enlarged prostate or rectal/pelvic mass, pelvic exam may reveal enlarged uterus or pelvic mass
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9
Q

Hydronephrosis: labs
* UA may shows
* What may be normal?
* What levels should be check?

A
  • UA may show hematuria, pyuria, proteinuria, bacteriuria
  • Urine sediment may be normal
  • Check BUN and creatinine
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10
Q

Hydronephrosis - Labs
* What may help in differentiating bladder causes of hydronephrosis?

A

Urodynamic testing (bladder/urethra function)

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11
Q

Hydronephrosis - Imaging
* What is used?
* What should be obtained to diagnose intra-abdominal or retroperitoneal causes?
* What can be used at times?

A
  • US imaging – 90% sensitivity and specificity
  • IV urogram and/or CT should be obtained to diagnose intra-abdominal or retroperitoneal causes.
  • MRI used at times
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12
Q

What may be used for those with high risk of AKI from contrast?

A

Antegrade urography (those that have nephrostomy tube in place)

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13
Q

Hydronephrosis - Differential Diagnosis (list sxs)
* Pyelonephritis:
* Cholelithiasis:
* Duodenitis:

A
  • Pyelonephritis – fever, chills, nausea, vomiting, diarrhea occurring with or without symptoms of cystitis
  • Cholelithiasis – pain is more typical in epigastrium and RUQ and often nausea and vomiting occurs
  • Duodenitis – Right flank pain, dull, better with food intake, worse when hungry
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14
Q

Hydronephrosis - Differential Diagnosis
* Other urologic disorders include what?
* Causes of unexplained renal failure in adults? (5)
* What account for most cases of acute renal failure?

A
  • Other urologic disorders include ureteropelvic junction obstruction, renal subcapsular hematoma and renal cell carcinoma.
  • Causes of unexplained renal failure in adults – hypoperfusion, acute tubular necrosis, interstitial, glomerular, or small vessel disease
  • Hypoperfusion and ATN account for most cases of acute renal failure
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15
Q

Hydronephrosis - Management
* Functional causes may be treated by what?
* Hydronephrosis with infection is a urologic emergency – treated by what? (usually performed by what? What are meds?

A

Functional causes may be treated by frequent voiding or catheterization

Hydronephrosis with infection is a urologic emergency – treated by prompt drainage using retrograde stent insertion or percutaneous nephrostomy
* Usually performed by urologist or IR depending on type
* Meds – adults with hydronephrosis, complicated by infection – should be treated with IV ABX for 3-4 weeks (1-2 of which are IV followed by PO)

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16
Q

Hydronephrosis - Prognosis
* Neonates and children with unresolved hydronephrosis: F/U when?
* Prognosis for an adult patient depends on what?
* Complete obstruction for 1-2 weeks usually leads to what?

A
  • Neonates and children with unresolved hydronephrosis – follow up on a regular basis with urine cultures, serum creatinine, US
  • Prognosis for an adult patient depends on the duration and completeness of the obstruction, if infected.
  • Complete obstruction for 1-2 weeks usually leads to at least partial return of renal function. After 8 weeks, recovery is unlikely.
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17
Q

Polycystic Kidney Disease (PKD)
* What is the adult onset?
* What is the infantile onset?
* Acoounts for what?

A
  • Adult onset = Autosomal dominant disorder = MC hereditary kidney disease
  • Infantile onset = autosomal recessive: a/w hepatic fibrosis -> death in 1st year of life
  • Accounts for 10% of ESRD
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18
Q

Polycystic Kidney Disease (PKD)
* What are the predominant characteristic?
* Patient presentation usually when (age)?
* Vasopressin stimulates what?

A
  • Predominant Characteristic – formation of cysts in the kidneys, may form cysts in other organs as well.
  • Patient presentation usually in 25-30’s
  • Vasopressin stimulates cystogenesis with ESRD eventually (50% develop ESRD by age 60)
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19
Q

PKD: DX
* What pain is present? (2)
* What happens with what peeing?
* What are the extrarenal/associated findings?(4)

A
  • Abdominal pain
  • Flank pain (predisposes to pyelonephritis)
  • Nocturia
  • Extrarenal/associated findings – subarachnoid hemorrhage due to cerebral “berry” aneurysms, liver cysts, Mitral valve prolapse, colonic diverticula
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20
Q

DX - PKD
* Dx most common with what? (what does it show)
* Genetic testing done when?

A
  • Diagnosis most common with Renal US -> Multiple cysts, large kidneys, cortical thickening, enlarge calyces
  • Genetic testing done post diagnosis
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21
Q

PKD-DX
* What does the physical exam revel?
* If you see what, thank about PKD?
* What does the UA showed? What is shown in late stage?

A
  • Physical Exam = may reveal large palpable kidneys
  • If you see Abdominal Mass + hematuria/HTN – think about PKD
  • Urinalysis – hematuria, proteinuria, concentrated urine
    Isosthenuria with hyperuricemia in late stage
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22
Q

DX - PKD
* Isosthenuria:

A

If you were to give the patient anti-diuretic hormone (ADH) or if he didn’t drink any water for 12 hours, and then the urinalysis was repeated and the specific gravity was still the same, it means that
* Kidneys have lost their concentrating ability–renal failure.
* “Isosthenuria”: urine has same osmolality as plasma

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23
Q

TX of PKD
* Single, simple cyst:
* Multiple cysts:
* What do you need to prevent and preserve?

A
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24
Q

PKD:
* What education?
* Ultimately refer to what?
* What to do for ESRD?

A
  • Patient and family education
  • Ultimately refer to nephrology if there are any clinical signs or symptoms of disease
  • Dialysis/transplantation for ESRD
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25
Q

PKD-Complication Treatment
* Pain:
* Hematuria:

A
  • Pain – bed rest, analgesics
  • Hematuria – usually due to rupture of cyst into the renal pelvis, but could be a stone or UTI – hydration and bed rest
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26
Q

Complications - PKD
* What are the sxs, dx and txt of renal infection?
* What is the tx for nephrolithiasis?

A
  • Renal Infection – flank pain, fever, leukocytosis – CT may show increased cyst wall thickness if cyst infected. Difficult to treat – needs a fluoroquinolone or Bactrim. Treatment may require IV abx followed by long-term PO abx.
  • Nephrolithiasis – increase hydration to 2-3 L/day to prevent precipitation of stones
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27
Q

Complications - PKD
* Cyst-induced ischemia appears to cause of what?
* Cerebral Aneurysms – 10-15% will have arterial aneurysms where? What is recommended?
* Other issues (3)

A
  • HTN – 50% will be hypertensive on presentation. Cyst-induced ischemia appears to cause activation of the renin-angiotensin system. Use an ACE inhibitor or an ARB
  • Cerebral Aneurysms – 10-15% will have arterial aneurysms in the circle of Willis. Screening recommended only if family hx positive, undergoing elective surgery, or in a high-risk profession (pilot).
  • Other – diverticulosis, aortic aneurysms, mitral valve prolapse
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28
Q

Prognosis - PKD
* Vasopressin receptor antagonists decreases what?
* Tolvaptan is FDA approved for what?
* Encourage the patient to drink what?
* What may slow down the progression?

A
  • Vasopressin receptor antagonists decrease the rate of change in total kidney volume and eGFR decline.
  • Tolvaptan is FDA approved for the treatment of autosomal dominant polycystic kidney disease.
  • Encourage the patient to drink at least 2 L of water daily.
  • Treatment of HTN and a low-protein diet may slow the progression – maybe.
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29
Q

Horseshoe Kidney (HK)
* Look for it in?
* 1 in 1000 have some type of what?
* What is the most common?
* Fused renal mass almost always contains what?

A
  • Congenital & typically asymptomatic, so look for it in neonates
  • 1 in 1000 have some type of renal fusion
  • Horseshoe kidney is the most common
  • Fused renal mass almost always contains two excretory systems and therefore two ureters
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30
Q

Horseshoe Kidney (HK)
* Renal mass may be what?
* May remain in?
* Seen quite frequently in who?
* What are complications? (3)

A
  • Renal mass may be entirely on one side or divided equally on the flanks
  • May remain in the pelvis and have alternate blood supply.
  • Seen quite frequently in Turner syndrome, Trisomy 13, 18, 21
  • Complications - stones, pyelonephritis, increased risk of renal cancer
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31
Q

Clinical Presentation - HK
* Most have what?
* Some develop what?
* What do the GI sxs mimic?

A
  • Most have no symptoms
  • Some develop ureteral obstruction (ureteropelvic junction obstruction)
  • GI symptoms that mimic peptic ulcer, cholelithiasis or appendicitis may be observed
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32
Q

Clinical Presentation - HK
* Infection is a risk if what?
* UA?
* Renal function?

A
  • Infection is a risk if ureteral obstruction and hydronephrosis or calculus develops
  • UA normal unless UTI
  • Renal function normal unless disease coexists in each of the fused renal masses
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33
Q

Dx, complications of HK
* What image clearly reveals it?
* What other imaging can you do?
* Prone to what? (4)

A
  • CT clearly reveals
  • However – plain x-ray may reveal, urogram, US
  • Prone to ureteral obstruction (UP junction-> dt urine stasis)
  • Hydronephrosis, stone formation, infection (pyelonephritis -> dt urine stasis)
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34
Q

What is the txt and prognosis of HK ?

A

No TX typically needed (if asymp-> do serial UAs)
Prognosis – usually excellent

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35
Q

Goals of general fluid management:
* Replace what?
What are sensible and insensible losses)

A

Replace Obligatory Fluid Losses
* Sensible (measurable) = urine
* Insensible (not easily measurable) = lung, perspiration

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36
Q

Goals of General Fluid Management
* Replace what that usually presents pathophysiologically?
* What are the examples (6)

A

Replace Exceptional Losses (present pathophysiologically)
* Diarrhea
* Vomiting
* NG tube
* Drains & Fistulas
* Blood
* Surgical evaporative losses (exploratory laparotomy)

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37
Q

Goals of General Fluid Management
* Daily what? why?
* Monitor what?

A
  • Daily weights- reflection of fluid (scale or a lift/bed)
  • Monitor I & O (intake and output) and electrolytes
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38
Q

Indications for IV Fluids
* When is isotonic used?
* When is hypotonic used? Caution with what?
* When is hypertonic used? Dangerous in the setting of what?

A
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39
Q

What are the types of IV fluids?

A
  • Normal Saline 0.9% (NS) – almost isotonic
  • 0.45% Normal Saline (1/2 NS)
  • Ringer’s Lactate or Lactated Ringers (LR/ RL) – surgeons favorite
  • Dextrose 5% with 0.45% Normal Saline (D5W & 0.45% NS)
  • 5% dextrose in water (D5W)
  • TGH Special: House Wine (D5 1/2NS with KCl 20mEq
  • 3% Saline: hypertonic
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40
Q

5% dextrose in water (D5W)
* Used in who?
* Showed be avoided in who? Why?

A
  • diabetics and people needing the free water
  • Should be avoided in Wernicke patient or alcoholics
  • Glucose oxidation is a thiamine-intensive process that may drive the insufficient circulating vitamin B-1 intracellularly
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41
Q

K is given to patients with what?

A

NG tube suctioning

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42
Q
A
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43
Q
  • Lactate turns into what? Good in what?
  • D5 sugar (solute) gets used by your body and you end up with what?
  • Glucose in D5W 0.45 is good when?
A
  • Lactate turns into bicarbonate – good in lactic/metabolic acidosis (counteracts it). Don’t give with High pH.
  • D5 sugar (solute) gets used by your body and you end up with free water w/o solute. So if theres high Na and hypovolemia – give D5W slowly to increase fluids.
  • Glucose in D5W 0.45 is good cause you’ve been NPO 8hrs after procedure.
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44
Q

Osmolality:
* What is osmotic pressure responsible for what?
* What does it depend on?
* Usually expressed as waht?

A
  • Osmotic Pressure responsible for water movement across cell membranes
  • Depends on the total number of solute particles (osmoles) dissolved in solution
  • Usually expressed as milliosmoles of solute per kilogram of solvent (mOsm/kg)
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45
Q

It is a lot but it is good patho!

Explain this picture

A

Proximal Tubule:
* Fluid is isosmotic to ECF (300 mOsm): The fluid entering the proximal tubule has the same osmolarity as the extracellular fluid.

Loop of Henle
* Descending Limb: Water is reabsorbed (H₂O) into the surrounding medulla due to the high osmolarity of the interstitial fluid. This results in the fluid becoming more concentrated (hyperosmotic).
* Ascending Limb: Here, Na⁺, Cl⁻, and K⁺ are actively transported out of the tubule without water following, creating a hypoosmotic fluid (lower osmolarity) by the time it reaches the distal tubule.

Distal Tubule
* Hypoosmotic Fluid (100 mOsm): The fluid entering the distal tubule is hypoosmotic due to the active transport of solutes in the ascending limb of the Loop of Henle.

Collecting Duct
* Permeability to H₂O Varies: The permeability of the collecting duct to water varies, which is influenced by the presence of antidiuretic hormone (ADH).
* Urine Osmolarity Depends on Permeability: If the collecting duct is permeable to water (high ADH), water is reabsorbed, leading to more concentrated urine. If it’s impermeable (low ADH), less water is reabsorbed, resulting in diluted urine.

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46
Q

Fill in

A
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47
Q

fill in the cover part

A
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48
Q

Hypernatremia
* What is the the serum sodium level? What is it due to?
* What are some causes? (6)
* What populations can be at risk? (3)

A
  • Serum sodium >145 mEq/L – DUE to free water loss
  • Causes – diarrhea, diuretics, sweating, fever, burns, diabetes insipidus
  • Infants, disabled, elderly who cannot take in adequate H20 (hot elderly syndrome)
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49
Q

Hypernatremia
* What is seen clinical?
* What does that exam show?

A
  • Clinical - thirst (MC initial symptom) , confusion, lethargy, fatigue, muscle weakness. If severe – seizure, coma, death.
  • Exam – dry mucous membranes, decreased skin turgor, tachycardia (early sign), hypotension (late sign) .
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50
Q

Hypernatremia:
* What are the 3 management steps?

A
  • Correct shock (Normal saline! or LR)
  • Treat underlying cause (fever, vomiting, diabetes insipidus, etc)
  • Replace water deficit
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51
Q

Hypernatremia
* What are hypovolemic causes?
* What are isovolemic/euvolemic causes?
* What are hypervolemic causes?

A
  • Hypovolemic causes – either renal (severe hyperglycemia or osmotic diuretics) or extrarenal (sweating, GI or Resp loss, dehydration)
  • Isovolemic/euvolemic causes – diabetes insipidus (lack of ADH)
  • Hypervolemic – mineralocorticoid excess, hypertonic saline
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52
Q

Hypernatremia:
* Clinical for all forms: what are sxs?

A

Clinical for all forms – dependent on rapidity and severity – CNS dysfunction (confusion, lethargy, fatigue)

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53
Q

Diabetes Insipidus
* What is it? What are the two types?

A

DI: inability of the kidney to concentrate urine, leading to production of large amounts of dilure urine
* Central DI: Deficiency of ADH production by hypothalamus (synthesized)-pituitary (released)
* Nephrogenic DI: Kidney resistance to ADH

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54
Q

Diabetes Insipidus
* What are the sxs?
* How do you dx it?

A

Sxs: Thirst and hypotonic polyuria (3-20 L daily)

Dx:
* Hypernatremia
* Daily urinary excretion of 3 liters or more
* Low urine specific gravity <1.010 or 24hr urine osmolality < 300 mOsm (LOW)
* Serum osmolarity (increased dt to increased urinary free water loss)

Normal Urine Sodium – 20mEq/L at random; 40-220 per day
Normal Urine osmolality – 50-800 at random (depending on hydration status), 500-850 mOsm/kg per day

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55
Q

Diabetes Insipidus
* What test can be deprivation? What is the issue? What does it differenitate?

A

Water deprivation test can be performed, but can cause severe dehydration
* Differentiates from psychogenic polydipsia (PP causes dilution hyponatremia and doesn’t respond to exogenous ADH admin)

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56
Q

DX and TX - Hypernatremia
* What do you need to look at for serum?
* Assess what?
* What is going on with urine sodium?

A
  • Serum – sodium, urine osmolarity, serum osmolarity
  • Assess volume status: (Hyperosmolality nearly always associated with hypernatremia)
  • Urine sodium: Urine osmolarity (low if urine dilute – diabetes insipidus), (high if urine concentrated due to extrarenal cause – dehydration)
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57
Q

TX - Hypernatremia
* What is the txt for euvolemic and hypovolemic?
* What is the rate of volumes?

A
  • Use hypotonic fluids in euvolemic: H2O, D5W, 0.45 NS, 0.2 NS
  • Use isotonic fluids if hypovolemic – NS or Lactated ringers.
  • Rate - >0.5 mEq/L/hr can result in cerebral edema ( do not want to go too fast)
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58
Q

Hyponatremia:
* What is the sodium level?
* What are the sxs?
* What are serious sxs caused by?
* Beware of what?

A
  • Sodium <135 (increased free water due to kidneys inability of kidneys to excrete excess water)
  • Symptoms include headache, vomiting, AMS, seizure
    * Serious symptoms caused by cerebral edema
  • Beware overcorrection- central pontine myelinolysis (osmotic demyelinating syndrome)
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59
Q

What are the 4 types of hyponatremia?

A
  • Pseudohyponatremia- saline contamination, hypertriglyceridemia, hyperproteinemia, hyperglycemia (add 1.6meq/L per 100mg/dL glucose)
  • Hypovolemic
  • Hypervolemic
  • Euvolemic
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60
Q

Hyponatremia
* What should you order?

A

Order urine and serum sodium and osmolality

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61
Q

Pance pearls: really good -> helped me a lot

Hyponatremia-
* What steps should you take to dx?

A
  • Step one: mearure serum (plasma osmolaliry)-> If true (hypotonic, low osmolality), go to step two
  • Step two: Assess volum status if hypotonic/decreased osmolality to asses if hypovolemic cs euvolemic vs hypervolemic. If hypovolemic, go to step 3
  • Step 3: Urine doium concentration. Urine sodium under 10 indicates extrarenal losss of volume (GI, blood or third spacing volume loss) with preserved renal ability to hold onto sodium (water and electrolyre conservation. Urine sodium over 20mmol suggests renal loss of volume (diuretics, vomiting, cortisol deficiency and salt wasting nephropathies
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62
Q

Pance

Urine osmolality:
* What is going if the patient has low urine sodium and low urine osmolality?
* What is going on if the patient has high urine sodium and osmolality?

A
  • Low: primary polydipsia or reset osmostat
  • High: SIADH
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63
Q

Hyponatremia- Treatment Strategy
* What can you do not and why?
* Always treat what?

A
  • DO NOT RAISE SODIUM LEVEL MORE THAN 6-12 meq/L in the first 24 hours-> Can cause Central Pontine Myelinosis
  • ALWAYS TREAT UNDERLYING DISORDER (IF KNOWN)
64
Q

Hyponatremia- Treatment Strategy
* How do you treat hypovolemic, hypervolemic and euvolemic states?
* In emergency situations/severe hyponatremia with neuro deficits, txt how?

A
  • Hypovolemic- Normal saline 500-1000mL/hr until BP stable, then 200mL/hr while checking sodium frequently to ensure only rising about 0.5meq/hr
  • Hypervolemic- Fluid restriction, treat underlying cause. In special cases: may use albumin, paracentesis; hemodialysis is definitive
  • Euvolemic- NS (small bolus) & Free water restriction. Caution: in SIADH, saline may worsen due to retaining the free water. No free water intake
  • In emergency situations/severe hyponatremia with neuro deficits -> hypertonic saline 3% may be used in 100mL bolus
65
Q

SIADH
* What is it?
* What does ADH do?produced by? released by?

A
  • Syndrome of inappropriate antidiuretic hormone secretion (SIADH)-body makes too much antidiuretic hormone (ADH) – opposite to diabetes insipidus
  • ADH-helps the kidneys control the amount of water the body loses through the urine
    * Produced in the hypothalamus, released by the pituitary gland
66
Q

SIADH
* What does it cause the body to do? Not deficient in what?
* Low what?

A
67
Q
A
68
Q

SIADH Pathophysiology
* What is the plasma sodium concentration? What is the equation?

A
  • The plasma sodium concentration (PNa) is a function of the ratio of the body’s content of exchangeable sodium and potassium (NaEand KE) and total body water (TBW) as described by Edelman’s classic equation:
  • PNa ≈ (NaE+ KE)/Total body water
69
Q

SIADH Pathophysiology
* Antidiuretic hormone (ADH, arginine vasopressin) secretion results in what?
* In addition, the increase in TBW (total body water) transiently expands what?

A
  • Antidiuretic hormone (ADH, arginine vasopressin) secretion results in a concentrated urine and therefore a reduced urine volume. The higher the plasma ADH, the more concentrated the urine. In most patients with SIADH, ingestion of water does not adequately suppress ADH, and the urine remains concentrated. This leads to water retention, which increases TBW. This increase in TBW lowers the plasma sodium concentration by dilution.
  • In addition, the increase in TBW transiently expands the extracellular fluid volume and thereby triggers increased urinary sodium excretion, which both returns the extracellular fluid volume toward normal and further lowers the plasma sodium concentration.
70
Q

SIADH Pathophysiology
* Hyponatremia can occur in SIADH even if what?
* In SIADH, the urine sodium concentration is what? Serum potassium? Acid base distrubance? Serum uric acid?

A
  • Hyponatremia can occur in SIADH even if the only fluid given is isotonicsaline.
  • In SIADH, the urine sodium concentration is usually above 40 mEq/L, the serum potassium concentration is normal, there is no acid-base disturbance, and the serum uric acid concentration is frequently low
71
Q

SIADH Treatment
* Treat what?
* What about fluids? Salt?
* Severe tx?

A
  • Treat underlying cause (hypothyroidism/adrenal insufficiency or infection)
  • Fluid restriction (~800ml/day)
  • Oral salt tablets
    * IV NS is frequently used in clinical practice, but may cause worsening hyponatremia
  • Hypertonic saline (if severe, aka seizures)
72
Q

SIADH Treatment
* What else can be used to txt but usually for specialist? How does it work?

A

Vasopressin receptor antagonists
* Conivaptan (IV in hospitalized)
* Tolvaptan (oral in outpatient)
* Produce a selective water diuresis without affecting sodium and potassium excretion

73
Q

What are some causes of SIADH?(5)

A
74
Q
A
75
Q

Low Volume Hyponaturia:
* What are causes?
* What do you see clinical?

A
  • Renal loss via diuretics, ACEI, ARBs, Hypoaldosteronism
  • Extrarenal loss – bleeding, pancreatitis, burns, GI loss
  • Clinical – dry mucous membranes, poor turgor, flat neck veins, hypotension, elevated hematocrit and serum protein, increased BUN: creatinine ratio (>20:1) (i.e. prerenal azotemia)
76
Q

Low Volume Hyponaturia:
* What is the txt?

A

TX – you manage all of this with Normal Saline to correct the volume
* Until which point will your Na raise with NS in the setting of hyponatremia

77
Q

Euvolemia or Hypervolemia hyponaturia
* Normal causes? (4)
* What do you see clinical?
* What is the txt?

A
78
Q

Euvolemia or Hypervolemia hyponaturia:
* What are high causes?
* What do you see clinically?
* How do you tx it?

A
  • High – Causes – Nephrosis, CHF
  • Clinical – EDEMA – peripheral and presacral, pulmonary edema, jugular venous distention, HTN, decreased hematocrit, decreased serum protein, decreased BUN: creatinine ratio
  • TX – treat acute/chronic renal failure, restrict H2O and salt
79
Q

Diuretics
* Loop diuretics MOA? adverse effect?
* Thiazide MOA? adverse effect?
* Potassium sparing diuretics MOA? adverse effect?

A
  • Loop diuretics inhibit Na+, K+, Cl-, transport and Ca+ and Mg+ absorption. ADVERSE effect – decreased electrolytes “drain everything”
  • Thiazide diuretics –decrease urinary calcium excretion & Most likely among diuretics to causehyponatremia. ADVERSE effects – decreases kidney’s ability to produce dilute urine, causes hypokalemia, hypomagnesemia, hypochloremia. “drain everything bur calcium’’
  • Potassium sparing diuretics (Triamterene/Spironolactone/Eplerenone/ACEI/ARBs) – ADVERSE effect - hyperkalemia
80
Q

Hypokalemia:
* What is the definition?
* Results from what?
* What is the most common etiology

A
  • Definition – serum potassium level less than 3.5 mEq/L
  • Results from insufficient dietary potassium intake, intracellular shifting of K+ from extracellular space, extrarenal potassium loss, or renal potassium loss.
  • Most common etiology – GI loss in diarrheal/Vomitingdisease
81
Q

Hypokalemia
* May produce what sxs?
* Assoicated with low what?
* What requires urgent treatment?

A
  • May produce non-specific symptoms- palpitations, weakness, fatigue, depression, myalgias
  • Associated with low magnesium levels
  • Hypokalemia + Acidosis – profound K+ depletion and requires urgent treatment
82
Q

Hypokalemia
* Hypokalemia can be induced by what?
* Increase the likelihood of what toxicity?
* Loop diuretics causes what?

A
83
Q

Clinical Appearance/clues of hypokalemia:
* What are common sxs?(5)

A
  • Fatigue
  • Malaise
  • Muscle cramps
  • Muscle weakness
  • Constipation
84
Q

Clinical Appearance/clues of hypokalemia:
* What are the severe cases sxs?
* Hypertension may be present due what?
* Renal manifestations includes what?

A
  • Severe cases; hyporeflexia, paralysis, hypercapnia, tetany and rhabdomyolysis
  • Hypertension may be present due to aldosterone or mineralocorticoid excess
  • Renal manifestations include nephrogenic KI and interstitial nephritis

Hypokalemia assfectsmyscle contraction and cardiac conduction but does not cause seizures

85
Q

Lab Findings, ECG and Treatment of hypokalemia
* K+ is low as result of what?
* What can the ECG show?

A

K+ is low as a result of diarrhea, vomiting and inappropriately high with renal loss
ECG – may show decreased amplitude, broadening of T waves (earliest sign), prominent U waves, premature ventricular contractions, and depressed ST segments.

86
Q

Treatment of hypokal
* What can you give? What is the dose?
* Also correct what?

A

Oral potassium is safest route – typically K-dur
* Can administer 2 doses of 40mEq PO 1hr apart

May give K+ IV for severe deficiency (slow infusion,~20mEq/hr)

Also correct Magnesium

87
Q

What does this show?

A
  • Flat T waves
  • U waves are present
  • Torades at the end
  • All of these point to low K+
88
Q

When do you need to refer for hypokalemia?

A
89
Q

Hyperkalemia:
* What is the definition?
* 90% of potassium is secreted through what?
* Where is potassium in the body?
* What are the common causes?(2)

A
  • Definition – serum potassium greater than 5.0 mEq/L (in some laboratories 5.2)
  • 90% of potassium is secreted through the kidney
  • 98% intracellular while only 2% circulates in the blood
  • Most common cause is hemolysis, most common “real cause” is renal failure
90
Q

Hyperkalemia
* What are the three steps in management?

A
  • Stabilize the cardiac membrane
  • Shift potassium into cells
  • Remove potassium from the body
91
Q

Hyperkalemia:
* What are some other causes?
* What drugs can cause it?
* What can be normal even if the hyperkalemia is life threatening?
* More common in who?

A
92
Q

Clinical presentation of hyperkalemia:
s/s? (Dr. V notes)
* impairs what?
* What are the EKG changes?
* What are terminal events?

A

*MURDER
Muscle weakness, Urine production, Respirataory failure, decreased cardiac contractility, Early muscle twiching and cramps, Rythm changes
* Impairs neuromuscular transmission – causes muscle weakness (progressive ascending), flaccid paralysis and ileus (paralyzes intestinal muscles)
* Do NOT rely upon ECG to catch hyperkalemia, but changes include bradycardia, PR interval prolongation, peaked T waves, QRS widening and biphasic QRS-T complexes. BBB and AV block may occur.
* V fib and cardiac arrest are terminal events

93
Q

What does this show?

A

Bradycardia, wide QRS, P wave flat
* Hyperkal

94
Q

Prevention, treat and refer for hyperkal:
* What drugs need to be mointor?
* Repeat what?
* Cheak what and why?

A
  • ACE inhibitors, ARBs and spironolactone, potassium-sparing diuretics should be used cautiously in patients with heart and/or liver failure and kidney disease
  • Repeat labs, check plasma potassium
  • Check renal panel – rule out kidney dysfunction
95
Q

Prevention, Treat, Refer hyperkal
* Treatment is emergent in who?
* Hold what?
* Refer if what?

A
  • Treatment emergent in patients with cardiac hx.
  • Hold exogenous potassium
  • Refer if hyperkalemia from kidney disease and with renal potassium excretion - nephrologist
96
Q

What does everyone get first?
Next?
What is not given if kidney function is not normal?
If glucose is less than 300 give what?
What is the definitive treatment, but not for everyone?

A
97
Q

Calcium concentration:
* What is normal?
* What is necessary for what?
* The calcium-sensing receptor, is what? What happens if receptor is defected?

A
  • Normal – Total 8.5 – 10.5 mg/dL, Ionized 4.6 – 5.3 mg/dL
  • Necessary for muscle and nerve function
  • The calcium-sensing receptor, is a transmembrane protein and is located in the parathyroid gland and kidneys.
  • Functional defects in this receptor are associated with diseases of abnormal calcium metabolism
98
Q

Causes of hypocalcemia
* What are the most common causes?
* Decreased what?
* Increased what?
* _ disease

A
  • The most common causes are advanced Chronic Kidney Disease due to decreased production of active vitamin D3, low albumin, hypoparathyroidism
  • Decreased intake or absorption
  • Increased loss
  • Endocrine disease
99
Q

Clinical presentation of Hypocalcemia:
* Increases what?
* What are the classic signs (2)
* other signs? DrV slide

A
  • Increases excitation of nerve, muscle cells (because decrease excitation threhold) – spasm, cramps, tetany, laryngospasm with stridor, seizure, paresthesia, pain
  • Classic sign – “Chvostek Sign” : The increased irritability of the facial nerve, manifested by twitching of the ipsilateral facial muscles on percussion over the branches of thefacial nerve
  • Classic sign – “Trousseau Sign”: inflation os BP cuff above systolic BP for 3 mins causes painful carpal spasms->carpopedal latent tetany

  • CRAMPS: Confusion, Reflexes hyperative, Arrythmia (prolonged QT interval), Muscle spasms, Positive Trousseaus, Signs of Chvostek
100
Q

Treatment hypocalcemia:
* What are the severe symptomatic presentation?
* What is the txt?

A
  • Tetany, arrhythmias, or seizures
  • IV calcium gluconate, continuous infusion
101
Q

Txt of hypocalcemia:
* What is the txt for asymptomatic?
* Check what?
* What does not require replacement?

A
  • Oral calcium – 1-2 g and Vit D.
  • Typically, calcium carbonate
  • Check urinary excretion of calcium – too high and it impacts renal function
  • low Ca associated with hypoalbuminemia does not requires replacement
102
Q

When to Refer, When to Admit for hypocalcemia?

A
103
Q

Hypercalcemia:
* What are most of the causes? (2)
* Must look at what?
* May affect what?(3)

A
  • 90% - primary hyperparathyroidism and malignancy
  • Must look at duration and for a neoplasm
  • May affect kidney, GI and neuro function
104
Q

Hypercalcemia
* What are the sxs?(5)

A

Weakness, loss of reflexes, fatigue, constipation, polyuria, nausea, vomiting, anorexia, renal colic, nephrolithiasis
* Pance: Nephrolithiasis, bones-bone pain, fractures, abominal groans-ileus, constipation. Decreased DTR and weekness, psychic moans (depression, anxiety, vognitive dysfunction) and increased vascular tone (HTN)

105
Q

Hypercalcemia
* What are the labs? When do you need to adjuct calcium?
* If severe think what?
* ECG?
* CXR?

A
  • Lab – ionized calcium exceeds 1.32 mmol/L
    * Remember- adjust calcium by adding /subtracting 0.08mg/dL for every 1.0 g/L albumin above or below 4 g/L
  • Severe: Think malignancy
  • ECG – shortened QT interval
  • CXR – granulomatous disease or malignancy
106
Q

Fill in for causes of hypercalcemia

A
107
Q

Treatment of hypercalcemia:
* Identify what?
* IVF’s to do what?
* Do not use what?
* What is the choice for hypercalemia of malignancy?

A
  • Identify cause and treat cause
  • IVF’s to increase hydration to increase calciuresis
  • Don’t use thiazide diuretics to assist – may worsen
  • Bisphosphonates are treatment of choice for hypercalcemia of malignancy (may take up to 72 hours to reach full effect)
108
Q

Treatment of hypercalcemia
* Dialysis with low calcium, may need what?
* Refer based on what?
* Symptomatic or severe hypercalcemia require what?
* Suspected malignancy may require what?

A
  • Dialysis with low calcium dialysate may be needed.
  • Refer based on etiology
  • Symptomatic or severe hypercalcemia require immediate treatment
  • Suspected malignancy may require urgent, expediated evaluat
109
Q

Hypercalcemia:
* What is calciphylaxis?

A

Calciphylaxis, also known as calcific uremic arteriolopathy (CUA), is a serious and rare condition typically seen in patients with end-stage renal disease (ESRD) on dialysis, but it can also occur in patients with normal kidney function. It is characterized by the calcification of small and medium-sized blood vessels, leading to blood flow obstruction, tissue ischemia, and necrosis. Here are some key points about calciphylaxis:

110
Q

Phosphorus Concentration Disorders
* Phosphorus Concentration Disorders what?
* What are primary determinants? (3)
* What is the msot important regulator?

A
  • Plasma phosphorus represents a small fraction of total body phosphate (2%)
  • Primary determinants – renal excretion, intestinal absorption, shift between intracellular and extracellular spaces.
  • Kidney is the most important regulator
111
Q

Phosphorus Concentration Disorders
* Renal proximal tubular reabsorption of phosphate is decreased by what?
* Growth hormone increases what?
* Intimately related to what?

A
  • Renal proximal tubular reabsorption of phosphate is decreased by volume expansion, corticosteroids and proximal tubular dysfunction.
  • Growth hormone increased proximal tubular reabsorption.
  • Intimately related to calcium metabolism
112
Q

Hyperphosphatemia
* MCC is what?
* Clinical manifestions?
* If calcium not low?
* Treat with what?(4)

A

Hyperphosphatemia – most common cause is ESRD – tx with phosphate binders, calcium acetate, calcium carbonate, or Sevelamer, hydrate
* Clinical manifestations: Usually due to low calcium (tetany, prolonged QT on EKG)
* If calcium not low pathological calcifications
* Treated with low phosphorus diet, saline infusion/loop diuretics, calcium acetate (PhosLo), dialysis

113
Q

Hypophosphatemia
* What are causes?
* What is the MCC?
* What are the clinical manifestations?
* Treated with what?

A

Hypophosphatemia – Vitamin D deficiency, respiratory alkalosis (shifts PO4 intracellularly), excessive IV glucose, decreased GI absorption – tx with phosphate repletion
* Alcoholism = MCC
* Clinical manifestations: weakness, CHF, respiratory failure (all muscles need PO4 to function), seizures, coma, AMS
* Treated with oral phosphorus and/or IV (sodium phosphate or potassium phosphate)

114
Q

Disorders of Magnesium Concentration
* Normal plasma mag is what?
* How does it exist in the body?
* Excreted through what?
* Physiologic effects on the nervous system mimic what?

A
  • Normal plasma magnesium concentration is 1.8 – 3.0mg/dL
  • One third bound to protein and two-thirds existing as free cation.
  • Excreted through kidney
  • Physiologic effects on the nervous system mimic those of calcium.
115
Q

Disorders of Magnesium Concentration
* Who are best friends?
* Remember – serum Mag may be normal in what?

A
  • Mag and Calcium are best friends (and coexists with K)– if one is not right, more than likely the other will not be right.
  • Remember – serum Mag may be normal in mag depletions – check urine mag
116
Q

Hypomagnesemia
* Shares many etiologies with what?
* what also occurs from hypomagnemia?
* What will not work until you correct the hypomag?

A
  • Shares many etiologies with hypokalemia
  • Renal potassium wasting also occurs from hypomagnesemia
  • Potassium replacement will not work until you correct the hypomagnesemia.
117
Q

Hypomagnesemia
* What does is show clinically?
* What do the labs show?
* What does the EGC show?

A
  • weakness, cramps, neuromuscular and central nervous system hyperirritability, tremors, nystagmus, Babinski, HTN, Tachycardia and ventricular arrhythmias.
  • Lab – urinary excretion of magnesium exceeding 10-30 mg/day, hypocalcemia and hypokalemia are often present.
  • ECG may show prolonged QT interval, pTH secretion is often suppressed.
118
Q

Hypomagnesemia
* What is the txt?

A

IV Magnesium Sulfate(over 1-2hr; if infused over 15 mins – acts a soft tissue muscle relaxant)

119
Q

Hypermagnesemia:
* Often associated with what?
* What are sources of mag?
* What is used IV mag used for?
* Very easy to induce hypermagnesemia when ?

A
  • Often associated with advanced CKD and impaired magnesium excretion or chronic intake of mag containing drugs.
  • Folks forget antacids and laxatives are sources of mag.
  • IV Mag used for preeclampsia and eclampsia
  • Very easy to induce hypermagnesemia when attempting to replace in CKD
120
Q

Clinical Appearance of Hypermag:
* Common sxs??
* Less common sxs?
* What do the labs show?
* ECG?
* At are serious issues?

A
121
Q

Treatment of hypermag:
* Stop what?
* What do you give?
* What might you need?

A
  • Stop any source of Mag
  • Calcium antagonizes – give calcium chloride 500mg or more at rate of 100mg per minute.
  • May need Hemodialysis or peritoneal dialysis to remove mag – especially in severe CKD
122
Q

Glomerular Filtration Rate (GFR)
* What does it measure?
* Tradionally calculated by what?

A
123
Q

Glomerular Filtration Rate (GFR)
* In practice, how do we measure it?
* What does it reflect?

A
  • In practice, this is estimated through prediction equations for GFR based on serum creatinine using age, gender, and ethnicity
  • Reflects the ability of the kidneys to filter fluids and various substances, including medications.
124
Q

Fill in

A
125
Q

Blood Urea Nitrogen (BUN)
* What are normal findings? Higher in who?
* What is a critical value?
* Rough measurement of what?
* Urea is formed by what? Therefore can be used as what?

A
  • Normal findings 10-20mg/dL (slightly higher in elderly, slightly lower in children)
  • Critical value >100mg/dL
  • Rough measurement of renal function/GFR
  • Urea is formed by liver and therefore is also measurement of liver function
126
Q

Blood Urea Nitrogen (BUN)
* Interpreted in conjunction with what?
* Many causes of elevation including what?

A
  • Interpreted in conjunction with creatinine- ie BUN/creatinine ratio
  • Many causes of elevation including dehydration, shock, burns, CHF, GI bleeding, ureteral obstruction, primary renal disease, nephrotoxic drugs
127
Q

Creatinine
* What is the normal finding?
* What is the critical value?
* Catabolic product of what?
* Unlike BUN, aside from dehydration, what can cause an increase?

A
  • Normal findings- 0.5-1.2 mg/dL (varies by gender and age)
  • Critical value >4mg/dL
  • Catabolic product of creatine phosphate
  • Unlike BUN, aside from dehydration, only renal disorders and urinary obstruction will cause elevation in creatinine
128
Q

Creatinine
* There is some fluctuation with what?
* used to est what?

A
  • There is some fluctuation with muscle mass, protein consumption, age
  • Used to estimate glomerular filtration rate (GFR)
129
Q

What is in a BMP?

A
130
Q

Urinalysis:
* How should you collect it? When?
* What is gold stand in Dx of UTI <2?

A
  • Collect it midstream or by cath
  • First morning specimen: urine is more concentrated & contains higher levels of cellular elements & other components
  • Suprapubic aspiration is gold-standard in Dx of UTI <2yo (rarely done)
131
Q

Urinalysis
* When should you do the dipstick?
* What is microscopy for?
* What is a normal sediment called?

A
  • Dipstick within 30-60mins of collection followed by microscopy if dipstick has positives
  • Microscopy – centrifuged urinary sediment – looking for crystals, cells, casts and infectious organisms
  • A normal sediment (made of Tamm-Horsfall proteins) is termed “bland”
132
Q

Suprapubic Aspiration
* how do you this?

A
133
Q

Urinalysis- Appearance, color, odor
* What is normal color?
* What is bright yellow, orange, purple, red and brown?

A
  • Normal: clear
  • Color: Straw Yellow
  • Bright yellow – B2
  • Orange – Pyridium
  • Purple – UTI
  • Red – food coloring
  • Brown – Bile or AGN
134
Q

Urinalysis- Appearance, color, odor
* DKA smell?
* Fecal order?
* Foul odor?
* Ammonia odor?

A
  • DKA- sweet smell of acetone
  • Fecal odor- enterovesical fistula
  • Foul odor- UTI
  • Ammonia odor – prolonged retention within bladder (BOO/underactivity)
135
Q

Urine Volume
* What are normal urine volumes?
* Varies with what?

A
  • Normal urine volume is 750 to 2000 ml/24hr
  • Varies with state of hydration, metabolic state, hormonal influence
136
Q

Urine Volume
* Causes of polyuria and oliguria?

A
  • Polyuria: DM, DI, Diuretic use, Psychogenic
  • Oliguria (<30cc/hr): Pre-renal vs. Renal vs. Post-renal causes
137
Q

Urinalysis- pH
* What is normal?
* How do the kidneys maintain acid base balance?
* Changes based on what?
* UTIs or citrus fruits and increases what?
* Certain stones form in what?

A
138
Q

Urinalysis- Protein
* Normal value?
* Normally not present, why?
* Dipstick is sensitive to what? May miss what? What can you do to check for the missing ones?

A
  • Normal: 0-8 mg/dL; Proteinuria = 150mg/24hrs; Nephrosis = >3.5g/24hrs
  • Normally not present because the glomerular membrane openings are too small to allow them to pass through
  • Dipstick is sensitive to albumin; may miss small concentrations of γ-globulins and Bence Jones proteins
  • Sulfosalicylic acid test method is a more sensitive precipitation test. It can detect albumin, globulins, and Bence-Jones protein at low concentrations.
139
Q

Urinalysis- Protein
* Proteinuria is a common and important indicator of what?
* Tamm-Horsfall Protein is exclusively produced by what?
* Follow-up testing may include what?

A
  • Proteinuria is a common and important indicator of renal disease
  • Tamm-Horsfall Protein is exclusively produced by renal tubular cells of the distal loop of Henle and is the most abundant normal urinary protein
  • Follow-up testing may include 24-hour urine protein measurement and urine protein/creatinine ratio
140
Q
A
141
Q

Urinalysis- Glucose
* What is normal and why?
* When it is elevated?
* Glycosuria occurs when? What are some causes?

A
  • Normal: none, because it is always reabsorbed by proximal tubule
  • Elevated in hyperglycemia or glomerulus damage
  • Glycosuria occurs when filtered load of glucose exceeds ability of tubule to reabsorb it (180- 200 mg per dL) i.e. “renal threshold”
    * Etiologies include DM, Cushing’s syndrome, liver pancreatic disease, & Fanconi’s syndrome (tubular waste disease).
142
Q

Urinalysis- Specific Gravity
* What is normal?
* Measure of what?
* What does high and low mean?
* Always in comparison to what?

A
  • Normal: 1.010-1.030 (some sources say 1.005-1.030)
  • Measure of concentration of waste and electrolytes in the urine
  • High = concentrated urine, Low = dilute urine
  • Always in comparison to distilled water
143
Q

Urinalysis- Specific Gravity
* Evaluates what?
* Overhydration becomes what?
* What will have SG >1.035?

A
  • Evaluates concentrating power of kidney
  • Overhydration becomes dilute while dehydration becomes concentrated
  • Any high-density radiopaque dyes, high glucose or any contamination with have SG >1.035
144
Q

Urinalysis- Leukocyte Esterase
* What is normal?
* Screen to detect what?

A
  • Normal: none
  • Screen to detect leukocytes present in the urine
  • 90% accurate in predicting WBCs in the urine
145
Q

Urinalysis- Nitrites
* Normal?
* What will produce the enzyme reductase?
* Reductase reduces what?
* indicated what?
* Negative nitrites do not do what?

A
146
Q

Urinalysis- Ketones
* What is normal?
* Generally ketones consist of what?
* Indicated what?
* Only what is detected on UA dipstick?
* What is specific for DKA

A

Normal: none

Generally, Ketones consist of beta-hydroxybutyric acid (78%), acetoacetic acid (20%), and acetone (2%)
* Indicates that insulin is lacking and fatty tissue is being metabolized
* Only acetoacetic acid is detected on UA dipstick
* Only beta-hydroxybutyric acid is specific for DKA

147
Q

Urinalysis- Ketones
* Indicates what?
* In absence of what suggest starvation?
* Can also be elevated in other diseases of ketosis: list them
* Occasionally seen in what?

A
  • Indicates hyperglycemia/ poorly controlled DM (typically type 1)
  • In absence of glycosuria, ketone bodies suggest starvation
  • Can also be elevated in other diseases of ketosis: alcoholism, fasting/starvation/dehydration, isopropanol ingestion
  • Occasionally seen in febrile illnesses in children
148
Q

Urinalysis- Bilirubin & Urobilinogen
* What is normal?
* Conjugated with glucuronic acid (direct) bilirubin can be what? When can unconjugated not be excreted in urine?

A
  • Normal: none
  • Conjugated with glucuronic acid (direct) bilirubin can be excreted into the urine after conversion to urobilinogen in intestines and reabsorbed
    * Unconjugated or indirect is bound to albumin, and is therefore not water soluble and cannot be excreted in the urine
149
Q

Urinalysis- Bilirubin & Urobilinogen
* Elevation indicates what?
* Urobilinogen indicates what?
* Less important marker of what?

A
  • Elevation indicates disease of bilirubin metabolism after conjugation
  • Urobilinogen indicates overproduction of bilirubin
  • Less important marker of liver disease than serum levels
150
Q

Urinalysis- Crystals
* Normal:
* Uric acid crystal:
* Phosphate and calcium oxalate crystals:
* What is the concern with crystals?

A
  • Normal: none but are commonly seen
  • Uric acid crystals: think gout
  • Phosphate and calcium oxalate crystals: think parathyroid abnormalities, malabsorption
  • Concern with crystals is formation of stones
151
Q

Urine Sediment
* Casts form when?
* WBC/RBC casts only form where?
* What acts like glue for casts?
* When do cellular casts form?

A

Casts form when urine flow is slow or glomerulus is inflamed
* WBC/RBC casts only form in DCT and CD
* Tamm-Horsfall protein and albumin act like glue for casts

If there are many red or white blood cells in urine, cellular casts form.

152
Q

Urine Sediment
* What are the hallmarks of acute tubular necrosis?
* What can be seen with pyelonephritis and intersitial nephritis?
* What is highly suggestive of glomerulonephritis?

A
  • Pigmented granular casts (called Muddy Brown casts) + renal tubular epithelial cells alone or in casts are hallmarks of acute tubular necrosis
  • White blood cells + white blood cell casts + proteinuria can be seen with pyelonephritis and interstitial nephritis.
  • Protein + hematuria with acanthocytes + red blood cells casts – highly suggestive of glomerulonephritis
153
Q
A
154
Q

Hematuria:
* Clinically significant if there are what?
* What if there is no casts?
* What are the reasons for false + on dipstick?
*

A
  • Clinically significant if there are more than three red cells per high-power field on at least two occasions.
  • No casts? = Distal to kidney bleed
  • False positives on dipstick – myoglobin, oxidizing agents, beets, rhubarb, hydrochloric acid, bacteria, factitious.
155
Q

Hematuria
* Transient hematuria is common and less often a concern in who?
* Exercise-induced hematuria is a relatively common, benign condition often associated with what?

A
  • Transient hematuria is common and less often a concern in younger population due to lower concern for malignancy
  • Exercise-induced hematuria is a relatively common, benign condition often associated with long-distance running. Repeat urinalysis 48-72 hour later should be negative.
156
Q

Pyuria
* What is it? What does it indicate?
* What may contamine urine?
* WBC’s may be transiently increased during what?
* Leukocytes have what?

A
157
Q

Squamous Epithelial Cells
* What does it help you distinguish?
* What does transitional epithelial cell clumps indicate?
* When are renal tubular cells seen?

A

Clinical Medicine 3 (27 decks)

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