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Renal > Renal Exam 1 > Flashcards

Renal Exam 1 Flashcards

1
Q

Location of kidneys in comparison to vertebral bodies and ribs

A
  • Between vertebral bodies T12-L3

- Anterior to ribs 11/12

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2
Q

Contents of renal corpuscles

A
  • Glomerulus (tuft of capillaries) and Bowman’s (glomerular) capsule
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3
Q

Contents of cortical labyrinth

A
  • PCT, Loop of Henle, DCT
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4
Q

Contents of renal medulla

A
  • Loop of Henle, collecting ducts, papilla. Note: no glomeruli
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5
Q

Define arterial supply to kidneys and subsequent divisions

A
  • Renal = interlobar = arcuate = interlobular = afferent arteriole = efferent arteriole = peritubular capillary beds = vasa recta (specifically at Loop of H) —- venous (reversal of names)
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6
Q

Describe layers that make up the renal corpuscle from area of capillaries out

A
  1. Blood lumen
  2. Fenestrated endothelium
  3. Basement membrane (glomerular basement membrane): lamina rara, densa, rara
  4. Podocytes (visceral layer of Bowman’s) with pedicels that interdigitate. Slits between each process.
  5. Urinary space
  6. Parietal layer of Bowman’s
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7
Q

Function of mesangial (aka intraglomerular mesangial) cells

A
  • Contractile: control GFR

- Phagocytic: clear immune cell complexes, clean BM

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8
Q

Function of glomerular BM

A
  • Lamina rara: negatively charged (heparin sulfate) traps cationic molecules and repels anionic
  • Lamina densa: composed of collagen type IV, restricts movement of molecules greater than 70 Kda
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9
Q

Describe flow of filtrate (ultimately urine) starting at glomerulus

A
  • Glomerulus = PCT (proximal convoluted tubule) = descending Loop of Henle = ascending Loop of Henle = DCT (distal) = collecting duct = papillary duct (many collecting ducts converge on these) = renal papillae (many papillary ducts converge on these) = minor calcyx = major calyx = renal pelvis = ureters = bladder = urethra
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10
Q

Compare and contrast between epithelium of PCT, descending Loop of Henle, ascending Loop of Henle, DCT, collecting tubules/ducts and calyces / renal pelvis

A
  • PCT: low simple columnar (to cuboidal) epithelium w/microvilli (brush border) d/t need for resorption
  • Descending Loop (thick walled): simple cuboidal transitioning to simple squamous
  • Ascending Loop (thin walled): simple squamous
  • DCT: low simple columnar (to cuboidal) epithelium. Note: no brush border.
  • Collecting tubules/ducts: simple cuboidal epithelium
  • Calyces (minor/major) and renal pelvis: transitional epithelium
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11
Q

Location of JGA (juxtaglomerular apparatus)

A
  • Adjacent to DCT and afferent arteriole
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12
Q

Contents and function of JGA

A
  • JGA refers to: macula densa, JG cells, lacis cells
  • Overall: regulates BP and GFR
  • Macula densa: cells contained within DCT at vascular pole that sense NaCl concentration in filtrate
  • JG cells: cells at vascular pole, release renin
  • Lacis cells (aka extraglomerular mesangial cells): cells at vascular pole, resemble smooth muscle cells, play role in blood flow regulation
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13
Q

Where is macula densa always located in kidney?

A
  • At vascular pole of glomeruli
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14
Q

Define normal constriction of ureters where kidney stones may become lodged

A
  • Junction of renal pelvis with ureter
  • Where ureters cross pelvic brim
  • Junction of ureter into urinary bladder as it enters infero-medially where a flap valve is created preventing backflow of urine into ureter
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15
Q

In what pelvis does bladder lie?

A
  • Lesser pelvis (aka true pelvis)
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16
Q

Epithelial lining of bladder

A
  • Transitional epithelium
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17
Q

Where is internal urethral sphincter muscle located?

A
  • Within neck of bladder
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18
Q

Innervation of detrusor muscle

A
  • Detrusor = smooth muscle in walls of blader

- Innervation = PSNS

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19
Q

Describe micturition reflex and what controls it

A
  • Mnemonic = store and pee
  • Store: SNS increases tone of internal urethral sphincter in neck of bladder allowing for storage
  • Pee: PSNS relaxes/inhibits internal urethral sphincter in neck of bladder allowing for peeing
  • Somatic involvement of this reflex is present. Specifically through pubococcygeus muscle of levator ani. This muscle controls angle of neck of bladder with the urethra and provides voluntary control of urination together with external urinary sphincter muscle.
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20
Q

Parts of male urethra

A
  • Intramural (pre-prostatic): neck of bladder surrounded by internal urethral sphincter muscle
  • Prostatic
  • Membranous: w/external urethral sphincter
  • Spongy (penile)
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21
Q

Narrowest and least distensible part of male urethra

A
  • Membranous
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22
Q

Innervation of external urethral sphincter muscle? Function?

A
  • Pudendal nerve

- Voluntary urination

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23
Q

Difference between male and female internal urethral sphincter muscle

A
  • Females: not as well organized
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24
Q

Location of visceral afferent fibers conveying pain sensation from urinary system

A
  • T10-L2 via DRG
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25
Q

Where is referred pain for kidney stones that pass through ureter

A
  • Loin to groin (ipsilateral lower quadrant of anterior abdominal wall to groin)
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26
Q

List the major functions of the kidney

A
  1. Excretion of metabolic waste products and foreign substances
  2. Regulation of body fluids and electrolyte balance, acid-base balance and arterial BP
  3. Elaboration of endocrine hormones (EPO, final step in activating vit D3, renin)
  4. Gluconeogenesis
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27
Q

How is the renal circulation unique in terms of circulation?

A
  • Two capillary beds structured in series from each other: glomerular capillaries and peritubular capillaries, separated by efferent arteriole
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28
Q

Which nephrons assist in formation of concentrated urine?

A
  • Juxtamedullary nephron with their vasa recta
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29
Q

Steps in urine formation in the kidney

A
  1. Glomerular filtration
  2. Re-absorption
  3. Secretion
  4. Excretion = filtration – reabsorption + secretion
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30
Q

Where in the nephron does the reabsorption of each of the following occur: glucose, amino acids, water, Na, Cl and K?

A
  • Glucose: 99% reabsorbed at PCT
  • Amino acids: 99% reabsorbed at PCT
  • Water: PCT, descending limb, DCT and collecting duct. Not ascending limb that is impermeable to water
  • Na: PCT (up to 70%)!&raquo_space; ascending limb > DCT and collecting duct where reabsorption fine tuning is done
  • Cl: PCT (up to 70%)&raquo_space; ascending limb > DCT ??
  • K: PCT (up to 70%)&raquo_space; ascending limb. DCT and collecting duct is where secretion or re-absorption can occur.
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31
Q

Where in the nephron does the counter current multiplication occur?

A
  • Loop of Henle
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32
Q

Where in the nephron does the counter current exchange occur?

A
  • Vasa recta
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33
Q

Where in the nephron does aldosterone have its effect? What is the effect?

A
  • Distal part of DCT which is the cortical collecting tubule at the principle cell
  • Increases Na reabsorption and K secretion
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34
Q

Where in the nephron does ADH have its effect? What is the effect?

A
  • Collecting tubule

- Increase permeability of collecting tubule to water = increase water reabsorption and less H2o excreted

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35
Q

Describe renal control of acid-base balance

A
  • HCO3- excretion leads to bases being removed from blood.
  • H+ are secreted into lumen by epithelium of tubule leading to acid being removed from blood.
  • If more H secreted than bicarb filtered, net loss of acid. If more bicarb filtered than H secreted, there will be net loss of base
  • Alkalosis: kidney will not re-absorb filtered bicarb increasing bicarb excretion leading to production of more bicarb and proton to drive acid production
  • Acidosis: kidney re-absorbs filtered bicarb decreasing excretion leading to drive that reduces acid accumulation
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36
Q

Explain forces governing glomerular filtration and tubular reabsorption

A
  • Net filtration pressure = sum of hydrostatic forces/pressure and colloid osmotic forces/pressure = glomerular hydrostatic pressure – Bowman’s capsule pressure – glomerular oncotic pressure. Note: glomerular hydrostatic pressure favors filtration while glomerular colloid osmotic pressure and Bowman’s capsule pressure oppose filtration.
  • Glomerular capillary filtration fraction coefficient (three layer barrier between the blood lumen and the urinary space)
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37
Q

Explain the effect of size and charge on the glomerular filtration. How does this change when a disease process causes the loss of the filtration barrier of the glomerulus?

A
  • Negatively charged BM impedes movement of both negatively charged and large (> 70 Kda) substances including proteins into glomerular filtrate. Increased permeability leads to protein entry into filtrate. This is seen in nephrotic syndrome. Proteinuria = reduced colloid oncotic pressure = edema and reduced plasma volume.
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38
Q

How is GFR affected by vasoconstriction of afferent arteriole? Vasodilation?

A
  • Vasoconstriction = decreased GFR

- Vasodilation = increased GFR

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39
Q

How is GFR affected by vasoconstriction of efferent arteriole? Vasodilation?

A
  • Vasoconstriction = increased GFR

- Vasodilation = decreased GFR

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40
Q

Ability for kidney to form urine that is more concentration than the plasma is essential for survival of mammals on land. What are the requirements for this?

A
  1. High osmolarity of renal medullary interstitial fluid

2. High level of ADH

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41
Q

Describe mechanisms for producing a hyperosmotic renal medulla

A

See SG for explanation

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42
Q

Describe how ADH is released

A
  • ADH: Increase in fluid osmolality surrounding osmoreceptors in hypothalamus leads to them shrinking. Shrinkage signals supraoptic nuclei to release ADH (posterior pituitary).
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43
Q

Describe mechanisms for release of renin

A
  1. Baroreceptor: increased pressure in afferent arteriole inhibits renin release, decreased pressure promotes renin release
  2. SNS: beta-1 adrenergic nerves stimulate renin release
  3. Macula densa: increased NaCl in distal nephron inhibits renin release; decreased NaCl promotes renin release
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44
Q

Function of renin downstream

A
  • Renin cleaves angiotensinogen into ang I
  • Ang I is converted into ang II via ACE
  • Ang II: vasoconstriction, renal retention of salt & water and stimulates aldosterone release
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45
Q

Effect of increased renal SNS nerve activity

A
  • Reduction in GFR by constriction of renal arterioles
  • Increase in tubular Na reabsorption
  • Increase in renin release
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46
Q

Why do we care about renal clearance?

A
  • Quantifies the excretory function of the kidneys.
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47
Q

How is GFR measured?

A
  • GFR = [Vdot x U(x)] / P(x)
  • Vdot = urine flow rate
  • U(x) = urine concentration of X
  • P(x) = plasma concentration of X
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48
Q

Explain why the clearance of creatinine is a reasonable estimate of GFR. Is Cr absorbed or secreted?

A
  • Creatinine is cleared almost entirely by glomerular filtration. Cr is freely filtered with a small amount secreted, so calculation is a slight over-estimation.
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49
Q

Explain why clearance of PAH (para-amino hippurate) is a measure of effect renal plasma flow rate.

A
  • Renal plasma flow: if substance is completely cleared from plasma, the clearance rate of that substance is equal to the total renal plasma flow
  • RPF = [U(s) x V] / P(s)
  • Waiting for Di Sole
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50
Q

What is filtration fraction? Calculate FF if given GFR and RPF. The FF is usually about what percentage of the renal plasma flow?

A
  • FF = fraction of RPF that is filtered into Bowman’s capsule at glomerulus.
  • FF = GFR / RPF.
  • FF is usually about 20% of GFR
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51
Q

Which factors are needed to calculate a patient’s GFR using Cockroft-Gault formula. What factors are needed to use the modification of diet in renal disease (MDRD) study formula for calculating GFR?

A
  1. Cockcroft-Gault: Age, body weight, plasma creatinine, gender
    - Equation Ccr = (140 – Age) x body weight (kg) / 72 x Pcr (mg/dl). Multiply x 0.85 for females.
  2. MDRD: Plasma creatinine, age, AA, gender
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52
Q

How can abnormalities in kidney function cause HTN?

A
  • Increase vascular resistance, decreased glomerular capillary filtration fraction coefficient, excessive tubular sodium re-absorption
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53
Q

Causes and effects of AKI (acute kidney injury)

A
  • AKI = sudden decrease in kidney function or damage (few hours or days) indicated by rapid decline in GFR
  • Causes:
    a. Pre-renal: kidney hypoperfusion
    b. Renal: vascular, glomerular, tubular or interstitial problems
    c. Post-renal: UT obstruction
  • Effect: water/hypernatremia (edema, HTN), hyperkalemia, metabolic acidosis, anuria
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54
Q

Define chronic kidney disease (CKD).

A
  • Progressive and irreversible loss of large number of nephrons. Clinical sx appear until nephrons fall to 75% below normal.
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55
Q

Three ways which body can regulate pH. Over what time frames does each operate?

A
  1. Bicarbonate buffer system: almost instantaneous
  2. Respiratory compensation: regulates PCO2 in matter of hours
  3. Renal compensation: regulates bicarb concentration and H excretion in matter of days
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56
Q

Define Henderson-Hasselbach equation to determine pH in the body

A
  • pH = 6.1 + log[(HCO3-)/0.03PCO2]
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57
Q

What effect does normal metabolism have upon acid-base balance?

A
  • Oxidation of nutrients generates CO2
  • Oxidation of methionine/cysteine and other sulfur-containing compounds generate sulfuric acid
  • Phosphate-containing compounds are consumed that form phosphoric acid
  • Metabolism of glutamate and aspartate forms bases
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58
Q

Do protons leave the body as free H? Explain.

A
  • Cannot leave as free H d/t limiting urine pH. Removed by binding to HPO4- (leaves as H2PO4) and NH3 (leaves as NH4+)
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59
Q

How are hydrogen ions secreted into tubular lumen?

A
  1. Proximal acidification: PCT
    - Na/K ATPase sets up energy gradient. Na/H secondary active antiporter moves H out into tubular lumen and Na comes back in.
  2. Distal acidification: DCT and collecting ducts
    - Low pH stimulates insertion of H/ATPase into luminal membrane, which moves H out into tubular lumen.
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60
Q

Describe the reabsorption of bicarbonate.

A
  • Virtually all reabsorbed (90% in PCT, 10% in collecting duct)
  • Proximal tubule: H+ in tubular lumen reacts with HCO3- to form H2CO3, which is broken down by carbonic anhydrase into water and CO2. These enter into tubular cell where they are formed back into H2CO3 via another carbonic anhydrase isoform. They dissociate into HCO3- and H+. HCO3- moves back into peritubular capillary with Na via symporter. Note: Na entered from tubular lumen via Na/H antiporter. Net = movement of NaHCO3 from filtrate to blood.
  • Collecting duct: Same as above (except H+ present in tubular lumen d/t H/ATPase). HCO3- exits renal tubular cell via HCO3-/Cl- antiporter.
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61
Q

Is bicarbonate always reabsorbed? Can it be excreted?

A
  • In metabolic alkaloses, bicarb can be actively secreted. This is accomplished by B-type intercalated cells of collecting duct.
  • Here, the cell reverses the polarity of the H/ATPase and bicarb/Cl antiporter to peritubular and tubular lumen respectively. Now proton reabsorbed into peritubular capillary and bicarb excreted.
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62
Q

Why does excretion of free H make a minimal contribution to pH regulation? What is meant by limiting urine pH?

A
  • H/ATPase stimulated by high acid load can raise the proton concentration in filtrate to a max vaue of 0.04 mmol/L, corresponding to urine pH of 4.4. At this pH, the transporter is inhibited. This is referred to as the limiting urine pH. The daily acid load is much higher than what can be eliminated using this method. Excretion of proton takes place therefore by H2Po4 and NH4+.
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63
Q

What is the role of phosphate in the excretion of H ions? Explain how this works.

A
  • Filtered HPO4- binds to proton and is excreted in urine. Each time this occurs, one H+ is eliminated and one new HCO3- is formed and added to blood. This corrects as acidosis.
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64
Q

Define titratable acid and describe how it is measured.

A
  • Titratable acid is the measure of protons excreted in urine as un-dissociated weak acid. The most abundant one is H2PO4.
  • Measured: Do 24 hr urine collection, measure amount of NaOH required to back-titrate urine pH to 7.4.
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65
Q

What is the role of NH4+ in the excretion of H ions? How are glutaminase and glutamate DH involved in this process?

A
  • NH4+ is a means to remove proton from the body in response to severe acidosis.
  • Glutamine converted to glutamate via glutaminase, which generates NH4+. Glutamate is converted to alpha-ketoglutarate by glutamate DH, which yields a second NH4+. When H+ combines with NH3 and excreted as NH4+, HCO3- is released to the blood. Net effect = 2 HCO3- added to blood.
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66
Q

What regulates the rate of H secretion by renal tubular cells?

A
  • pH dependent

- Low pH activates Na/H antiporter and H/ATPase

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67
Q

List what happens in kidney during acidosis

A
  • H+ secretion increases, all bicarb reabsorbed, titratable acid excreted in form of H2PO4, NH4+ production/excretion increased
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68
Q

List what happens in kidney during alkalosis

A
  • HCO3- secreted in urine via B-type intercalated cells of collecting duct
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69
Q

Normal lab values for arterial PCO2, arterial pH, arterial bicarb, urinary titratable acid, urinary ammonium ion

A
  • Arterial PCO2: 40 torr
  • Arterial pH: 7.35 – 7.45
  • Arterial bicarb: 24 mmol/L (rarely measured)
  • Urinary titratable acid: 0-20 mmol/day. Up to 40 seen in acidosis
  • Urinary ammonium ion: 20-40 meq/day. Upon to 250 seen in acidosis
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70
Q

Define anion gap. How is it calculated? What conditions might produce a large anion gap?

A
  • Difference between primary measured cations and anions in serum. Commonly performed in patients who present with AMS, unknown exposures, acute renal failure and acute illnesses.
  • Calculated: [Na plasma] – [Bicarb plasma] + [Cl plasma]
  • Normal = 8-12 meq/L
  • Large gap d/t ingestion of production of fixed acid
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71
Q

Define base deficit.

A
  • Difference between measured bicarb concentration and bicarb concentration predicted by normal buffer slope at that pH given buffering/compensation.
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72
Q

View cases from L5

A

View cases from L5

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73
Q

Who are more at risk for urolithiases?

A
  • Men, elderly until age 60, history
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74
Q

Primary CT signs of ureteral obstructions d/t stones

A
  • Stone seen in ureter on symptomatic side, inspected along course, with soft tissue rim sign (ureteral wall edema surrounding stone)
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75
Q

Secondary CT signs of ureteral obstructions d/t stones

A
  • Perinephric stranding (edema): non-crisp kidney border, collecting system dilation, ureteral dilation, nephromegaly, decreased enhancement
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76
Q

What is the first line choice in workup of flank pain suspicious for urinary calculi?

A
  • Non-contrast CT

- US appropriate in pregnant population

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77
Q

First line imaging test in patient with unexplained hematuria or renal dysfunction

A
  • Ultrasound
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78
Q

Major method for imaging and characterizing cystic and solid renal lesions

A
  • CT w/ and w/o contrast
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79
Q

Most common renal mass

A
  • Simple cyst
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80
Q

Does CT or US have better sensitivity for detecting solid mass?

A
  • CT. 95% compared to 77%
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81
Q

Define attenuation. Define enhancement?

A
  • Attenuation: Decrease in intensity of x-ray beam caused by absorption of photons in tissue. Air (very black)
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82
Q

How do you differentiate between a complicated cyst in the kidney vs a renal cell carcinoma?

A
  • Can be indistinguishable
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83
Q

US is most cost effective method of defining and confirming a benign cyst. What are the properties of a simple cyst on US?

A
  • Sonolucent (aka anechoic), demonstrates enhancing through transmission, thin/almost imperceptible wall
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84
Q

Properties of a simple cyst on CT

A
  • HU
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85
Q

Features that makes a cyst non-simple?

A
  • Calcification, hyperattenuation on CT (> 20 HU), septations, multiloculated, nodularity, thick wall/septations (> 2mm), enhancement on CT (> 15)
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86
Q

Bosniak classification of cystic masses. What is management (workup / follow up)?

A
  • I: thin walls, fluid with water attenuation, no septa, no calcifications. Benign, no imaging follow-up.
  • II: benign, thin septa, fine/linear calcifications in walls/septa, minimal wall / septal enhancement is sometimes present. Almost all benign. If hyperattenuating > 3 cm, followup, otherwise no imaging f/u.
  • IIF: more complex with further increase in septa and calcifications, may be thicker and more nodular, enhancement may be present but not in tissue in which calcification is present. Majority benign. May need additional imaging/followup.
  • III: indeterminate for benignity or malignancy, thick/irregular walls or septa +/- calcifications, wall or septal enhancement can be clearly appreciated. Close followup, many will require surgical excision.
  • IV: malignant thick irregular enhancing walls or septa containing small or large amounts of calcium, soft tissue enhancement may extend from walls or septa. Surgical excision.
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87
Q

Most common primary solid renal tumor

A
  • Renal cell carcinoma. Note: increased incidence in VHL disease.
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88
Q

What condition are angiomyolipomas associated with?

A
  • Tuberous sclerosis. Note: angiomyolipomas are benign.
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89
Q

How are renal masses characterized?

A
  • Shape (tumefactive aka ball, infiltrative), composition, epicenter
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90
Q

Compare and contrast what the findings are for tumefactive vs infiltrative renal masses

A
  • Tumefactive (aka ball): CYST, RENAL CELL CARCINOMA, angiomyolipoma, oncocytoma, metastases, abscess
  • Infiltrative: infiltrating tumor (TRANSITIONAL CELL CARCINOMA, scc, lymphoma, RCC (ball-like) rarely!, metastases), infection (focal pylenonephritis), infarction
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91
Q

What imaging will detect fat in renal mass?

A
  • Non-contrast CT

- US cannot always

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92
Q

Imaging characteristics of transitional cell carcinoma?

A
  • Shape: infiltrative
  • Composition: soft tissue
  • Epicenter: renal sinus
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93
Q

Imaging characteristics of renal cell carcinoma?

A
  • Shape: tumefactive
  • Composition: soft tissue
  • Epicenter: parenchymal
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94
Q

Define an adrenal incidentaloma

A
  • Incidental adrenal mass discovered on imaging study obtained for other reasons with no overt sign of adrenal hyperfunctioning.
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95
Q

Risk of malignancy of adrenal incidentalomas

A
  • 1 in 1 million w/ rate of metastatic dz 1%

- If you called every adrenal incidentaloma

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96
Q

Size cutoff for adrenal incidentaloma vs malignancy

A
  • 3 cm: 95% malignant.
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97
Q

Describe workup of > 6cm, 3-6 cm and

A
  • > 6 cm = surgery
  • 3-6 cm = surgery biopsy or other imaging

-

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98
Q

Define enhancement between adenomas and malignancy/metastases

A
  • 60% or more washout (ie. rapid washout) = adenoma
  • Lower washout (ie. slow washout) = more chance of met/malignancy
  • Note: generally
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99
Q

Best test for determining whether an incidental adrenal mass is an adenoma?

A
  • CT scan with pre and post contrast delayed imaging
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100
Q

F/u of benign adrenal adenoma

A
  • Once it is determine to be a benign adenoma without hyperfunction, forget out it. Don’t have to repeatedly image.
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101
Q

Types of renal congenital defects. Describe each.

A
  • Agenesis: kidneys fail to differentiate and are absent, enlarged adrenals seen, incompatible with life if bilateral (commonly)
  • Hypoplasia: failure of kidneys to develop into normal size, UNILATERAL
  • Ectopic: kidney in another location, usually above pelvic brim, KINKING OR TORTUOSITY OF URETER MAY OCCUR PREDISPOSING TO INFECTION
  • Horseshoe: common, increased chance for infection, compatible with life
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102
Q

Kidney cystic diseases

A
  • ADPKD (Autosomal Dominant Polycystic Kidney Disease)
  • ARPKD (Autosomal Recessive PKD)
  • Acquired cystic disease (dialysis associated)
  • Simple cysts
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103
Q

Mutations involved in ADPKD

A
  • PKD1 or PKD2
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104
Q

What is ADPKD?

A
  • Multiple expanding cysts in kidney that eventually destroy them by 50s when renal failure occur. It is the 4th leading cause of ESRD.
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105
Q

In patient with ADPKD, what else should they be checked for?

A
  • Hepatic cysts, splenic cysts and berry aneurysms (Circle of Willis) resulting in SAH in ~10% of patients.
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106
Q

Gross appearance of kidneys in ADPKD

A
  • Grossly enlarged, multiple cysts containing blood, no recognizable kidney tissue
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107
Q

In what age group is ADPKD seen typically?

A
  • ADults (mnemonic: AD)
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108
Q

In what age group is ARPKD seen typically?

A
  • Childhood
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109
Q

Mutation(s) involved in ARPKD

A
  • PKHD1 (PKHD = polycystic kidney and hepatic disease)
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110
Q

Gross appearance of kidneys in ARPKD

A
  • Hugh, white, smooth-surfaced kidneys at birth with cysts 1-2 mm developing from collecting ducts
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111
Q

What else should ARPKD patients be checked for?

A
  • Hepatic fibrosis that is congenital
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112
Q

Compare and contrast: focal vs diffuse and global vs segmental in terms of renal pathology

A
  • Focal = 50% of glomeruli

- Global = whole glomerulus; segmental = portion of glomerulus

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113
Q

Immunoglobulins present and not present in glomerular disease

A
  • GAM present

- Not ED. Mnemonic: don’t want your friends to get ED.

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114
Q

Pathogenesis of glomerular disease

A
  • Antibodies against native GBM, antibodies against planted antigens, trapping of ag-ab complexes, antibodies against glomerular cells, cell mediated immunity
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115
Q

3 main clinical renal syndromes. Define where injury is and main clinical Ssx?

A

**

  • Nephritic syndrome: breaks in glomerular capillary loops. Sx = hematuria, HTN, RBC casts. Renal failure can happen, in which case it is called acute nephritic syndrome.
  • Nephrotic syndrome: defects in glomerular filtration, with podocyte processes effaced. Sx = severe proteinuria (> 3.5 g/24 hr), hypoalbuminemia (edema), fatty casts
  • Acute renal failure: tubular injury. Sx = oliguria and rapid rise in serum Cr.
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116
Q

Gross and microscopic findings of chronic renal failure

A
  • Note: results from untreated on unresponsive nephrotic syndrome/nephritic syndrome or acute renal failure
    1. Gross: kidneys small, cortex thinned, increased pelvic fat
    2. Micro: glomerular sclerosis, interstitial fibrosis, tubular atrophy
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117
Q

Causes of nephrotic syndrome

A
  1. Primary = minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, membranoproliferative glomerulonephritis (MPGN)
  2. Secondary = diabetic nephropathy, SLE, amyloidosis
  3. Other systemic disorders: DM, amyloidosis, SLE, drugs, infection, malignancies
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118
Q

What is the most common cause of nephrotic syndrome in children 2-6 yo?

A
  • Minimal change dz (MCD aka minimal change glomerulopathy / lipoid nephrosis)
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119
Q

What is minimal change disease?

A
  • Glomerular disease. One of causes of nephrotic syndrome and most common cause of this in children 2-6 yo.
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120
Q

Microscopic findings (LM, IF and EM) in MCD

A
  • LM: normal, maybe lipid in tubular cells *different to FSGS
  • IF: normal
  • EM: diffuse epithelial foot process effacement *like FSGS
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121
Q

Tx of MCD

A
  • Almost always responsive to steroids
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122
Q

What is focal segmental glomerulosclerosis (FSGS)? Causes? Describe morphologic course?

A
  • What? Progressive glomerular scarring (fibrosis) disease that leads to nephrotic syndrome. Has some nephritic syndrome components (HTN often, microscopic hematuria).
  • Causes: 80% idiopathic, other = virus associated (incl. HIV), drug associated (incl. HEROIN), genetic, hemodynamic adaptations
  • Morphologic course: Early in disease, glomerulosclerosis = focal and segmental. Late in disease, becomes diffuse and global.
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123
Q

Microscopic findings (LM, IF and EM) in FSGS

A
  • LM: segmental sclerosis (“hyalinosis”) if early stage *different to MCD
  • IF: mild IgM and C3 or negative *different to MCD
  • EM: diffuse epithelial cell injury (foot process effacement)* like MCD
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124
Q

Tx of FSGS

A
  • Responds to steroids variable
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125
Q

What is membranous glomerulopathy (aka membranous nephropathy/glomerulonephritis)?

A
  • Glomerular disease with deposition of Ag-Ab complexes that leads to nephrotic syndrome.
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126
Q

Microscopic findings (LM, IF and EM) in membranous glomerulopathy (aka membranous nephropathy/glomerulnephritis)?

A
  • LM: thickened stiff capillary walls (SPIKES) on silver stain
  • IF: GRANULAR IgG and C3 along glomerular BM
  • EM: subepithelial deposits of ab/ag complex
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127
Q

What is membranoproliferative glomerulonephritis (MPGN)? Type 1 vs type 2? Cause? Tx?

A
  • What: Slow progressive glomerular disease that leads to nephrotic syndrome with a nephritic component (hematuria). 50% progresses to CRF within 10 years.
  • Type 1: subendothelial deposits present + mesangial hypercellularity (increase in number). Cause = idiopathic or 2ndary to chronic immune complex disorders (SLE, hep B/C, etc.)
  • Type 2: intramembranous deposits present + mesangial hypercellularity (increase in number). Cause = 70% have C3 nephritic factor (C3NeF – an autoantibody which stabilizes C3 convertase) stopping enzymatic degradation of C3 and leading to persistent C3 activation. Therefore low serum C3 seen.
  • Tx: No treatment effective (steroids and immunosuppressives).
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128
Q

Microscopic findings (LM, IF and EM) in MPGN type 1?

A
  • LM: thickening of GBM (TRAM TRACKS) seen with silver stain
  • IF: granular C3 (often with IgG) *only C3 in MPGN type 2
  • EM: SUBENDOTHELIAL and mesangial deposits – between endothelial and GBM
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129
Q

Microscopic findings (LM, IF and EM) in MPGN type 2?

A
  • LM: thickening of GBM (TRAM TRACKS) seen with silver stain
  • IF: granular C3 only! *with IgG in MPGN type 1
  • EM: INTRAMEMBRANOUS deposits within lamina densa of GBM
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130
Q

In what MPGN disease is low serum C3 seen?

A
  • MPGN type 2
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131
Q

What is acute nephritic syndrome?

A
  • Nephritic syndrome + renal failure
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132
Q

Pathological conditions / change seen in acute nephritic syndrome? Diseases seen with each change?

A
  1. Diffuse proliferative glomerulonephritis: acute post-strep GN
  2. Crescentic glomerulonephritis: Goodpasture’s dz, Lupus nephritis, ANCA-associated diseases
    * These aren’t diseases per se, but describe pathological changes and are associated with specific disease.
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133
Q

What is acute post-infectious GN (pka acute post-strep GN). Cause? Who is affected? SSx? Lab findings? Tx? Microscopic findings on LM, IF and EM?

A
  • What: This is an acute nephritic syndrome occurring 1-3 weeks following infection.
  • Cause: infectious (strep, staph, pneumococcus etc.). Typically seen with strep.
  • Affected: children
  • SSx: Hematuria, azotemia, oliguria, HTN
  • Lab findings: low C3, ASO (anti-streptolysin O abs) titer serially elevated
  • Morpho findings
    a. LM = diffuse proliferative GN (mesangial and endothelium) with NEUTROPHILS (acute)
    b. IF: scattered (STARRY SKY) IgG, IgM and C3 along GBM AND IN MESANGIUM
    c. EM: subepithelial HUMPS, which is IgG, IgM and C3 focally
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134
Q

What is crescenteric glomerulonephritis? Causes? What are the components of the crescents?

A
  • What: Glomerular disease where glomerular crescents are formed leading to severe renal failure and death if untreated.
  • Causes: type I, II or III – see subsequent flash cards for diseases associated with these
  • Components: anti-GBM abs (eg. Anti-fibrinogen), immune complexes, anti-PMN abs, fibrin forms leading to proliferation of epithelial cells, influx of monocytes and macrophages.
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135
Q

Type I crescenteric glomerulonephritis causes. Lab findings? Tx?

A
  • Goodpasture’s disease (aka anti-GBM disease): autoimmune dz with production of abs against collagen IV in BM of glomerulus, lungs etc. Results in vasculitis esp. in lungs and kidneys causing a pulmonary-renal syndrome.
  • Labs: anti-GBM ab elevated
  • Tx: high dose steroids, cytotoxic agents, plasmapheresis
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136
Q

Type II crescenteric glomerulonephritis causes. Lab findings? Tx?

A
  • Lupus nephritis: SLE where kidney is affected by deposition of all immunoglobulin GAM + C3/4. Lab findings = anti-dsDNA ab etc.
  • IgA nephropathy (aka Berger dz): asymptomatic isolated hematuria (sometimes with mild proteinuria). It is the most common type of primary GN worldwide. Affects children and non-AA young adults (commonly).
  • Henoch-Schönlein purpura
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137
Q

Type III crescenteric glomerulonephritis cause

A
  • ANCA-associated disease (eg. Wegener’s granulomatosis): group of vasculitis disorders esp. affecting small vessels and can cause pulmonary-renal syndrome. ANCA (anti-neutrophil cytoplasmic antibody).
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138
Q

IF findings for type I crescenteric GN

A
  • Type I = Goodpasture’s disease
  • IF findings: linear capillary loop IgG (CIGARETTE SMOKE): capillary loops in glomerulus are outlined by linear anti-GBM ab
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139
Q

IF findings for type II crescenteric GN

A
  • Type II = Lupus nephritis, IgA nephropathy, Henoch-Schönlein purpura
  • IF findings: granular deposits of immunoglobulin in mesangium or capillary loops (LUMP-BUMPY)
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140
Q

IF findings for type III crescenteric GN

A
  • Type III = ANCA-associated disease (eg. Wegener’s granulomatosis)
  • IF findings: absent or minimal
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141
Q

Microscopic findings (LM, IF, EM) in IgA nephropathy?

A
  • LM: mesangial proliferation (> 3 per region)
  • IF: mesangial IgA
  • EM: mesangial deposits
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142
Q

What diseases causes asymptomatic isolated hematuria?

A
  1. IgA nephropathy
  2. Alport syndrome (hereditary)
  3. Thin GBM disease (hereditary)
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143
Q

What is the most common type of primary GN worldwide?

A
  • IgA nephropathy
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144
Q

What is Alport syndrome? Which group is affected? SSx? Microscopic morphology seen?

A
  • What: genetic defect (X-linked dominant with incomplete penetrance) of glomerular basement membrane d/t mutation in gene encoding alpha-4 chain of collagen type IV. **Don’t confuse with Goodpasture’s, which is autoimmune dz with abs against GBM, specifically type IV collagen.
  • Group: affects males, females carriers (incomplete penetrance)
  • SSx: SENSORINEURAL DEAFNESS, microscopic hematuria, progresses to renal failure (progression noted by proteinuria)
  • Microscopy: GBM thickening, splitting and lamination (BASKET-WEAVE PATTERN)
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145
Q

Microscopic findings (LM, IF and EM) seen in thin-GBM disease

A
  • LM: normal
  • IF: negative
  • EM: thin GBM
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146
Q

What is the only glomerular disease with deposition of all Igs?

A
  • Lupus nephritis. Deposition of GAM w/C3 and 4
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147
Q

Pathology findings in amyloidosis glomerulonephropathies

A
  • Congo red shows apple-green birefringence under polarized light
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148
Q

What is acute tubular necrosis (ANT)? Etiologies

A
  • Destruction of renal tubular epithelium leading to loss of renal function.
  • Two types:
    1. Ischemia: shock
    2. Nephrotoxic: drugs, heavy metals, organic solvents, radiocontrast dyes, myoglobin (rhabdo)
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149
Q

Microscopic findings in ANT

A
  • Necrotic debris in tubules, dilated tubules with flattened epithelium
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150
Q

Drugs that can cause acute interstitial nephritis. SSx / presentation.

A
  • Synthetic penicillins, rifampin, ibuprofen, thiazide diuretics.
  • SSx: 2 weeks following use of these meds = fever, eosinophilia, rash and acute renal failure (oliguria + increased Cr)
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151
Q

Most common pathogen responsible for acute pyelenonephritis? How does infection occur?

A
  • E.coli. Ascending (ie. reflux obstruction)
152
Q

Etiology of chronic pyelonephritis

A
  • Obstruction (congenital or acquired) **

- Other = instrumentation, vesicoureteral reflux, pregnancy, F»>M, previous lesions, immunosuppression/deficiency

153
Q

Microscopic findings between acute and chronic pyelonephritis

A
  • Acute: neutrophils and neutrophil casts in tubule
  • Chronic: lymphocytes (mononuclear), pitting/geographic scarshallmark, thyroidization (appears like colloid in thyroid gland) d/t destruction of architecture, tubular atrophy
154
Q

Benign vs malignant tumors

A
  • Benign: adenoma, angiomyolipoma, fibroma, oncocytoma
  • Malignant: renal cell carcinoma (histotypes: clear cell = majority, papillary, chromophobe), urothelial carcinoma, Wilms, medullary carcinoma
155
Q

Where are papillary adenomas found in the kidney?

A
  • Always within cortex. Usually small
156
Q

Gross findings of papillary adenomas of kidney

A
  • Pale, yellow, well-circumscribed nodules in cortex of kidney
157
Q

Risk factors for renal cell carcinoma

A
  • **Tobacco, CRF and acquired cystic renal disease

- Obesity, HTN, unopposed E therapy, asbestos, heavy metals

158
Q

Sx of renal cell carcinoma

A
  • ** hematuria, abdominal mass

- Flank pain, HTN, weight loss, fever

159
Q

Describe spread of RCC. Where does it invade early?

A
  • Hematogenous. Invades renal vein early.
160
Q

Genetic change seen with clear cell RCC

A
  • Loss of tumor suppressor VHL
161
Q

Genetic change seen with papillary RCC

A
  • Activation of oncogene MET
162
Q

Genetic change seen with chromophobe RCC

A
  • Loss of multiple chromosomes
163
Q

Gross and microscopic findings of clear cell RCC

A
  • Gross: solitary, unilateral, YELLOW-ORANGE, sharply define margins, grey-white necrosis and foci of hemorrhagic discoloration
  • Microscopic: rounded/polygonal shape, clear abundant (NOT eosinophilic) granular cytoplasm, abundant capillaries
164
Q

Gross and microscopic findings of papillary (chromophil) RCC

A
  • Gross: thick capsule with reactive changes and hemorrhage (red/brown)
  • Microscopic: papillary structures which enclose foamy macrophages, tumor cells with abundant eosinophilic cytoplasm and mildly atypical nuclei, sparse capillaries
165
Q

VHL syndrome has an increased incidence of what cancer?

A
  • RCC
166
Q

Gross and microscopic findings of urothelial (transitional cell carcinoma) of renal pelvis

A
  • Gross: cauliflower-like structure

- Microscopic: papillary growth lined by urothelials with mild atypia and pleomorphism

167
Q

Most common renal malignancy of early childhood (2-4 yo). Etiology? SSx? Microscopic findings?

A
  • Loss of function mutation of tumor suppressor genes WT1 or WT2 on c/s 11
  • SSx: huge palpable flank mass and or hematuria
  • Microscopic: embryonic glomerular structures, tumor epithelial (abortive tubules and glomeruli) surrounded by metanephric blastema and tumor immature spindled cells stroma
168
Q

T/F. Maintenance fluids are related to weight in pediatric patient.

A
  • False. Related to metabolism
169
Q

What is insensible heat loss?

A
  • Heat loss through evaporation from skin and from respiratory tract
170
Q

Who has higher body weight BMR: infants or adults?

A
  • Infants. Think about their vitals.
171
Q

Calculate daily fluid requirements in normally hydrated pediatric patient

A
  • This is Holliday-Segar formula. Useful up to 80 kg.
    1. 3-10 kg: 100 ml/kg
    2. > 10 20 kg: 1500 ml + 20 ml/kg for every extra kg over 20
172
Q

Calculate fluid deficit for mild / moderate / severe older child and infant (1 month to 1 year)

A
  1. Older child
    - Mild: 3% dehydrated (30 ml/kg)
    - Moderate: 6% (60 ml/kg)
    - Severe: 9% (90 ml/kg)
  2. Infant
    - Mild: 5% (50 ml/kg)
    - Moderate: 10% (100 ml/kg)
    - Severe: 15% (150 ml/kg)
173
Q

Define mild dehydration

A
  • All findings normal except irritable yet consolable. See findings in moderate and severe.
174
Q

Define moderate dehydration

A
  • Skin tenting, dry skin, dry buccal mucosa, deep set eyes, reduced tears, soft fontanelle, irritable and not consolable, slight HR, - 2 sec cap refill, decreased urine output
175
Q

Define severe dehydration

A
  • No skin turgor, clammy skin, buccal mucosa/lips are parched/cracked, sunken eyes, no tears, sunken fontanelle, lethargic/obtunded, increased HR, > 3 sec cap refill, anuric
176
Q

What are the indications for fluid bolus in normonatremic dehydrated pediatric patient? How much? What type of fluid?

A
  • CV instability: tachycardia, cap refill, low BP (last thing to go): seen in 9 and 15% patient.
  • How much: 10 ml/kg for neonates, 20 ml/kg for infants and children, 10 ml/kg for adolescents
  • Fluid: NS or LR
177
Q

Describe how you would treat a normonatremic dehydrated pediatric patient generally as far as fluids go?

A
  1. Calculate premorbid weight. This is weight of patient before their % of dehydration. Eg. 9 kg today, but 10% dehydrated. 9/90 = x/100. Premorbid = 10 kg.
  2. Give bolus NS or LR for CV instability as quickly as possible
  3. Reassess after bolus and if CV stable, then proceed.
  4. Calculate deficit and subtract bolus from that (called sequential deficit/maintenance). Give this amount of D5 .45 NS in 8 hours.
  5. Add 20 meq/L of KCL after first void to all fluids (deficit and maintenance).
  6. Calculate maintenance fluids for 24 hours. Get amount per hour and multiple by 1.5 OR take amount and divide by 16. This gets you the hourly amount that will get a full days fluid in within 16 hours (the remainder of day). Example: 1100 ml maintenance for 24 hours. This is 45.83 ml/hour. To get total in over 16 hours you need to infuse at rate of (45.83 x 1.5) = 68.75 ml/hr. This is D5 0.45 NS fluid.
  7. Replace any ongoing losses ml for ml (ie. diarrhea, vomiting, chest tube output etc.)
178
Q

What are the requirements for K, Na and Cl for peds patients each day?

A
  • 1, 2, 3
  • K: 1 meq/kg/day
  • Na: 2 meq/kg/day
  • Cl: 3 meq/kg/day
179
Q

What fluid replacement should be given to hypernatremic dehydration patient? Over what time frame? Why?

A
  • Give D5 .2 NS over 48 hours instead of 24 hours. Must be corrected slowly to avoid brain edema. Standard replacement models as described above don’t apply.
180
Q

What should be done in mildly dehydrated child (ie. no signs of CV instability)?

A
  • Oral rehydration
181
Q

Role of calcium

A
  • NM/nerve conduction, NT release, muscle contraction, membrane potential maintenance, intracellular signaling, bone formation, coagulation cascade, enzyme regulation
182
Q

Where is calcium distributed in body?

A
  • 99% in bone
  • Extracellular: 50% bound, 50% free
  • Intracellular
183
Q

What can confound total serum calcium?

A
  • Abnormalities in albumin. 50% of calcium in bound form to for example albumin.
184
Q

How do you calculate corrected calcium with drop in albumin?

A
  • For every 1 gram / dl drop in serum albumin below 4 g/dl, measured serum calcium decreases by 0.8 mg/dl
  • Corrected Ca (mg/dl) = measured Ca (mg/dl) + (0.8 (4 – measured albumin g/dl) )
  • Example: 80 yo with lung cancer, serum Ca 8 mg/dl and albumin 2 g/dl. Correct Ca = 8 + 0.8 (2) = 9.6 mg/dl
185
Q

Organs involved in calcium homeostasis

A
  • Bone, kidney, gut
186
Q

Regulatory hormones of calcium metabolism

A
  • PTH, Calcitonin, Vit D
187
Q

PTH Function

A
  • From chief cells of parathyroid gland
  • Overall: increases serum Ca and decreases serum PO4
  • How: increases osteoclastic resorption of Ca & PO4, increases DCT calcium reabsorption with decrease in phosphate reabsorption, increase gut absorption of Ca via Vit D production in kidney
188
Q

Calcitonin function

A
  • From parafollicular thyroid gland cells
  • Overall: decreases serum Ca and PO4
  • How: inhibits osteoclastic resorption, decreases renal tubular reabsorption of Ca and PO4, decrease gut absorption of PO4
189
Q

Vit D function

A
  • Overall: increases serum Ca and PO4
  • How: similar to PTH; increase intestinal absorption of Ca & PO4, increase bone resorption of Ca and PO4 through osteoclastic activity, increase renal reabsorption of Ca & PO4, decrease production of PTH
190
Q

SSx of hypercalcemia

A
  • CNS: lethargy, psychosis, coma
  • NM: myalgias, weakness
  • CV: EKG w/ bradycardia, short QT, short QRS
  • Renal: polyuria, decreased GFR, nephrolithiasis, nephrocalcinosis
  • GI: anorexia, nausea, constipation
  • Metastatic calcifications (calciphylaxis): seen in chronic renal failure (lack of vit D activation = disinhibition of PTH = high PTH)
191
Q

Most common cause of hypercalcemia. Other etiologies

A
  • Primary hyperparathyroidism (adenoma, hyperplasia, parathyroid cancer)
  • Other: malignancy (PTHrP expressing commonly from lung), drug-induced (vit D, thiazides, lithium, milk-alkali), granulomatous diseases/TB (extra-renal 1,25 hydroxy vit D production), immobilization (increase osteoclastic/decreased osteoblastic), acidosis (decreases bound calcium)
192
Q

Tx of hypercalcemia

A
  • 1st thing = ECF volume restoration with normal saline

- Next: loop diuretics (not thiazides!), bisphosphonate therapy, calcitonin therapy, glucocorticoid therapy, dialysis

193
Q

SSx of hypocalcemia

A
  • Paresthesias, tetany (Chvostek’s, Trousseau, laryngeal muscle spasms), cardiac (long QT and arrhythmias incl. Torsades), seizures
194
Q

How does low calcium cause depolarizations (tetany etc)?

A
  • Calcium acts to stabilize the membrane potential. When low, RMP moved closer to threshold making it easier to depolarize.
195
Q

Causes of hypocalcemia

A
  • Hypoalbuminema, hypoparathyroidism, parathyroid dz, postparathyroidectomy, sepsis, pancreatitis, liver dz, kidney dz, disorders of Vit D, acute complexation/deposition of calcium, sepsis, osteoblastic bone mets, drugs, alkalosis
196
Q

Lab findings in hypoparathyroidism

A
  • Hypocalcemia, hyperphosphatemia, low PTH
197
Q

What are the vit D resistance disorders?

A
  1. Vit D dependent rickets type 1: 1-alphahydroxylase deficiency
  2. Vit D dependent rickets type 2: mutation of vit D receptor
198
Q

Role of phosphorus

A
  1. Structural component of biological membranes
  2. Present in nucleotides and nucleic acids
  3. Signal transduction
  4. Temporary storage and transfer of energy derived from metabolic fuels
  5. Enzymatic regulation
199
Q

With hyperphosphatemia, what other electrolyte abnormality is seen?

A
  • Hypocalcemia
200
Q

Sx of hyperphosphatemia

A
  • Related to hypocalcemia: spasms, paresthesias etc.

- Underlying condition: fatigue, SOB, edema, lack of appetite, nausea/vomiting

201
Q

Most common cause of hyperphosphatemia

A
  • Renal failure

- Other = acute phosphate load (tumor lysis, rhabdo, lactic and ketoacidosis, exogenous phosphate)

202
Q

SSx of hypophosphatemia

A
  • Mild: asymptomatic
  • Severe: weakness, bone pain, rhabdomyolysis, mental status change, hypercalciuria (inhibition of Ca reabsorption), anemia, WBC abnormalities, platelet defects, respiratory failure
203
Q

Major conditions associated with hypophosphatemia

A
  1. Chronic alcoholism
  2. IV hyperalminentation without phosphate ie. refeeding syndrome
  3. Chronic ingestion of antacids
  4. DKA
204
Q

Role of magnesium

A
  • Enzyme cofactor, required for oxphos, bone development, DNA/RNA synthesis, transport of calcium and K across cell membranes, nerve impulse conduction, muscle contraction
205
Q

Where is magnesium reabsorbed in kidney?

A
  • Mostly in ascending loop
206
Q

Most common cause of hypermagnesemia

A
  • Renal failure. Hypermagnesemia is rare

- Other = magnesium infusion (PE patients), oral ingestion, magnesium enemas

207
Q

Sx of hypomagnesemia

A
  • Arrhythmias is main concern (if severe = Torsades), nistagmus, fatigue, seizures, muscle spasms, weakness: diaphragm, numbness
208
Q

EKG changes seen with hypomagnesemia. Tx?

A
  • Prolongation leading to Torsades

- Tx = magnesium

209
Q

Causes of hypomagnesemia

A
  1. Renal losses: loop, thiazide diuretic use; volume expansion, etoh, etc.
  2. GI losses: diarrhea, less commonly vomiting, primary intestinal hypomagnesemia, acute pancreatitis, PPIs
210
Q

Normal serum Na range

A
  • 135 – 145 mmol/L
211
Q

T/F. Disorders of Na are almost always caused by Na itself.

A
  • False. Caused by disorders of water balance.
212
Q

Define hyponatremia, severe hyponatremia. Define hypernatremia, severe hypernatremia?

A
  • Hyponatremia 145 mmol/L

- Severe hypernatremia > 155 mmol/L

213
Q

Sx of hyponatremia

A
  • Non-specific
  • CNS related (cellular edema of brain): WEAKNESS (unique feature), nausea, vomiting, HA, fatigue, seizure, coma, death
  • ** note: severity of sx related to rapidity and severity of hyponatremia
214
Q

What is osmotic adaptation? Why do I care?

A
  • Brain cells have ability to excrete or produce osmols to protect against over hydration and dehydration respectively depending on hypo- or hyper-osmolar state in serum.
  • Hypo-osmolar state: brain cells excrete osmols to protect against cellular overhydration
  • Hyper-osmolar state: brain cells produce osmols to protect against cellular dehydration
  • Why care? Take this process into account when you are treating. Overly aggressive correction of abnormalities can make patient worse.
215
Q

What is osmotic demyelination syndrome?

A
  • Severe neurologic disorder of demyelination of CNS (esp. pons) that may occur with overly rapid correction of severe hyponatremia. Mechanism unclear.
  • Sx: parapesis (partial paralysis of lower extremities), dysarthria, dysphagia, seizure, coma and death.
216
Q

What is primary polydipsia? Sx? Is hypo- or hyper-natremia seen?

A
  • Excessive H2o intake overwhelming kidneys ability to excrete water load. It is uncommon. Typically results from psychogenic etiology.
  • Sx: polyuria, complaint of increased thirst
  • Hyponatremia is seen
217
Q

What is pseudohyponatremia? Tx?

A
  • In states of severe hyperlipidemia or hyperproteinemia, the fraction of plasma water (usually ~93%) is reduced. Lab measurements of Na are artificially lowered d/t reduction in plasma water as lipids and proteins occupy larger volume of total plasma. Very uncommon.
  • Tx = tx underlying causes (hyperlipidemia, hyperproteinemia d/t myeloma etc.)
218
Q

Types of hypo-osmolar (aka hypotonic) hyponatremia

A
  1. Hypovolemic
  2. Hypervolemic
  3. Euvolemic
219
Q

Etiologies of hypo-osmolar (aka hypotonic), hypovolemic hyponatremia. What is urine concentration of sodium in each case?

A
  • Large decrease in Na and smaller decrease water
    1. Renal causes (losses): diuretics (esp. HCTZ!), osmotic diuresis (severe hyperglycemia leads to glycosuria). High urine Na seen here d/t diuretic process.
    2. Non-renal / extra-renal (losses): blood loss, diarrhea, vomiting. Low urine Na seen here because you are trying to hold onto it.
  • How? Reduction in water with Na in ECF, resulting in hypotonicity in ECF, therefore shift of water further from ECF to ICF.
220
Q

Etiologies of hypo-osmolar (aka hypotonic), hypervolemic hyponatremia. What is urine concentration of sodium in each case.

A
  • Increase in Na with larger increase in water
    1. Renal causes: renal failure = retention of both Na and water. High urine Na.
    2. Extra-renal causes: CHF, cirrhosis and nephrotic syndrome: high ECF but decrease in effective circulating volume d/t low protein. Results in ADH secretion = more water retention. Low urine Na.
221
Q

Etiologies of hypo-osmolar (aka hypotonic), euvolemic hyponatremia

A
  • Increase in water only without change in Na
    1. Hypoadrenalism: cortisol functions to inhibit ADH secretion. No cortisol = no inhibition of ADH secretion with increase in CRH. CRH mimics ADH function. Increase in water.
    2. Hypothyroidism: thyroid hormone normally inhibits ADH. NO thyroid hormone = disinhibition of ADH secretion = high ADH = increase in water.
    3. SIADH: varying etiologies lead to inappropriate elevation of ADH despite hyponatremia and euvolemia. Urine osmolarity is elevated inappropriately.
222
Q

Etiology of SIADH

A
  • CNS diseases (meningitis, cancer, stroke), drugs, pulmonary dz (pneumonia, severe asthma, cancer, SCLC), pain, stress
223
Q

Describe diagnostic characteristics (PE and labs) of SIADH

A
  • Serum: hyponatremia, hyposmolality
  • Urine: elevated urine osmolality (d/t elevated ADH)
  • PE: normovolemic (no edema or signs of decreased effective circulating volumes)
  • Normal renal, adrenal and thyroid functions.
224
Q

Tx of hypo-osmolar (aka hypotonic), hypovolemic hyponatremia?

A
  • Give 0.9% NS slowly.
225
Q

Tx of hypo-osmolar (aka hypotonic), hypervolemic hyponatremia?

A
  • Restrict free H2o intake.
  • Other options: Demeclocycline to increase urinary water loss. Vasopressin (vaptans) antagonist to increase urinary water loss.
226
Q

Tx of hypo-osmolar (aka hypotonic), euvolemic hyponatremia?

A
  • Restrict free H2o intake. Demeclocycline to increase urinary water loss. Vasopressin (vaptans) antagonist to increase urinary water loss.
227
Q

Treatment of severe hyponatremia or symptomatic hyponatremia

A

**

  • Hypertonic 3% saline slowly.
228
Q

Differentiate between hypernatremia and hyponatremia based on sx

A
  • Cannot, non-specific and same.
229
Q

Etiologies of hypernatremia. What is most common?

A
  1. Most common = water loss
    - Insensible (burns, sweating, respiratory), renal (diabetes insipidus), GI (diarrhea, vomiting with inadequate free water replacement), hypothalamic disorder (hypodipsia), severe exercise w/water redistribution to cells
  2. Na+ retention (uncommon): administration of hypertonic NaCl / NaHCO3; salt pills
230
Q

What is diabetes insipidus? General sx? What electrolyte abnormality is seen? Types?

A
  • Reduction in water reabsorption by kidney and a diuresis of dilute urine leading to hypernatremia. Sx include polyuria, polydipsia, dilute urine, thirst.
  • Two types:
  1. Nephrogenic DI (NDI): failure of response to ADH
  2. Central DI (CDI): failure of ADH production/secretion
231
Q

Etiology of central DI

A
  • All etiologies involve dysfunction of ADH production/secretion d/t idiopathic, neurosurgery, head trauma, hypoxic/ischemic encephalopathy, cancer
232
Q

Etiology of nephrogenic DI

A
  • Congenital or acquired (** hypercalcemia, hypokalemia, lithium/demeclocycline, renal parenchymal dz etc.) leading to reduced or absence of renal responsiveness to ADH.
233
Q

Compare and contrast signs/sx/lab findings of CDI to NDI

A
  • CDI: polyuria (up to 20 L/day), polydipsia, low urine osmolality (dilute urine), undetectable ADH
  • NDI: polyuria (3-4 L/day), polydipsia, low urine osmolality (dilute urine), ADH normal
234
Q

Which DI is corrected after ADH administration: CDI or NDI?

A
  • CDI
235
Q

What does rapid correction of hypernatremia lead to?

A
  • Increased brain water (cerebral edema). Go slow!!
236
Q

When is hypernatremia tx indicated?

A
  • Symptomatic, volume depleted, hypernatremia is severe (> 155 mmol/L)
237
Q

Define tx of hypernatremia

A
  • Correct underlying cause if possible
  • **Correct volume depletion first!! Use 0.9 NS for fluid resuscitation followed by hypotonic (1/2 NS or ½ NS or D5W) to correct hypernatremia
  • If CDI: replaced with ADH
  • If NDI: make sure patient takes in adequate water
238
Q

See case L11

A

See case L11

239
Q

Function of K

A
  • Cellular function/metabolism including NM function, membrane potential. Disorders affect heart and cardiac system.
240
Q

Normal K range.

A
  • 3.5 – 5.5 mmol/L
241
Q

Define hypokalemia

A

-

242
Q

Causes of hypokalemia

A
  1. Increased entry to cells: increased pH, insulin effect, beta adrenergic effect
  2. GI losses: vomiting, diarrhea
  3. Urinary losses: diuretics, mineralocorticoid excess, hypomagnesemia
  4. Decreased intake (rare)
243
Q

EKG findings with hypokalemia

A

** Increase in amplitude of U waves!

244
Q

Tx of hypokalemia

A
  1. Tx underlying cause if possible
  2. Oral or IV K. KCl preferred. Don’t exceed 10-20 mmol/hr***
  3. Monitor EKG
245
Q

Why is KCl preferred tx for hypokalemia

A
  • Metabolic alkalosis (HCl depletion) is commonly associated with hypokalemia esp. in cases of vomiting.
  • KCl treats both hypokalemia and alkalosis
246
Q

Causes of hyperkalemia. What drugs can cause this?

A
  • Most common = increased intake, pseudohyperkalemia, insulin deficiency and hyperglycemia (insulin normally causes K entry into cell with glucose), tissue catabolism), renal failure, circulating volume depletion, hypoaldosteronism (aldosterone causes excretion of K normally)
  • Drugs: NSAIDs, ACEi, aldosterone antagonists (spironolactone, amiloride, eplerenone), renin inhibitors
247
Q

SSx of hyperkalemia. EKG findings?

A
  • Muscle weakness, cardiac abnormalities (EKG: tall/peaked symmetrical T wave = first change**, widened QRS, P wave absent)
  • Probably will be exam Q on this.
248
Q

Tx of hyperkalemia, MOA?

A
  • Calcium (in form of Ca gluconate): used only with symptomatic severe hyperkalemia as best initial therapy. Give 10 ml 10% over 2-5 mins, repeat PRN. MOA: antagonizes deleterious membrane action of hyperkalemia
  • Glucose & Insulin (insulin only if hyperglycemic). MOA: shifts K and glucose into cells increasing Na/K ATPase.
  • NaHCO3: use if patient has coexisting metabolic acidosis. MOA: shifts K intracellularly.
  • Beta-2 agonists (albuterol most commonly). MOA: shifts K intracellularly via Na/K ATPase.
  • Diuretics. MOA: increase urinary K loss by increasing flow rates.
  • Cation Exchange Resin (Na polystyrene sulfonate). MOA: exchanges K for Na.
  • Hemodialysis: fastest and most efficient means to lower serum K***.
249
Q

What is the best initial therapy for severe hyperkalemia where muscle weakness and EKG changes are seen and immediate intervention is needed?

A
  • Calcium gluconate (10 ml 10%) over 2-5 minutes (too quickly and arrhythmia can result), repeat PRN.
250
Q

What treatment is of greatest value in hyperkalemic patient with coexisting metabolic acidosis?

A
  • NaHCO3
251
Q

What treatment is the fastest and most efficient means to lower serum K in hyperkalemia?

A
  • ***Hemodialysis
252
Q

Caution for calcium tx in hyperkalemia

A
  • Potential for dig toxicity, don’t give with HCO3- containing solns as it can cause precipitation of Ca.
253
Q

Caution for glucose/insulin tx in hyperkalemia

A
  • Hypoglycemia, hyperglycemia
254
Q

Caution for NaHCO3 tx in hyperkalemia

A
  • Volume overload

- Hypernatremia

255
Q

Caution for beta-2 agonists in hyperkalemia

A
  • Tachycardia, angina pectoris
256
Q

Caution for cation exchange resin in hyperkalemia

A
  • Given PO or rectal enema. Constipation, bowel injury and volume overload.
257
Q

Review L13 cases

A

Review L13 cases

258
Q

Diagnostic approach in evaluating renal function

A
  1. Estimate GFR (using Cockcroft-Gault or other method)
  2. Determine if pre-renal, renal or post-renal cause

a. Renal:
i. Glomerular: nephritic, nephrotic

ii. Non-glomerular: vascular, tubular, interstitial

259
Q

Is BUN measure of renal function?

A
  • Indirect and rough measurement of renal function if normal liver function exists. Remember, Urea excreted by liver.
260
Q

Causes of BUN increase (aka azotemia)

A
  • Dehydration, hypovolemia, shock (third spacing?), CHF, MI, GI bleed, protein supplementation, starvation, pyelonephritis, ATN (acute tubular necrosis), bladder obstruction
261
Q

Causes of BUN decrease

A
  • Liver failure, overhydration, negative nitrogen balance (malnutrition/malabsorption), pregnancy, nephrotic syndrome
262
Q

Utility of Cr

A
  • Proportional to GFR: as GFR decreases, Cr goes up
263
Q

Limitations of Cr

A
  • Slight increase in creatinine after large meals (and esp. large meaty meals), increased if patients take supplemental creatine
264
Q

Causes of Cr increase

A
  • Diseases affecting renal function
265
Q

Causes of Cr decrease

A
  • Decreased muscle mass (debilitation, muscular dystrophy, Myasthenia gravis, elderly, children)
266
Q

What does BUN/Cr ratio tell you?

A

**Where “pathology” is

  1. Pre-renal: BUN:Cr > 20:1
  2. Post-renal OR Normal: BUN:Cr 10-20:1
  3. Renal:
267
Q

Factors that Cockcroft-Gault equation takes into account when estimating GFR

A
  • Age, sex, weight, creatinine
268
Q

Normal urine pH

A
  • 4.5-8.0
269
Q

Causes of glucosuria

A
  • Inability of kidney to reabsorb filtered glucose despite normal plasma levels (renal glucosuria)
  • Spillage of glucose d/t abnormally high plasma glucose (> 180)
270
Q

What does high vs low SG of urine mean?

A
  • High = dehydration

- Low = overhydration, renal dz that diminish concentrating ability

271
Q

Markers in urine indicating UTI

A
  • Leukocyte esterase: presence of WBCs (whole or lysed)
  • Nitrites: reduction of nitrates to nitrites by many bacteria
  • Combine leuk esterase with nitrites with microscopy for most sensitive result
272
Q

When are ketones present in urine?

A
  1. DM & hyperglycemic
  2. Alcoholism
  3. Fasting/starving/dehydration
273
Q

What is next test if blood is present in UA?

A
  • Normal: 0-2 RBC/HPF transiently.

- Follow up with microscopy

274
Q

+ve muscle pain, +ve blood on urine dipstick and microscopy

A
  • Rhabdomyolysis

- Myoglobin causes dipstick to be +ve for blood

275
Q

How much protein is normal in urine / 24 hours?

A

-

276
Q

When should 24 hour urine collection for proteinuria be ordered?

A
  • If mildly abnormal microalbumin or dipstick x 3 (more than +1)
277
Q

Nephrotic range of proteinuria

A
  • > = 3500 mg (3.5 g) / day
278
Q

T/F. Very high proteinuria has a tubular etiology

A
  • False. Glomerular. Usually albumin.
279
Q

Should asymptomatic bacteriuria be treated?

A
  • No. Certain cases are exception.
280
Q

Is it normal to find WBCs in urine?

A
  • Transiently has no clinical significance. Persistent = infection, chronic pyelonephritis, tubulointerstitial dz.
281
Q

Glomerular source of hematuria presents with what findings in urine

A
  • +ve hematuria, +ve proteinuria, +ve erythrocyte casts, +ve dysmorphic RBCs
282
Q

Non-glomerular renal source of hematuria presents with what findings in urine

A
  • +ve hematuria, +ve proteinuria
283
Q

Urologic hematuria resulting from tumors, calculi and infection results in what findings in urine

A
  • +ve hematuria only
284
Q

Which epithelial cells in urine is important?

A
  • Only epithelial cells in casts, which = tubular origin
285
Q

RBC casts found in what disease

A
  • Glomerulonephritis (nephritic)
286
Q

WBC casts found in what disease

A
  • Pyelonephritis
287
Q

Tubular epithelial cell casts found in what disease

A
  • ATN (acute tubular necrosis)
288
Q

Fatty casts found in what disease

A
  • Nephrotic syndrome, hypothyroidism
289
Q

Granular casts found in what disease

A
  • Many diseases, can be seen after exercise
290
Q

Waxy/broad casts found in what disease

A
  • Advanced renal failure
291
Q

Calcium oxalate crystals in UA + acute renal failure, think…

A
  • Ethylene glycol poisoning
292
Q

FENA values

A
  • 2% = acute tubular necrosis
293
Q

Most common intrinsic cause of acute renal failure in hospitalized patient group

A
  • ATN
294
Q

Etiology of ATN

A
  • Acute ischemic: Hypotension

- Acute nephrotoxic: contrast, MTX, ethylene glycol, rhabdo, myeloma, tumor lysis syndrome

295
Q

+ve UA for eosinophils think…

A
  • Allergic interstitial nephritis
296
Q

Tx of PSGN

A
  • Pts typically get better by themselves, monitor, tx symptoms
  • Do kidney biopsy if not improving, kidneys getting worse
297
Q

Indications for kidney biopsy

A
  1. Isolated glomerular hematuria with proteinuria
  2. Nephrotic syndrome
  3. Acute nephritic syndrome
  4. Unexplained acute or rapidly progressive renal failure
298
Q

Review L14/15 case studies

A

Review L14/15 case studies

299
Q

pH that is compatible with life

A
  • 6.8 – 7.8
300
Q

What are the mixed acid/base disorders that one can have?

A
  • Can have a metabolic acidosis with metabolic alkalosis
  • Metabolic acidosis or alkalosis can be combined with respiratory acidosis or alkalosis
  • Can never have both respiratory alkalosis and acidosis
301
Q

Define acidosis/alkalosis

A
  • Acidosis: pH 7.45

- Note: 7.35 and 7.45 themselves are normal

302
Q

Normal HCO3

A
  • 25 mmol/L
303
Q

Lab values that change with metabolic alkalosis/acidosis vs respiratory alkalosis/acidosis

A
  • Metabolic alkalosis = increased HCO3- (> 40 mmol/L in primary metabolic alkalosis **); Metabolic acidosis = decreased HCO3- (
304
Q

Compensation expected in metabolic alkalosis

A
  • Respiratory acidosis (hypoventilation to increase pCO2)
305
Q

Causes of metabolic alkalosis

A
  • GI: hydrogen loss as in vomiting or nasogastric suction
  • Renal: hydrogen loss as in primary aldosteronism, loop or thiazide diuretic use (production of more bicarb, secretion of H)
  • Intracellular shift of hydrogen: as in hypokalemia (for example)
  • Alkali administration
  • Contraction alkalosis: massive diuresis
  • Maintainers: chloride depletion, hypokalemia, effective circulating volume depletion, hyperaldosteronism
306
Q

What is contraction alkalosis?

A
  • Diuretics trigger secretion of H & K along with loss of volume leading to shrinkage of total body fluid. To counteract hypovolemia, aldosterone is released which leads to Na/H20/HCO3 retention and secretion of H & K.
  • Bicarb is the same, but the volume is lower making it seem as if bicarb is elevated.
307
Q

Tx of metabolic alkalosis

A
  • Correct underlying cause
  • Correct electrolyte abnormalities
  • If diuresis is required, use K-sparing diuretic (amiloride, triamterene, spironolactone or eplerenone) or acetazolamide (interferes with HCO3- reabsorption in kidneys)
308
Q

Causes of metabolic acidosis

A
  • Increased acid generation
  • Loss of bicarb (hyperchloremic acidosis with severe diarrhea – AG is normal here)
  • Diminished renal acid excretion (d/t renal failure or renal tubular acidosis). Results in hyperchloremic acidosis with normal AG.
309
Q

Compensation expected with metabolic acidosis

A
  • Respiratory alkalosis (hyperventilation to decrease pCO2)
310
Q

What is plasma anion gap? What is increase in AG caused by? When is it used? Calculation? Normal value?

A
  • Measure of difference between anions and cations. Not some cations and anions are not included in the equation because of their relatively low concentrations. Therefore an increase in AG is caused by increase in the unmeasured anions typically. Used to differentiate causes of metabolic acidosis. Results either high or normal (aka non-AG)
  • Calculation: AG = Na – (Cl + HCO3)
  • Normal = 12 mmol/L
311
Q

In what metabolic acidosis situation (s) can AG gap be normal?

A
  • # 1: Substantial loss of HCO3 (as in severe diarrhea). Kidneys compensate for loss of volume by retaining NaCl. Net effect is equal amount of exchange of chloride for bicarb loss therefore causing AG to remain same. This is called hyperchloremic metabolic acidosis
  • # 2: Defective renal acidification (in renal failure or renal tubular acidosis): failure to excrete normal quantities of acid. Hyperchloremic state happens because conjugate base is excreted as sodium salt and NaCl retained.
312
Q

Do I need to know anything about urine anion gap?

A

Do I need to know anything about urine anion gap?

313
Q

Causes of high AG metabolic acidosis

A
  • Mnemonic = MUDPILES
  • Methanol (wood alcohol and winder wiper fluid), uremia (CRF), DKA, propylene glycol, I: infection/iron/INH, lactic acidosis, ethylene glycol (antifreeze), salicylates
314
Q

DKA. Triad presentation? What other history is found? Tx?

A
  • Triad: hyperglycemia, high AG metabolic acidosis, ketonemia
  • Other hx: history of T1 DM, poor compliance with insulin pump
  • Tx: IV fluids and insulin. If severe, may administer NaHCO3 to obtain pH > 7.1, but controversial.
315
Q

How is serum osmolal gap (SOG) aka osmolality of serum calculated? Normal SOG?

A
  • [2 x Na] + glucose/18 + BUN/2.8

- Normal = 10-15 mosm/kg

316
Q

Two common causes of increased SOG?

A
  • Methanol intoxication or ethylene glycol intoxication

- Note: both are causes of high AG metabolic acidosis

317
Q

Early and late symptoms of ASA intoxication. How does acid-base status present during each of these? Net effect?

A
  • Early: tinnitus, vertigo, nausea, vomiting and diarrhea. Initially: respiratory alkalosis (d/t ASA stimulating respiratory center)
  • Late: AMS, hyperpyrexia, non-cardiac pulmonary edema, coma. Later: metabolic acidosis with high AG.
  • Net: mixed – primary respiratory alkalosis + primary metabolic acidosis
318
Q

Tx of ASA intoxication

A
  • Activated charcoal if recently ingested
  • Give NaHCO3!!
  • Monitor serum salicylate []. > 100 mg/dl associated with morbidity and mortality. This is absolute indication for hemodialysis!
319
Q

Fastest way to treat ASA, ethylene glycol and methanol intoxications?

A
  • Hemodialysis
320
Q

How to check for appropriate respiratory compensation to metabolic acidosis?

A
  • Winter’s formula: PCO2 = (1.5 x [HCO3]) + 8 +/- 2.
  • If this value corresponds to the patient’s PCO2 value, then compensation is adequate. If PCO2 is higher, then respiratory acidosis. If PCO2 is lower, then respiratory alkalosis.
321
Q

What is delta ratio? What is it used for?

A
  • Delta ratio = delta AG / delta HCO3 = (measured AG – normal AG) / normal HCO3 – measured serum HCO3)
  • Used to determine metabolic acidosis is mixed with metabolic alkalosis
  • If delta ratio 2, then underlying metabolic alkalosis is present too!
322
Q

Clinical strategy in determining acid-base problems

A
  1. Look at history
  2. Check pH and see if acidemic or alkalemic
  3. Check serum HCO3 and PCO2 to see what primary disturbance is – respiratory or metabolic –osis?
  4. Is AG high or normal? Applicable only in metabolic acidosis.
  5. Appropriate compensation using Winter’s formula? Applicable only in metabolic acidosis. If metabolic alkalosis: is pH normal or between 7.35 – 7.45?
  6. Is mixed disorder present? Only applicable in metabolic acidosis to see if metabolic alkalosis also present.
  7. Diagnosis
  8. Treatment
323
Q

Define microscopic hematuria

A
  • > 3 RBCs / HPF. Note: not just chemical test. Must see RBCs.
324
Q

Non glomerular causes of hematuria

A
  1. Upper urinary tract: pyelonephritis, urolithiasis, RCC, urothelial/TCC, urinary obstruction, benign hematuria
  2. Lower urinary tract: bacterial cystitis, BPH, strenuous exercise, urothelial/TCC, spurious hematuria (menses, vaginal atrophy), instrumentation, benign hematuria
325
Q

Risk factors for significant urologic dz

A
  • Age > 40, males, hx of cigarette smoking, hx of chemical exposure, pelvic radiation, irritative voiding sx (urgency, frequency, dysuria), prior urologic dz/tx
326
Q

Second most common GU cancer

A
  • Bladder CA (males > females, mean age 70)
327
Q

Most common bladder cancer?

A
  • > 90% = urothelial/TCC
328
Q

Bladder cancer associated with chronic urothelial irritation

A
  • SCC
329
Q

Biggest risk factor for bladder cancer

A
  • Cigarette smoking (4x risk)
330
Q

Patient presents with painless gross hematuria. What is diagnosis?

A
  • Bladder cancer until proven otherwise. This is classic presentation in > 80% cases.
  • Note: hematuria often intermittent
331
Q

Which test has the most/highest specificity for detecting bladder tumor?

A
  • Urine cytology. Has high specificity (good at detecting TNs, therefore + ve results good at ruling IN). Because low sensitivity though, -ve result isn’t helping at ruling out.
  • Note: FISH has highest combined sensitivity and specificity, but expensive.
332
Q

Main categorizations of bladder cancer staging

A
  • T1 and less (non-invasive) = mucosa or lamina propria, not invasive. This is 70% of all bladder cancers with 5-year survival of 80-100%. 70-80% of these cancers do recur within 2 years.
  • T2 + (invasive) = into muscle and now has access to blood vessels, lymphatics for metastatic potential.
333
Q

Typical met sites for bladder cancer

A
  • Pelvic LNs, lung, liver, bone
334
Q

What is the surveillance of non-invasive bladder cancer?

A
  • Most recurrences within first 2 years.
    1. Cystoscopy and urine cytology/FISH q 3 months for 1-2 years; q 6months for following 1-2 years, then annually for life. Consider stopping after 5 years in low grade dz. Note: any recurrence restarts this protocol.
    2. Periodic upper tract imaging: renal US/IVP/CT urography q 1-2 years esp with high grade tumors.
335
Q

Tx options for non-invasive bladder cancer

A
  1. TURBT
  2. Adjuvant therapy
    - BCG (Mb Bovis): used in high grade Ta and T1. Decreases recurrence by 40%**
    - Mitomycin C: single instillation after TURBT for patient that don’t tolerate BCG
    - BCG failures: IFN-alpha, Doxorubicin, valrubicin, epirubicin
    * Note: recurrent high-grade T1 despite BCG may require radical cystectomy
336
Q

Tx options for muscle invasive bladder cancer

A
  • Surgery: radical cystectomy **standard of care, partial cystectomy (small solitary in posterior wall or dome of bladder)
  • Radiation
  • Chemo
  • Note: met dz has dismal prognosis despite systemic therapy
337
Q

Micturition cycle. What controls each part?

A
  • Storage: SNS T10-L2
  • Emptying (Pee): PSNS (S2-4), pontine micturition center initiates voluntary void
  • Mnemonic: store & pee
338
Q

What should happen to pressure in the bladder with filling?

A
  • Very little rise until stretch limit reached at which time contraction happens leading to urination.
339
Q

What is urinary incontinence? Types?

A
  • Any involuntary loss of urine
    1. Bladder dysfunction
    a. Urge: involuntary urine leak accompanied by or immediately preceded by a strong, sudden desire to urinate.
    b. Overflow: extreme frequency/constant urine dribbling at extremes of bladder volumes or when volume reaches limit of bladder properties
    2. Outlet dysfunction (stress UI)
    a. Anatomic: involuntary urine leak with any sudden increase in abdominal pressure d/t urethral hypermobility.
    b. Intrinsic sphincter deficiency: involuntary urine leak with any sudden increase in abdominal pressure d/t weakness of urinary sphincter.
    3. Mixed incontinence: combo of urge and stress
340
Q

Causes of potentially reversible transient UI

A
  • Mnemonic: DIAPERS
  • D: delirium/cognitive impairment
  • I: infections
  • A: atrophic vaginitis/urethritis
  • P: pharmaceuticals/meds
  • E: excessive UOP/polyuria
  • R: restricted mobility
  • S: stool impaction/constipation
341
Q

How is UI evaluated?

A
  • UA, urine culture, PVR (post-void residual volume measurement nml
342
Q

What is OAB (over active bladder)?

A
  • Frequency and urgency with or without urge incontinence
343
Q

Tx of OAB and urge incontinence

A
  • Behavior (control fluid intake, timed voiding)
  • Lifestyle changes (weight loss, dietary changes, smoking cessation)
  • PT
  • Meds: anticholinergics, beta-3 agonist (mirabegron), vaginal E therapy in post-menopausal women
  • Surgery: sacral nerve modulation, intravesicular Botox, bladder augmentation or diversion
344
Q

Overflow UI. Causes? Sx? Tx?

A
  • Causes: meds, constipation, obstruction, sphincter dysfunction/dyssynergia, hx of pelvic surgery/trauma
  • Sx: extreme frequency and/or constant dribbling of urine
  • Tx: tx underlying obstruction or chronic catheterization
345
Q

Causes of stress UI

A
  1. Anatomic: urethral hypermobility

2. Intrinsic sphincter deficiency: weakness of urinary sphincter

346
Q

Tx of stress UI

A
  • Behavior modification (control fluid intake, timed voiding)
  • Lifestyle changes (weight loss, dietary changes, smoking cessation)
  • Meds: none!
  • PT, Kegels
  • Pessary
  • Surgery: urethral bulking agents, urethral slings (mainstay tx)* w/tx of pelvic organ prolapse if any
347
Q

Compare and contrast UT infection, contamination vs colonization. Which require tx?

A
  • UTI: pathogen + sx and / or inflammatory response. Tx.
  • Contamination: organisms introduced during collection or processing. No tx.
  • Colonization: this is asymptomatic bacteriuria. Often doesn’t require tx.
348
Q

Compare and contrast between uncomplicated, complicated, recurrent, reinfection, persistent UTI

A
  • Uncomplicated: infection in healthy pt with normal GU tract
  • Complicated: infection with factors that increase chance of acquiring bacteria or decreased therapy efficacy (abnormal GU tract, immunocompromised, MDR bacteria)
  • Recurrent: occurs after documented resolved infection
  • Reinfection: a new event with reintroduction of bacteria into GU tract
  • Persistent: recurrent UTI by same bacteria
349
Q

Risk factors for UTIs

A
  • Poor fluid intake, chronic dehydration, infrequent voiding, incomplete bladder emptying, chronic constipation/fecal incontinence, post-menopausal vaginal atrophy, staghorn calculi, chronic urinary cath, abnormal urinary tract, underlying dz (DM, immunosuppression), poor hygiene, sexual activity
350
Q

Empiric tx for UTIs

A
  • TMP-SMX or fluoroquinolones

- Note: adjust based on cultural sensitivities for persistent sx and complicated/recurrent UTIs

351
Q

Define interstitial cystitis/bladder pain syndrome. Pathognomonic findings? Sx? Tx?

A
  • Syndrome of chronic pain/pressure or discomfort associated with bladder usually accompanied by lower UT sx > 6 weeks! Has been associated with fibromyalgia, IBS, endometriosis, vulvodynia, multiple allergies.
  • No specific markers, lab findings, radiographic findings that are pathognomonic for this. Diagnosis of exclusion. Etiology really not really known. May find glomerulations and Hunner’s ulcers on cystoscopy.
  • Sx: urinary frequency, nocturia, pain with bladder filling, sx exacerbated with stress and certain intake, pelvic floor tension, dyspareunia, hematuria, small bladder
  • Tx: dietary modifications, pelvic floor PT, cystoscopy to cauterize any lesions/ulcerations, meds (sodium pentosanpolysulfate to replenish GAG layer; TCAs for neural pain; antihistamines for mast cell release), sacral neuromodulation, urinary diversion = last resort
352
Q

Types of bladder fistulas

A
  1. Vesicovaginal fistula

2. Vesicointestinal fistula

353
Q

AD disease associated with epilepsy, mental retardation, adenoma sebaceum, multi-organ hamartomas and angiomyolipomas (AML)

A
  • Tuberous sclerosis
354
Q

Presence of fat within a renal lesion w/-20 HU or lower is virtually diagnostic of?

A
  • AML. RCC is excluded.
355
Q

Presentation and tx of angiomyolipomas

A
  • Presentation: typically incidental, spontaneous bleeding 10% with pain
  • Tx: observe 4cm or atypical do embolization, partial nephrectomy or radical nephrectomy
356
Q

What is an oncocytoma?

A
  • Benign tumor derived from distal tubules of kidneys

- Can coexist with RCC

357
Q

Most lethal of all GU cancers?

A
  • RCC
358
Q

Etiology of RCC

A
  • Arises from PCT typically. Two types: clear cell and papillary types
359
Q

What is VHL disease?

A
  • AD disorder d/t mutations in VHL tumor suppressor gene on c/s 3.
  • Characterized by development of RCC (50% of patients, clear cell), pheochromocytoma, retinal angiomas and hemangioblastomas of brain stem/cerebellum or spinal cord
360
Q

RCC triad presentation

A
  • Flank pain, hematuria, palpable abdominal mass
361
Q

In what % of patients are paraneoplastic syndromes found? Which syndromes?

A
  • 20% of patients with RCC

- Syndromes: hypercalcemia (PTHrP), HTN (renin), polycythemia (EPO), non-met liver dysfunction (Stauffer’s syndrome)

362
Q

Most common RCC subtype? Rarest?

A
  • Conventional/clear cell

- Rarest: collecting duct, medullary

363
Q

Study of choice to diagnose RCC

A
  • CT urogram (w/ and without contrast)

- Note: > 50% found incidentally on imaging (CT or US)

364
Q

What is the best imaging study to evaluate indeterminate renal lesions on CT and to evaluate extent of renal vein/IVC involvement?

A
  • MRI
365
Q

Does renal biopsy have utility in RCC?

A
  • Sensitivities and specificities of needle biopsy for dx of RCC are similar to appearance on imaging alone so biopsy doesn’t alter treatment
366
Q

Sites of metastases for RCC

A
  • Retroperitoneal LNs, lung, liver, bone, brain

- Note: 1/3rd of RCC patients will have metastatic dz at presentation

367
Q

What is Fuhrman system?

A
  • System of grading tumor size and staging of clear cell RCC

- Independent predictor of survival

368
Q

Single most important prognostic factor for RCC

A
  • Pathologic staging
369
Q

Tx for localized RCC

A
  • Active surveillance: small renal lesions
370
Q

What to watch for after radical nephrectomy?

A
  • Glomerular hyperfiltration in contralateral kidney to restore filtration capacity. Prolonged leads to renal injury and focal segmental glomeruloscelorosis. First sign = proteinuria. Partial nephrectomy helps prevent hyperfiltration injury.
371
Q

Is radical nephrectomy cancer free survival comparable to partial nephrectomy?

A
  • Equivalent for T1 and T2 tumors.
372
Q

Tx of metastatic RCC

A
  • Resistant to radiation and chemo
  • Systemic immunotherapy: IL2, IFN
  • Targeted antiangiogenic agents: sunitanab, sorafenib, temsirolimus. Less toxic than IL-2.
373
Q

Common tumor of renal pelvis and ureter

A
  • TCC
374
Q

Sx of TCC

A
  • Hematuria primarily. Sometimes flank pain if obstruction present.
375
Q

Tx of TCC

A
  • Radical nephroureterectomy is gold standard

Renal (2 decks)

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