Term
| Why is the left kidney taken during a donor transplantation? |
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Definition
| Longer renal vein- pg 504 |
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Term
| What are the 6 major sections of a nephron? |
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Definition
Classified by location of glomerulus as superficial, mid-cortical, juxtamedullary, ect.
1) Bowman's capsule (Tuft of capillaries for Glomerular filtration)
2) Proximal tubule
3) Thin limbs of loop of henle (Descending and Ascending)
4) Thick ascending limb of loop of Henle
5) Distal convoluted tubule
6) Collecting duct. |
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Term
| What is the basic structure of a glomerulus? |
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Definition
Pg 504
Formed by blood vessels, epithelium (Bowman's capsule), intervening BM and stalk of support cells (Mesangial cells).
Vascular and Urinary poles
1) Afferant arteriole branches to form tuft of glomerular capillaries (fenestrated), where filtration occurs, and then merge to form efferant arteriole (both surrounded by smooth muscle)
2a) Parietal epithelium of Bowman's capsule lines urinary space
2b) Visceral epithelium (PODOCYTES) interdigitate at their pedicles (coated in sialic acid) via nephrin-cytoskeleton interactions and cover glomerular capillaries
3) BM lies between capillary endothelium and podocyte processes and is organized into
a) Lamina rara externa (contracts podocytes)
b) Lamina densa (central dense layer of collagen IV that limits permeability)
c) Lamina rara interna (contracts capillary endothelium)
**Lamina rara externa and interna contain laminin and fibronectin anchoring proteins, as well as heparan sulfate-rich anionic proteoglycans which repel negatively charged plasma proteins and attract positively charged plasam proteins |
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Term
| What is the anatomical course of the ureters once they leave the kidneys? |
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Definition
Pass UNDER Uterine artery and ductus deferens (retroperitoneal)
"Water (ureters) under the bridge (artery, ductus deferens)" |
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Term
| Describe the fluid compartment distribution of the body. |
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Definition
60-40-20
1) TBW is 60% of TB weight (kg)
2) ICF is 2/3 of TBW (K+, Mg2+, ATP/ADP) and ECF is 1/3 of TBW (Na+, Cl-, HCO3-)
3) Plasma is 1/4 of ECF (albumin and globulin) and interstitial fluid is 3/4 of ECF (hyperfiltrate) |
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Term
How are plasma volume and extracellular volume measured?
What about TBW, interstitial fluid and ICF?
What is the normal Osmolarity of the body? |
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Definition
1) Plasma= radiolabeled albumin (evan's blue)
ECF= Inulin
2) TBW= titrated water
Interstitial fluid= ECF (inulin)- PV (evan's blue)
ICF= TBW - ECF (inulin)
3) 290 mOsm |
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Term
| What is the glomerular filtration barrier and how is it disrupted in nephrotic syndrome? |
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Definition
Size and Charge barriers
1) GFB is composed of
- size barrier (fenestrated capillary endothelium)
- negative charge barrier (fused BM with heparan sulfate)
- epithelial layer of podocyte food processes
2) Fused basement membrane with heparan sulfate is disrupted to charge barrier is lost, resulting in albuminuria, hypoproteinemia, generalized edema and hyperlipidemia |
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Term
| How is urine clearance of a substance determined and how does it relate to GFR? |
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Definition
Cx (mL/min)= UxV/Px,
where V is urine flow rate
If Cx>GFR: net tubular secretion of x
If Cx If Cx = GFR: no net secretion or reabsorption |
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Term
What happens to tubular secretion of a substance if the urinary flow rate increases?
What if the plasma concentration of that substance decreases? |
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Definition
Clearance= UV/P
GFR= C (inulin)
1) If V increases, so does urine clearance of the substance. C>GFR, then there will be net tubular secretion, since substance will be lost faster than it is reabsorbed.
2) If P increases, C will decrease, and if C < GFR, there will be net reabsorption of the substance. |
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Term
| How is GFR ideally and normally determined, respectively? |
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Definition
Normal GFR= 100 mL/min
1) "Ideal" is clearance of inulin, which is freely filtered and neither reabsorbed nor secreted.
2) Creatinine clearance is used as an approximate measure, but slightly overestimates, because Cr is secreted slightly by tubules.
C= UV/P
C= Kf[{Pgc -Pbs) - (PIgc - PIbs)]
gc= glomerular capillary
bs= Bowman's space |
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Term
What is "effective renal plasma flow (ERPF) and how is it determined?
Why is it useful clinically? |
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Definition
Used to ultimately estimate RBF
1) Estimated using para- aminohippurate (PAH) clearance, which is both filtered and actively secreted in the proximal tubule.
**underestimates ERPF by 10%**
2) RBF= RPF/ (1-Hct)= UV/P(1-Hct) |
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Term
| What is the glomerular filtration factor (FF) and how is it calculated? |
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Definition
""How much incoming fluid is actually filtered by the glomerulus"
FF= GFR/RPF= (Cr clearance)/(PAH clearance).
- Normally 20%
Filtered load= GFR * Plasma concentration |
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Term
| Describe the basic process of filtration anatomically at the glomerulus. |
|
Definition
1) Fluid enters the glomerular capsule via the afferent arteriole
**PGE dilate afferent arteriole, increasing RPF and GFR (FF remains constant). NSAIDS inhibit this**
2) 20% is filtered and 80% leaves the glomerular capillaries by the efferent arterioles to become the peritubular capillary circulation.
**Ang-II preferentially constricts the efferent arteriole, increasing the GFR but decreasing the RPF (FF increases)** |
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Term
What effect does Lisinopril have on glomerular filtration?
Why doesn't ASA have the same effect? |
|
Definition
1) Decreases Filtration Fraction
Ace-i prevents Ang-II mediated vasoconstriction of efferent arteriole, which normally increases GFR and decreases RPF (increasing FF).
2) ASA inhibits PGE, thereby preventing PGE-mediated dilation of the afferent arteriole. However, this will decreases RPF and GFR equivalently, so FF will remain constant. |
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Term
What is the effect of each of the following on glomerular filtration fraction?
1) Afferent arteriole constriction (NSAID use)
2) Efferent arteriole constriction (Ang-II)
3) Increased plasma protein concentration
4) Decreased plasma protein concentration
5) Constriction of ureter |
|
Definition
1) RPF decreases, GFR decreases, FF NC
2) RPF decreases, GFR increases, FF increases
3) RPF NC, GFR decreases, FF decreases
4) RPF NC, GFR increases, FF increases
5) NC, GFR decreases, FF decreases |
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Term
How would you calculate each of the following measures of reabsorption and secretion?
1) Filtered load
2) Excretion rate
3) Reabsorption
4) Secretion |
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Definition
1) GFR x Px
2) V x U
3) Filtered- secreted
4) Excreted- filtered
**reabsorption= 2x filtered - excreted** |
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Term
| Why might glucose appear in the urine? |
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Definition
Marker for DM
At normal plasma level, glucose is completely reabsorbed in proximal tubule by Na+/glucose cotransport.
- At levels of 160-200 mg/dL (threshold), it begins to appear in urine
- At 350 mg/DL, all transporters are saturated (Tm) |
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Term
| Why might a patient have diarrhea, dermatitis and dementia despite a diet full of vitamin and fat-soluble vitamins? |
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Definition
3 D's of Pellagra, but Niacin (B3) is clearly in diet.
Hartnup's disease, a deficiency of neutral AA (tryptophan) transporter.
All AA clearance occurs by Na-depent transporters in proximal tubule (subject to competitive inhibition). |
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Term
Which of the following does NOT occur in the early proximal tubule?
1) Reabsorption of amino acids
2) Reabsorption of glucose and sodium
3) sodium/hydrogen exchange
4) hypotonic absorption
5) ammonia generation |
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Definition
4- Absorption in the PT is ISOtonic.
-4mV:0mV Lumen:interstitium
- The early PT contains brush border, which reabsorbs all glucose (Na/glucose co-transport), amino acids, most Cl- (HCO3-/Cl- exchange), Na+ and H2O
- PT generates and secretes NH3+, which acts as buffer for secreted H+ |
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Term
How do each of the following compounds affect the PT?
1) PTH
2) AT II
3) Acetazolamide |
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Definition
1) Inhibits Na+/Phosphate co-transport, leading to net phosphate excretion
2) Increases Na+/H+ exchange, leading to water reabsorption and permitting contraction alkalosis.
3) CA-i that prevents CA secretion from PT into filtrate
- Carbonic acid cannot be broken down to H2O and CO2 in lumen, and therefore cannot pass into the PT for bicarbonate synthesis and reabsorption. |
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Term
Which of the following DOES NOT occur in the thick ascending loop of henle
1) Impermeable to water
2) Active reabsorption of Na+, K+ and Cl
3) Paracellular reabsorption of Mg2+ and Ca2+
4) Urine concentration
5) ROMK-mediated K+ recycling |
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Definition
4-TAL is a DILUTING segment
+7mV:0mV Lumen:interstitium
- Apical Na+/K+/2Cl- transporter actively reabsorbs these ions (inhibited by Loop diuretics). Basolateral Na+/K+ ATPase reabsorbs Na+ (10-20% in TAL) and K+/Cl- transport occurs passively down electrochemical gradient.
- ROMK channels secrete K+, creating gradient for Mg2+/Ca2+ paracellular transport |
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Term
How do each of the following drugs act?
1) Spironolactone
2) Hydrochlorothiazide
3) Furosemide
4) Ethacrynic acid |
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Definition
1) 1 of 3 K+ sparing diuretics (the K+ STAys- Sprinolactone, Triamterene, Amiloride, eplerenone)
- Competitive aldosterone receptor antagonist in cortical collecting tubule
- Amiloride and Triamterene inhibit NCC channel in CCT
2) Thiazide diuretic that inhibits inhibits NaCl reabsorption in early distal tubule, reducing diluting capacity and decreases Ca2+ excretion
3) Sulfonamide loop diuretic that inhibits Na/K/2Cl transport in TAL, abolishes hypertonicity of medulla and prevents concentration of urine.
- Increases Ca+ secretion and stimulates PGE release
4) Phenoxyacetic acid derivative that acts like furosemide (non-sulmonamide) |
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Term
| What happens in the thin descending and ascending loops of henle? |
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Definition
1) This descending= concentrating segment (makes urine hypertonic)
- passive reabsorption of water via medullary hypertonicity (impermeable to sodium)
-10mV:0mV Lumen:interstitium
2) Thin ascending loop- passive diluting segment
- permeable to ions (Na and Cl), but NOT to water |
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Term
Which of the following DOES NOT occur in the DCT?
1) Paracellular Ca2+/Mg2+ co-transport
2) Active Na+/Cl- co-transport
3) Urine dilution
4) PTH-sensitive Ca2+/Na+ exchange
5) 5-10% of Na+ reabsoprtion |
|
Definition
1- Paracellular transport of these ions occurs in the TAL, where a positive gradient is generated by apical ROMK channels.
- In the diluting DCT, Ca2+ is reabsorbed through apical Ca2+ channels and then basolaterally by Ca2+/Na+ exchange (can be stimulated by PTH- 4)
- Na/Cl co-transport occurs apically (inhibited by thiazides and activated by Ang-II)
-10mV:0mV Lumen:interstitium |
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Term
Which of the following DOES NOT occur in the collecting tubules?
1) Na+ reabsorption in exchange for K+ from principle cells
2) Water reabsorption through aquaporin channels
3) Active H+ secretion from intercalated cells
4) HCO3- secretion
5) Aldosterone-mediated apical Na+ channel insertion |
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Definition
Page 508
4- in the CD, HCO3- is reabsorbed in basolateral HCO3-/Cl- exchange that takes place in intercalated cells
-50mV:0mV Lumen:interstitium
Principal Cells
- Aldosterone stimulates Na+ channel insertion into apical membrane (Amiloride/Triamterene-sensitive) (5)
- ADH acts on basolateral V2 receptors to induce apical Aquaporin insertion for water reabsorption (2)
- Apical K+ channels for secretion (1)
Intercalated cells
- H+ATPase is present in apical membrane (3)
- H+/K+ exchangers to bring in K+ secreted in principal cells
- Basolateral HCO3-/Cl- exchangers for HCO3- reabsorption |
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Term
| How does Digoxin affect the nephron? |
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Definition
Inhibits basolateral Na+/K+ ATPase in PCT.
Its active form is excreted by the kidney, so cardiac toxicity, hypoglycemia and electrolyte disturbances can occur in renal failure/elderly |
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Term
What happens to the relative concentration of each of the following substances in the tubular fluid and plasma as they move along the proximal tubule?
1) Creatinine/Inulin
2) Chloride
3) Sodium
4) HCO3-
5) PAH |
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Definition
1) Tubular concentration increases (not amount) due to water reabsorption (TF/P increases)
2) Constant, as it drives H2O reabsorption
3) Tubular concentration is higher, because it absorbed more slowly than sodium (then plateaus after first 1/3)
4) TF/P decreases because it is highly reabsorbed in PCT (like glucose and AA)
5) Tubular concentration increases because filtration and secretion (estimates ERPF) |
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Term
Which of the following is FALSE regarding the RAAS system?
1) Angiotensinogen is produced in the liver
2) Renin is released from kidneys in response to decreases in BP, Na+ delivery or increases in sympathetic tone
3) ACE is released from the lungs and kidneys, and converts Ang-1 to Ang-2
4) Ang-II inhibits thirst centers in the hypothalamus
5) Ang-II stimulates aldosterone release from the adrenal gland |
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Definition
4- Ang-II stimulates hypothalamic thirst centers and stimulates ADH release from the posterior pituitary, to increase insertion of Aquaporin channels into the apical membrane of principal cells of the CD for H2O reabsorption.
Angiotensinogen is produced by the liver and then activated to Ang-I by renin (kidneys), and then Ang-II by ACE (lungs and kidneys).
Ang 2 does 5 main things
1) Increases BP
- acts on AT-II receptors on vascular smooth muscle for vasoconstriction
2) Increases FF
- Constricts efferent arteriole to preserve renal function (GFR) in low volume states (low RBF)
3) Increases H2O reabsoprtion
a) ADH release from posterior pituitary binds V2 receptors in basolateral membrane of principal cells, leading to aquaporin insertion into apical membrane in CD.
b) Increases Na+/H+ activity in proximal tubule, permitting contraction alkalosis
4) Stimulates aldosterone release from adrenal gland, - increases Na+ channels and Na+/K+ pump insertion in principle cells
- Up-regulates K+ channels in principal cells and H+ channels in intercalated cells
5) Stimulates thirst
- stimulates hypothalamus |
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Term
| What are the 5 major functional consequences of Angiotensin II release? |
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Definition
Released in response to low BP (JG cells), low Na+ delivery (MD cells) or increased sympathetic tone (B1 receptors)
1) Increases BP
- acts on AT-II receptors on vascular smooth muscle for vasoconstriction
**affecting baroreceptor function, limits reflex bradycardia, which might normally accompany pressor effects**
2) Increases FF
- Constricts efferent arteriole to preserve renal function (GFR) in low volume states (low RBF)
3) Increases H2O reabsoprtion
a) ADH release from posterior pituitary binds V2 receptors in basolateral membrane of principal cells, leading to aquaporin insertion into apical membrane in CD.
b) Increases Na+/H+ activity in proximal tubule, permitting contraction alkalosis
4) Stimulates aldosterone release from adrenal gland, - increases Na+ channels and Na+/K+ pump insertion in principle cells
- Up-regulates K+ channels in principal cells and H+ channels in intercalated cells
5) Stimulates thirst
- stimulates hypothalamus |
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Term
| Why does reflex bradycardia not occur with Angiotensin II-mediated increases in BP, thirst, water reabsorption and glomerular filtration? |
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Definition
| Ang-II affects baroreceptor function to limit bradycardia |
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Term
| How does Aldosterone release from the adrenal glands create a favorable environment in the nephron for Na/H2O reabsorption? |
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Definition
Primarily regulated blood volume in response to Ang-II production and primarily affects CD
1) Up-regulate Na+ channel and Na/K ATPase insertion into principle cells
2) Enhances K+ excretion by increasing apical K+ channels in principle cells
3) Enhances H+ secretion by increasing H+ channels in intercalated cells. |
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Term
| How stimuli are known to increase renin release from the kidney? |
|
Definition
Released from JG cells when BP drops and too much absorption is occuring
1) Low BP sensed baroreceptors next to JG cells
2) Low NaCl concentration sensed by macula densa in DCT
- Decreases resistance to blood flow in afferent arteriole
- Increases renin release from JG cells
3) Increased sympathetic tone in JG B1 receptors |
|
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Term
What are the primary functions of each of the following?
1) Ang II
2) ANP
3) ADH
4) Aldosterone |
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Definition
1) Affects baroreceptor function; limits reflex bradycardia, which would normally accompany its pressor effects
2) released from atria in response to increased volume, acting as a "check" for RAAS system
- relaxes vascular smooth muscle via cGMP, causing increased GFR and decreased renin.
3) Regulates osmolarity but also responds to low blood volume, which takes precedence
4) Regulates blood volume (in low-volume states, both ADH and aldosterone are active) |
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Term
| What is the Juxtaglomerular apparatus and what is its clinical importance? |
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Definition
Composed of JG cells (modified smooth muscle cells in afferent arteriole) and Macula dense (Na+ sensor in DCT).
JG cells secrete renin in response to decreased RPF, decreased Na+ delivery to DCT and increased sympathetic tone (B1)
Renin will become Ang-II, which restores BP, maintains GFR (increasing FF), causes aldosterone and ADH release (osmolarity/fluid balance) and stimulates thirst. |
|
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Term
| What are the major endocrine functions of the kidney? |
|
Definition
1) Release EPO
- in repone to hypoxia from endothelial cells of peritubular capillaries
2) 1,25- (OH)2 vitamin D
- Produced by 25-OH vit D in PCT cells when stimulated by PTH, increasing reabsorption of Calcium and Phosphate and increasing intestinal absorption.
3) Renin
- Secreted by JG cells in response to decreased renal arterial pressure and increased renal sympathetic discharge (B1 receptors)
4) PGE2
- Paracrine secretion vasodilates afferent arterioles to increase GFR (inhibited by NSAIDS) |
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Term
| Why might a patient on ASA have renal failure? |
|
Definition
| PGE2 inhibition, which is a paracrine signal that is critical for afferent arteriole dilation and maintenance of GFR. |
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Term
Which of the following descriptions of ANP is INCORRECT?
1) Secreted in response to increased atrial pressure
2) Causes increased GFR
3) Causes increased Na+ filtration and reabsorption
4) Net effect of volume loss
5) Causes cGMP-mediated vasodilation of vascular smooth muscle |
|
Definition
3- ANP increases GFR and Na+ filtration WITHOUT a compensatory increase in reabsorption. This is why ANP release results in a net volume AND Na+ loss!
Its mechanism to increase GFR and decrease renin release is cGMP-mediated vascular smooth muscle dilation |
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Term
What is the "net effect" of each of the following chemicals?
1) ANP
2) PTH
3) Angiotensin II
4) Aldosterone
5) ADH (Vasopressin) |
|
Definition
1) Na+ and Volume loss
- Increase GFR and Na+ filtration without increased reabsorption.
2) Increased Ca2+ reabsorption (DCT) and Phosphate reabsorption (PCT), as well as 1,25 (OH)2 Vitamin D production
- causes calcium and phosphate absorption in GUT
3) Preservation of renal function in low-volume state (FF) with simultaneous Na+ reabsorption and reduced volume loss
- Efferent arteriole constriction (Increase GFR and FF) WITH compensatory Na+ reabsorption in PCT and Distal nephron
4) Maintains blood volume
- Secreted in response to low blood volume (AT-II) and high plasma [K+]
- Increased Na+ reabsorption (channel insertion in apical membrane of principle cells), K+ secretion and H+ secretion
5) Increases water reabsorption in response to low Osmolarity or Blood volume
- Binds V2 receptors in basolateral membrane of principle cells, leading to Aquaporin insertion into apical membrane. |
|
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Term
| How do the actions of ANP and ATII differ in terms of sodium handling? |
|
Definition
Both increase GFR (ANP via vasodilation and AT-II through efferent arteriole constriction).
1) ANP has NO compensatory increase in sodium reabsorption due to increased filtration, so there is a net sodium and fluid loss.
2) AT-II DOES have a compensatory response, so sodium is reabsorbed to maintain renal function in low-volume states |
|
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Term
| What factors lead to Aldosterone release from the adrenal cortex? |
|
Definition
1) Low blood volume
- AT-II stimulate aldosterone release, which will increase Na+ reabsorption and increase water reabsorption as well.
2) Increased plasma K+ concentration
- Increases Na+ channel insertion in apical membrane of CD, thereby increasing K+ secretion and excretion. |
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Term
Which of the following factors would cause K+ to shift OUT of cells, causing hyperkalemia?
1) Insulin
2) Alkalosis
3) B-adrenergic agonists
4) Digitalis
5) Hypo-osmolarity |
|
Definition
4- Digitalis blocks Na+/K+ ATPase in basolateral membrane, which prevents K+ uptake into cells.
INsulin shifts K INto cells
1) Insulin increases Na/K ATPase activity
2) B-adrenergic agonists increase Na/K ATPase activity
3) Alkalosis increases K+/H+ exchanger (exchange of intracellular H+ for extracellular K+) in intercalated cells, to increase H+ in the extracellular space and correct the alkalosis
4) Hypo-osmolarity favors ion absorption. |
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Term
Which of the following factors would cause K+ to shift IN to cells, causing hypokalemia?
1) B-adrenergic antagonists
2) Insulin deficiency
3) Digitalis
4) Hypo-osmolality
5) Cell lysis
6) Acidosis/Severe exercise |
|
Definition
4- Hypo-osmolality will favor ion reabsorption into cells, which would cause hypokalemia
- B-adrenergic antagonists, Digitalis and Inulin deficiency all lead to decreased Na/K ATPase activity, which limits K+ uptake into cells
- Cell lysis causes K+ release into the extracellular fluid
- Acidosis or severe exercise increase the H+/K+ exchanger activity, moving K+ out of cells and extracellular H+ into cells. |
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|
Term
What electrocyte imbalance could account for each of the following symptoms?
1) Disorientation, stupor, coma
2) Tetany, NM irritability
3) Peaked T waves, wide QRS, arrhythmias
4) U waves on ECG, flattened T waves, arrhythmias, paralysis
5) Delirium, decreased DTRs, cardiopulmonary arrest |
|
Definition
1) Low serum Na+
2) Low serum Ca2+ (without tetany could be Mg2+)
3) High K+
4) Low K+
5) High Mg2+ |
|
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Term
What clinical symptoms might you expect with low serum electrolyte levels of each of the following?
1) Na+
2) K+
3) Cl-
4) Ca2+
5) Mg2+
6) PO4_3- |
|
Definition
1) Disorientation, stupor, coma
2) U waves, flattened T waves, arrhythmia, paralysis
3) Secondary to metabolic alkalosis, hypokalemia, hypovlemia, increased aldosterone
4) Tetany, NM irritability
5) NM irritability, arrhythmias
6) Low-mineral ion product causes bone loss, osteomalacia |
|
|
Term
What clinical symptoms might you expect with high serum electrolyte levels of each of the following?
1) Na+
2) K+
3) Cl-
4) Ca2+
5) Mg2+
6) PO4_3- |
|
Definition
1) Neurologic: irritability, delirium, coma
2) Secondary to non-anion gap acidosis
3) Peaked T waves, wide QRS, arrhythmia
4) Delirium, renal stones, abdominal pain, not necessarily calciuria
5) Delirium, decreased DTRs, cardiopulmonary arrest
6) Renal stones, metastatic calcifications |
|
|
Term
What kind of acid-base abnormality is described by each of the following?
1) pH= 7.2, pCO2 37 mmHg, [HCO3-] low
2) pH= 7.7, pCO2 36 mmHg, [HCO3-] high
3) pH= 7.7, pCO2 37 mmHg, [HCO3-] low
4) pH= 7.2, pCO2 43 mmHg, [HCO3-] high |
|
Definition
Remember, respiratory compensation is immediate, but metabolic HCO3- compensation is DELAYED.
1) Compensated primary metabolic acidosis
- Low HCO3- caused hyperventilation, which decreased pCO2
2) Non-compensated, primary metabolic alkalosis
- basic pH and high bicarbonate, but no hypoventilation to increase pCO2
3) Primary respiratory alkylosis with metabolic compensation
- pH is basic, pCO2 is low and bicarbonate is low to compensate
4) Primary respiratory acidosis with metabolic compensation
- pH is acidic and pCO2 is high, so bicarbonate is increased to compensate |
|
|
Term
| How can one determine is respiratory compensation for a metabolic acidosis is appropriate? |
|
Definition
Winter's Formula
pCO2= 1.5 (HCO3-) + 8 +/- 2
pCO2 should increase 0.7 for every 1 mEq/L HCO3- |
|
|
Term
What are the possible causes of the following acid/base abnormality?
pH= 7.3
pCO2= 47mmHg
[HCO3-]= 27 mEq/L |
|
Definition
Primary respiratory acidosis with metabolic compensation
pCO2= 47mmHg (35-45)
[HCO3-]= 27 mEq/L (22-26)
CAUSE IS HYPOVENTILATION
- airway obstruction
- acute lung disease
- chronic lung disease
- opioids, narcotics, sedatives
- weakening of respiratory muscles |
|
|
Term
What are the possible causes of the following acid/base abnormality?
pH= 7.3
pCO2= 30mmHg
[HCO3-]= 20 mEq/L
[Na+]= 140
[Cl-]= 100 |
|
Definition
pCO2 30 (35-45)
[HCO3] 20 (22-26)
30= 20 + 8 +/- 2= 30 (sufficient)
Primary metabolic acidosis with respiratory compensation
AG= 140 - (20 +100)= 20, INCREASED
MUDPILES
- Methanol (formic acid)
- Uremia
- Diabetic KA
- Paraldehyde or Phenformin
- Iron or INH
- Lactic acidosis
- Ethylene glycol (oxalic acid)
- Salicylates (aspirin) |
|
|
Term
Which of the following would NOT produce an AG metabolic acidosis?
1) Methanol
2) Uremia
3) Paraldehyde
4) Hyperchloremia
5) Lactic acidosis
6) DKA |
|
Definition
4- Hyperchloremia produces a normal AG, as does glue sniffing, renal tubular acidosis and diarrhea
AG MA is MUDPILES
Methanol, Uremia, DKA, Paraldehyde, Iron/INH, Lactic acidosis, Ethylene glycol (oxalic acid) , Salicylates |
|
|
Term
What are the possible causes of the following acid/base abnormality?
pH= 7.3
pCO2= 30mmHg
[HCO3-]= 20 mEq/L
[Na+]= 136
[Cl-]= 105 |
|
Definition
pCO2 30 (35-45)
[HCO3] 20 (22-26)
30= 20 + 8 +/- 2= 30 (sufficient)
Primary metabolic acidosis with respiratory compensation
AG= 136 - (20 +105)= 11, NORMAL
1) Diarrhea
2) Sniffing glue
3) Hyperchloremia
4) Renal tubular acidosis |
|
|
Term
What are the possible causes of the following acid/base abnormality?
pH= 7.6
pCO2= 30mmHg
[HCO3-]= 20 mEq/L
[Na+]= 140
[Cl-]= 100 |
|
Definition
pCO2= 30 (35-45)
HCO3= 20 (22-26)
Primary respiratory alkalosis with metabolic compensation (delayed)
1) Hyperventilation (early high-altitude exposure)
2) Aspirin ingestion (early, PGE inhibition) |
|
|
Term
What are the possible causes of the following acid/base abnormality?
pH= 7.6
pCO2= 46mmHg
[HCO3-]= 28 mEq/L
[Na+]= 140
[Cl-]= 100 |
|
Definition
pCO2= 46 (35-45)
HCO3= 28 (22-26)
Primary metabolic alkalosis with respiratory compensation (immediate hypoventilation)
1) Diuretic use
2) Vomiting
3) Antacid use
4) Hyperaldosteronism |
|
|
Term
What type of renal tubular acidosis is described by each of the following?
1) Defect in collecting tubules ability to excrete H+. Associated with hypokalemia and risk of calcium-contaiing kidney stones.
2) Hypoaldosteronism or lack of collecting tubule response to aldosterone. Associated with hyperkalemia and inhibition of ammonium excretion in PCT.
3) Defect in PCT HCO3= reabsorption. Associated with hypokalemia and hypophosphatemic rickets. |
|
Definition
Cause on non-AG MA
1) Type 1 ("distal")
- Can't excrete H+ so you get acid buildup and you can't reabsorb K+.
2) Type 4 ("Hyperkalemic")
- Without aldosterone effects, you don't get apical Na+ channel insertion into CD, so you don't get K+ secretion.
- Urine is acidic and how defective buffering capacity
3) Type 2 ("Proximal")
- Without HCO3- reabsorption proximally, you won't get H+ secretion and K+ reabsorption distally. |
|
|
Term
What type of renal tubular acidosis is described by each of the following?
1) Defect in collecting tubules ability to excrete H+. Associated with hypokalemia and risk of calcium-contaiing kidney stones.
2) Hypoaldosteronism or lack of collecting tubule response to aldosterone. Associated with hyperkalemia and inhibition of ammonium excretion in PCT.
3) Defect in PCT HCO3= reabsorption. Associated with hypokalemia and hypophosphatemic rickets. |
|
Definition
Cause on non-AG MA
1) Type 1 ("distal")
- Can't excrete H+ so you get acid buildup and you can't reabsorb K+.
2) Type 4 ("Hyperkalemic")
- Without aldosterone effects, you don't get apical Na+ channel insertion into CD, so you don't get K+ secretion.
- Urine is acidic and how defective buffering capacity
3) Type 2 ("Proximal")
- Without HCO3- reabsorption proximally, you won't get H+ secretion and K+ reabsorption distally. |
|
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Term
What can each of the following urine casts indicate about the underlying pathophysiology?
1) RBC casts
2) WBC casts
3) Granular (muddy brown) casts
4) Waxy casts
5) Hyaline casts |
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Definition
Hematuria without casts can be "non-renal" origin, like Bladder cancer or Kidney stones.
1) Glomerulonephritis, ischemia or malignant hypertension
2) Tubulointerstial inflammation, acute pyelonephritis, transplant rejection
3) Acute tubular necrosis
4) Advanced renal disease/CRF
5) Non-specific |
|
|
Term
What is meant by the term "focal, segmental, glomerulosclerosis"?
What about "diffuse, membranous glomerulonephritis"? |
|
Definition
1) Focal means few glomeruli are involved and Segmental means that only a portion of those glomeruli are involved.
FSGS in particular is the most common glomerular disease of HIV patients.
2) Diffuse membranous glomerulonephritis is a form of nephrotic syndrome that involves inflammation of numerous glomerular membranes. |
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Term
| What are the major Nephritic and Nephrotic (and combination) diseases? |
|
Definition
1) Nephritic (inflammatory process producing hematuria and RBC casts in urine)
- Acute post-strep glomerulonephritis
- Rapidly progressive glomerulonephritis
- Berger's IgA glomerulonephropathy
- Alport syndrome
2) Nephrotic (massive proteinuria, hyperlipidemia, fatty casts and edema)
- FS glomerulosclerosis
- Membranous glomerulonephritis
- Minimal change disease
- Amyloidosis
- Diabetic glomerulonephropathy
3) Both
- Diffuse proliferative glomerulonephritis
- Membrano-proliferative glomerulonephritis |
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Term
Describe the characteristic LM, EM and IF findings:
4 year old with h/x of URI with hematuria and RBC casts in urine. They are only having 200 ml/d or urine, and it is dark in color. BUN/Cr is also elevated. |
|
Definition
Description of Nephritic syndrome (RBC casts, hematuria, oliguria, pepsi urine and azotemia).
Age and infection h/x suggests post-streptococcal glomerulonephritis (tends to spontaneously resolve)
1) LM: Enlarged, hyper-cellular glomeruli with PMNs and "lumpy bumpy" appearance.
2) EM: Sub-EPITHELIAL immune complex (IC) humps
3) IF: Granular appearance with IgG, IgM and C3 deposition along GBM and mesangium. |
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Term
| What are the possible causes of rapidly progressive glomerulonephritis? |
|
Definition
"Crescentic" glomerulonephritis with poor prognosis and rapid decline in renal function (days to weeks)
1) Goodpasture's- type II hypersensitivity; antibodies to GBM and alveolar BM, with linear IF
- hematuria and hemoptosis
2) Wegener's granulomatosis (c-ANCA)
3) Microscopic polyangiitis (p-ANCA) |
|
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Term
| What types of glomerular disease can present as nephritic and nephrotic syndrome simultaneously? What are the LM, EM and IF findings? |
|
Definition
LM: "wire-looping" of capillaries
EM: sub-endothelail and sometimes intramembranous IgG-based ICs often with C3 deposition
IF: Granular (full house for SLE)
1) Diffuse proliferative glomerulonephritis (SLE)
2) Membranoproliferative glomerulonephritis (can cause DPGN) |
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Term
What glomerular disease is associated with IgA-based immune complex mesangial deposits on IF?
What other disease is it associated with? |
|
Definition
1) Berger's disease (IgA nephropathy producing nephritic)
- Often presents/flares with URI or acute gastroenteritis
- LM: mesangial proliferation EM; mesangial IC deposits
2) Henoch shonlein disease (kid with purpura on thighs and buttocks) |
|
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Term
| What is the molecular defect and associated complications of Alport syndrome? |
|
Definition
1) X-linked mutation in type IV collagen leading to split BM
2) Nerve disorders, ocular disorders, deafness |
|
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Term
| What are the classic signs/symptoms of nephrotic syndrome and what are the major forms of associated glomerular disease? |
|
Definition
1) Massive proteinuria (>3.5g/d, frothy urine), Hyperlipidemia, Fatty casts and Edema.
- Loss of AT-III in urine pre-disposes to thrombosis and loss of IG predisposes to infection.
2)
a) FSGS- HIV
b) Membranous glomerulonephritis- Drugs, infections, SLE, tumors
c) Minimal change disease (lipoid nephrosis)- children
d) Amyloidosis- associated with chronic disease (MM, RA, TB)
e) Diabetic glomerulonephropathy- sub-endohelial ICs
f) Membrano-proliferative glomerulonephritis (mixed)- non-enzymatic glycosylation |
|
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Term
Patient has massive proteinuria (>3.5g/d, frothy urine), Hyperlipidemia, Fatty casts and Edema.
Diagnose each of the following and describe microscopy findings.
1) Most common glomerular disease of HIV
2) Triggered by recent infection in children and treated with corticosteroids
3) Associated with TB, RA and Multiple myeloma
4) "Tram tracking" LM appearance on EM
5) Non-enzymatic glycosylation of GBM, increasing permeability and thickening.
6) Most common cause of adult nephrotic syndrome
(Caused by drugs, infections, SLE and solid tumors) |
|
Definition
1) FSGS (most common type in adults)
- LM shown segmental sclerosis and hyalinosis
2) Minimal change disease
- LM shows normal glomeruli, but EM shows foot process effacement
- Selective albumin loss, but not globulins due to BGM polyanion loss
3) Amyloidosis
- LM shows congo red stain and apple-green birefringence
4) Type 1 MPGN (can be nephritic)
- Sub-endothelial ICs (rebuilt GBM) with granular IF
- Associated with HBV, HCV
- Type II would have "dense deposits" and is associated with C3 nephritic factor
5) Diabetic glomerulopathy
- NEG of efferent arterioles leads to increased GFR and mesangial expansion
- LM shows mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis (Kimmelsteil-Wilson lesion)
6) Membranous glomerulonephritis (diffuse membranous glomerulopathy)- SLE nephrotic presentation
- LM shows diffuse capillary and GBM thickening
- EM shows "spike and dome" appearance with sub-EPITHELIAL deposits
- IF- granular, full house |
|
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Term
| Which forms of glomerular disease present with Sub-endothelial vs. Sub-epithelial deposits? |
|
Definition
1) Sub-endothelial
- Membranoproliferative Glomerulonephitis (Type I with "tram-tracking" and HBV/HCV association or Type II with "dense deposits" on EM and C3 nephritic factor)
- Somtimes Berger's (IgA) glomerulonephritis
2) Sub-epithelial
- Post-streptococcal glomerulonephritis
- Diffuse proliferative glomerulonephritis/Membranous glomerulonephitis (drugs, SLE, solid tumors, infection) |
|
|
Term
| What is the difference between Type 1 and Type 2 membranoproliferative glomerulonephritis? |
|
Definition
Can present as nephritic or nephrotic, with Subendothelial ICs and granular IF appearance.
1) Type 1
- "tram tracking" on LM and GBM splitting from mesangial overgrowth
- Associated with HBV and HCV
2) Type 2
- "dense deposits" on EM
- Associated with C3 nephritic factor |
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Term
What type of kidney stone is described by each of the following and what causes them to form?
1) Common crystals that precipitate at neutral or acidic pH in individual with multiple myeloma and are radio-opaque on x-ray.
2) Precipitates at basic pH in patient with previous infection and are radio-opaque on X-ray
3) Precipitate at acidic pH and are radiolucent on X-ray
4) Rare hexagonal crystals that precipitate at acidic pH and are radio-opaque |
|
Definition
1) Calcium oxlalate or Calcium phosphate stone (most common)
- Conditions that cause hypercalcemia (cancer, increased PTH)
- Oxalate can be result of ethylene glycol poisoning (would also see AG MA) or vitamin C abuse
2) Ammonium magnesium phosphate (15%)
- Caused by infection with urease-positive bugs (Proteus, Staph, Klebsiella)
- Can form staghorn calculi and be nidus for UTI
3) Uric acid (5%) crystals associated with hyperuricemia (gout or polycythemia or leukemia).
- Seen in leukemia because of increased cell turnover
4) Cystine (1%) from cystinuria
- Treat with alkalization |
|
|
Term
|
Definition
Can be caused by stone or other urinary tract obstruction.
Causes dilation up to obstruction and, in chronic cases, parenchymal thinning (can ultimately kill kidney) |
|
|
Term
| What is the genetic association of the most common renal malignancy? |
|
Definition
von Hippel-Linau syndrome and gene deletion in chromosome 3p
vHL is a E3 ligase that targets and degrades HIF-1a, a hypoxia-induced transcription factor involves in vasculogenesis. |
|
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Term
| What paraneoplastic syndromes are associated with the kidney cancer associated with von Hippel-Lindau mutations in chromosome 3p |
|
Definition
Renal cell carcinoma (most common renal cancer). Cancer cells are filled with lipids and carbs in men ages 50-70 (smoking and obesity association)
1) Ectopic EPO- might see polycythemia
2) ACTH
3) PtHrP
4) Prolactin |
|
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Term
What kidney cancer is associated with polycythemia, flank pain, fever and weight loss.
Where does it metastasize to? |
|
Definition
1) Renal cell carcinoma (association with vHL syndrome and paraneoplastic syndromes).
Most common renal cell carcinoma (common in obese, male smokers ages 50-70).
2) Metastasizes to bone and lung. |
|
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Term
| What is the genetic abnormality associated with the most common renal malignancy of early childhood (age 2-4) |
|
Definition
Wilm's tumor (nephroblastoma).
Deletion of tumor suppressor gene WT1 on chromosome 11p and associated with WAGR complex: Wilm's tumor, Aniridia, GU malformation and mental Retardation |
|
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Term
3 year old boy presents with palpable flank mass and hematuria.
You look in their eyes and they have absent irises. What else is associated with this syndrome? |
|
Definition
Aniridia and Wilm's tumor (WT1 on 11p) as part of WAGR complex.
- Tumor will contain embryonic structures
G= genitourinary malformation
R= mental Retardation |
|
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Term
| What are the important risk factors for the form of GU cancer that presents with painless hematuria? |
|
Definition
Bladder Cancer- Transitional cell carcinoma (most common cancer of urinary tract)
Pee SAC
1) Phenacetin
2) Smoking
3) Aniline dyes
4) Cyclophosphamide (also hemorrhagic cystitis) |
|
|
Term
| What structures are most common involved in the most common cancer of the urinary tract? |
|
Definition
Transitional cell carcinoma
Renal calyces, Renal pelvis, Ureters, Bladder (painless hematuria)
Associated with Pee SAC (Phenacetin, Smoking, Aniline dyes, Cyclophosphamide) |
|
|
Term
| What features distinguish acute pyelonephritis from the chronic form? |
|
Definition
1) Acute
- affects cortex with sparing of glomeruli and vessels
- presents with fever, CVA tenderness, nausea and vomiting
2) Chronic (caused by vesicoureteral reflux)
- Coarse, asymmetric corticomedullary scarring, blunted calyx
- Tubules contain eosinophilic casts (thyroidization of kidney)
- WHITE CELL CASTS in urine |
|
|
Term
Which of the following descriptions of chronic pyelonephritis is FALSE?
1) Causes coarse, asymmetric corticomedullary scarring
2) White cell casts in urine are associated
3) Caused by Vesicoureteral reflux
4) Presents with Nausea and vomiting
5) Eosinophilic, "thyroid-like" cats in tubules |
|
Definition
4- This is an acute presentation, along with fever and CVA tenderness
WBC casts are classic |
|
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Term
Which of the following descriptions of acute pyelonephritis is FALSE?
1) Effects cortex and spares glomeruli/vessels
2) Presents with fever, nausea, vomiting and CVA tenderness
3) Neutrophillic infiltration of renal interstitum
4) Lymphocytic invasion with variable fibrosis. |
|
Definition
4- This is CHRONIC
Symptoms are classic, as is glomerular/vessel sparing, but infiltrate is PMN ONLY without fibrosis. |
|
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Term
27 year old male presents with fever, rash, hematuria and CVA tenderness.
What is the MOST likely cause? |
|
Definition
Drug-induced interstitial nephritis
Pyuria (eosinophils usually) and Azotemia 1-2 weeks after administration of drug (NSAIDs, diuretics, PCN-derivatives, sulfonamides, rifampin), which act as haptens, inducing type II hypersensitivity. |
|
|
Term
| What is the common cause of Diffuse cortical necrosis and why is it so concerning? |
|
Definition
Acute, generalized cortical infarction of both kidneys
1) DCN is caused by combination of vasospasm and DIC
2) Associated with obstetric catastrophe (abruptio placentae) and septic shock. |
|
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Term
| What is the most common cause of renal failure in the hospital and what are the 3 classic stages? |
|
Definition
Acute Tubular Necrosis (muddy brown casts), which is self-reversible, but fatal if left untreated (death during initial oliguric phase)
**associated with renal ischemia (shock, sepsis), crush injury (myoglobinuria), toxins.
1) Inciting event
2) Maintenance phase- oliguric; lasts 1-3 weeks; risk of hyperkalemia
3) Recovery- polyuric; BUN/Cr fall; risk of hypokalemia |
|
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Term
| You find "muddy brown" casts in a hospitalized patient. Why are you worried? |
|
Definition
Indicates Acute Tubular Necrosis, which is usually self-reversible, but can cause death in initial oliguric phase if left untreated.
ATN is caused by renal ischemia (sepsis, shock), toxins, crush injury
1) Inciting event
2) Maintenance phase- oliguric; lasts 1-3 weeks; risk of hyperkalemia
3) Recovery- polyuric; BUN/Cr fall; risk of hypokalemia |
|
|
Term
| Why might a patient present with gross hematuria and proteinuria following a recent infection if they DO NOT have nephrotic syndrome? |
|
Definition
Renal Papillary Necrosis (sloughing of renal papillae)
1) DM
2) Acute pyelonephritis
3) Chronic phenacetin use (acetaminophen is a derivative)
4) Sicke cell anemia and trait |
|
|
Term
| What are the usual causes of pre-renal, renal and post-renal AKI? |
|
Definition
AKI is "acute decline in renal funcion with elevated Cr and BUN over period of several days"
1) Pre-renal (Osm>500, Una<10, Fe_na <1%, sBUN/Cr>20)
- Decreased RBF (hypotension) leading to Na+/H2O retention, leading to increased BUN:Cr ratio
2) Renal (Osm<350, Urine Na>20, Fe_na>2%, sBUN/Cr<15)
- ATN or ischemia/toxins
- Sometimes RPGN
- Patchy necrosis leads to debris obstructing tubule and causes backflow, decreasing GFR and impairing BUN reabsorption.
3) Post-renal (Osm<350, Una>40, Fena>4%, sBUN/Cr>15)
- Outflow obstruction (strones, BPH, neoplasia, congential anomalies)
- must be BILATERAL |
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|
Term
What are common causes of each of the following lab data/AKI
1) Osm>500, Una<10, Fe_na <1%, sBUN/Cr>20
2) Osm<350, Urine Na>20, Fe_na>2%, sBUN/Cr<15
3) Osm<350, Una>40, Fe_na>4%, sBUN/Cr>15 |
|
Definition
AKI is "acute decline in renal funcion with elevated Cr and BUN over period of several days"
1) Pre-renal azotemia
- Decreased RBF (hypotension) leading to Na+/H2O retention, leading to increased BUN:Cr ratio
2) Intrinsic renal AKI
- ATN or ischemia/toxins
- Sometimes RPGN
- Patchy necrosis leads to debris obstructing tubule and causes backflow, decreasing GFR and impairing BUN reabsorption.
3) Post-renal AKI
- Outflow obstruction (strones, BPH, neoplasia, congential anomalies)
- must be BILATERAL |
|
|
Term
Which of the following DOES NOT occur in renal failure?
1) Pulmonary edema and htn
2) Hyokalemia
3) Metabolic acidosis
4) Uremia
5) Anemia |
|
Definition
2- you see hyperkalemia
Urine is not being produced and nitrogenous wastes cannot be excreted.
1) HTN/edema/CHF from Na+/H2O retention
2-3) Metabolic acidosis from low HCO3-, which is why you see hyperkalemia
4) Uremia from nitrogenous waste |
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Term
Which of the following is not characteristic of Uremia?
1) Asterixis
2) Nausea and weight loss
3) Coagulation factor deficiency
4) Encephalopathy
5) Platelet dysfunction
6) Pericarditis |
|
Definition
3- This would more likely be seen in cirrhosis.
Clinical syndrome associated with elevated BUN and Creatinine in renal failure.
Uremia= Asterixis, Encephalopathy, Pericarditis, Platelet dysfunction and Nausea/anorexia |
|
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Term
Which of the following is NOT seen renal failure?
1) Renal osteodystrophy
2) Growth retardation and developmental delay
3) Metabolic acidosis
4) Polycythemia
5) Dyslipidemia
6) Hyperkalemia |
|
Definition
|
|
Term
| Why is renal osteodystrophy common in renal failure? |
|
Definition
Hydroxylation of 25(OH)-vitamin D occurs proximal tubule cells in response to PTH, and is critical for absorption of calcium and phosphate in intestine, and renal phosphate excretion.
In renal failure, you lose calcium in urine and retain phosphate, causing secondary hyperparathyroidism. This causes sub-periosteal thinning of bones
**Hyperphosphatemia is independent of decreased serum Ca2_, whereas decreased 1,25(OH)2 vitamin D causes decreased intestinal Ca absorption**
You end |
|
|
Term
What type of renal cyst is described by each of the following?
1) Autosomal dominant genetics presenting with acute flank pain, hematuria, hypertension, urinary infection and progressive renal failure
2) Autosomal recessive genetics associated with congenital haptic fibrosis and Potter's facies
3) Cortical and medullary cysts from dialysis treatment
4) Benign, common cysts that are thin, non-enhancing and fluid-filled cystic structures
5) Associated with kidney stones (70%) and small kidney on ultrasound |
|
Definition
1) ADPKD
- Adult form that will ultimately destroy kidney parenchyma
-PKD1 or PKD2 gene mutations cause HTN (renin production)
2) ARPKD
- Potter's associated with significant renal failure in utero
- Later concerns are HTN, portal HTN and progressive renal insufficiency
3) Dialysis cysts of cortex and medulla
4) Simple cysts- found in >40% of elderly
5) Medullary cystic disease
- Can lead to fibrosis and progressive renal insufficiency with inability to concentrate urine
- Poor prognosis |
|
|
Term
| What autosomal dominant disease is associated with liver disease, berry aneurysms and mitral valve prolapse? |
|
Definition
ADPKD- PKD1 or PKD2 mutations that cause HTN (renin production)
Ultimately destroy kidney parenchyma (distended, multiple fluid-filled cysts) |
|
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Term
Which part of the nephron do each of the following agents act on?
1) Acetazolamide
2) Mannitol
3) Thiazides
4) K-sparing diuretics
5) ADH antagonists
6) Loop diuretics |
|
Definition
1) CA-inhibitor acts on PCT
- used for alkylosis associated with altitude, glaucoma, metabolic alkalosis and urinary alkalization (for acid stones)
2) Osmotic diuretic that acts on PCT
- Used for shock, drug overdose and to treat high intracrania/intraocular pressure
3) Inhibits NCC in DCT to reducing urine concentrating ability and decrease Ca2+ excretion
- Used in HTN (not when CHF or DM-2 is co-morbid), CFH, idiopathic hypercalciuria, nephrogenic diabetes insipidus
4) Amiloride/Triamterene act on collecting duct ENaC
Spironolactone is aldosterone receptor antagonist
- Used in hyperaldosteronism, K+ depletion and CHF
5) Vaptans and Tetracyclines act on collecting duct to prevent water reabsorption
6) Furosemide (sulfonamide) and Ethacrynic acid (phenoxyacetic acid derivative inhibit Na,K,2Cl transporters in TAL
- Diuresis |
|
|
Term
| What are the major toxicities of the sulfonamide drug that is used to treat Edema, hypertension and hypercalcemia? |
|
Definition
Furosemide (loop diuretic)
OH DANG
1) Ototoxicity
2) Hypokalemia
3) Dehydration
4) Allergy (sulfa- use Ethacrynic acid)
5) Nephritis (interstitial)
6) Gout |
|
|
Term
| What is the mechanism of action of Furosemide? |
|
Definition
Loops Lose calcium (use thiazide to prevent this)
1) Sulfonamide that inhibits Na,K,2Cl channels in TAL, abolishing hypertonicity of medulla, so urine cannot be concentrated
2) Stimulate PGE release (vasodilatory effect on afferent arteriole), which is inhibited by NSAIDs |
|
|
Term
| Why might a patient be placed on Ethacrynic acid? When would you avoid its use? |
|
Definition
Sulfa Allergies!
Diuretic with same action as Furosemide (Na,K,2Cl), but that is a phenoxyacetic acid derivative, rather than a sulfonamide.
Can cause hyperuricemia though, so don't use with gout! |
|
|
Term
| Why might you be cautious to use Acetazolamide to treat a patient's Glaucoma? |
|
Definition
ACIDazolamide causes ACIDosis
CA-i that can cause Hyperchloremic metabolic acidosis
Also neuropathy, NH3 toxicity and sulfa allergy |
|
|
Term
When might you avoid using the following drugs?
1) Mannitol
2) Ethacrynic acid
3) Hydrochlorothiazide
4) Spironolactone |
|
Definition
1) Osmotic diuretic- Pulmonary edema, dehydration, anuria, CHF
2) Gout (causes hyperuricemia)
3) HyperGLUC
- Causes Hypokalemic metabolic acidosis, hyponatremia, hyperGlycemia, hyperLipidemia, hyperUricemia and hyperCalcemia. Sulfa allergy
4) Hyperkalemia (K-sparing) |
|
|
Term
What happens to each of the following with use of a diuretic?
1) Urine NaCl
2) Urine K+
3) Blood pH
4) Urine Ca2+ |
|
Definition
1) Increases with all diuretics (serum may decrease)
2) Increases in all except spironolactone, amiloride and triamterene (serum may decrease)
3) Acidemia occurs with Ca-i and K-sparing diuretics
Alkalemia with loop diuretics and thiazides
4) Increases with loop diuretics: decreases paracellular Ca+ reabsorption
Decreases with thiazides: enhanced paracellular reabsorption in proximal tubule and loop of henle |
|
|
Term
| Why do loop diuretics and thiazides cause alkalemia? |
|
Definition
3 mechanisms
1) Volume contraction- increases AT-II leads to increased Na/H exchange in proximal tubule, increased bicarbonate formation (contraction alkalosis)
2) K+ loss leads to less K+ exiting all cells (via H+/K+ exchanger) in exchange for H+ entering cells
3) In low K+ state, H+ is exchanged instead of K+ for Na+ in CCD, leading to alkalosis and "paradoxical aciduria" |
|
|
Term
| What diuretics can cause acidemia and how? |
|
Definition
1) CA-i like Acetazolamide
- Decrease HCO3- absorption
2) K+-sparing aldosterone blockage
- Prevents K+ secretion and H+ secretion
- Hyperkalemia leads to K+ entering cells and H+ exiting them. |
|
|
Term
| What are the important toxicities associated with the thiazide used to prevent calcium loss? |
|
Definition
Thiazide
HyperGLUC
1) Hypokalemic metabolic acidosis
2) Hyponatremia
3) HyperGlycemia
4) HyperLipidemia
5) HyperUricemia
6) HyperCalcemia
7) Sulfa allergy |
|
|
Term
| How do ACE inhibitors work and why might you prescribe them? |
|
Definition
1) Give them for HTN, CHF, diabetic renal disease, and to prevent unfavorable heart remodeling as a result of chronic HTN
2) Inhibit ACE, preventing AT-II production and preventing inactivation of bradykinin, a potent vasodilator
- Renin release is increased due to loss of feedback inhibition |
|
|
Term
| Why might you give an ARB (-sartan) instead of an ACE-i? |
|
Definition
Captopril, enalopril, lisinopril cause COUGH!
ARBs do not increase kallikrein, so you don't get a cough |
|
|
Term
| What are the side effects associated with ACE-inhibitor use? |
|
Definition
Don't give with bilarteral renal artery sternosis because of decrease in GFR
CAPTOpRIL and Hyperkalemia
1) Cough
2) Angioedema
3) Pregnancy problems
4) Taste changes
5) hypOtension
6) Rash
7) Increased renin
8) Lower AT-II |
|
|
Term
| What is the most common cause of nephrotic syndrome in adults? |
|
Definition
|
|
