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228 Cards in this Set
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Why is the left kidney taken during living donor transplantation?
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Because the left renal vein is longer.
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What course do the ureters take from the kidney to the urethra?
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"Water under the bridge"
Ureters pass under uterine artery and ductus deferens (retroperitoneal) |
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List the different body fluid compartments and their relative volumes.
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TBW: 40% nonwater mass, 60% total body water
Total body water: 1/3 ECF, 2/3 ICF ECF: 1/4 plasma, 3/4, interstitial |
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Is sodium or potassium high inside the cell?
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"HIKIN"
High K INtracellular |
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What is the 60-40-20 rule?
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60% total body water
40% ICF 20% ECF |
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How can plasma volume be measured?
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Radiolabeled albumin.
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How can extracellular volume be measured?
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Inulin
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What is the typical osmolarity?
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290 mOsm
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What does the glomerular filtration barrier consist of?
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1. Fenestrated capillary endothelium
2. Basement membrane fused with heparin sulfate (negative charge barrier). 3. Epithelial layer consisting of podocyte foot processes (pedicles). |
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What happens to the charge barrier in nephrotic syndrome?
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Charge barrier is lost resulting in albuminuria, hypoproteinemia, generalized edema, and hyperlipidemia.
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What equation describes the renal clearance?
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Cx=(Ux)(V)/Px
Cx is clearance of drug x Ux is urine concentration of drug x Px is plasma concentration of drug x V is urine flow rate |
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What are the units for clearance of a compound?
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mL/min
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Relating the clearance of a compound to the glomerular filtration rate can tell you what? Provide examples.
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Whether the compound is reabsorbed or secreted.
Cx<GFR, reabsorption Cx>GFR, secretion Cx=GFR, no net secretion or absorption |
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What compound can be used to calculate the GFR and why?
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By monitoring inulin because it is freely filtered, but neither secreted nor reabsorbed.
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Creatinine clearance can be used to estimate the GFR. What are the limitation to its use in this regard?
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Creatinine is moderately secreted by the renal tubules, so it slightly overestimates GFR.
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What equation can be used to calculate GFR based upon inulin clearance?
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GFR=Cinulin=(Ui)(V)/Pi
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What can be used to estimate the effective renal plasma flow?
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Clearance of PAH (para-aminohippurate) because it is both filtered and excreted.
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How closely does the effective renal plasma flow estimate the true renal plasma flow?
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It underestimates RPF by approximately 10%
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How can one calculate the filtration fraction?
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FF=GFR/RPF
GFR estimated with creatinine clearance RPF estimated with PAH clearance |
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What is the normal filtration fraction?
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20%
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What is the filtered load calculated as?
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GFR x plasma concentration
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What compounds dilate afferent arterioles, leading to increased RPF and GFR?
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Prostaglandins (inhibited by NSAIDs).
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When prostaglandins are produced, what happens to the filtration fraction?
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It remains constant since both RPF and GFR increase proportionally.
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What compound constricts efferent arterioles, leading to decreased RPF and increased GFR?
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Angiotensin II (inhibited by ACE inhibitors).
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When angiotensin II is produced, what happens to the filtration fraction?
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It increases because RPF decreases and GFR increases.
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What effect does increased plasma protein concentration have on the RPF, GFR, and FF?
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RPF unchanged
GFR decreases FF decreases |
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What effect does decreased plasma protein concentration have on RPF, GFR, and FF?
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RPF is unchanged
GFR is increased FF is increased |
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What effect does constriction of the ureter have on RPF, GFR, and FF?
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RPF is unchanged
GFR is decreased FF is decreased |
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What is the definition of free water clearance (CH2O)?
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The volume of blood plasma that is cleared of solute-free water per unit time.
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How can free water clearance be calculated?
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CH2O=V-Cosm
V=urine flow rate Cosm=UosmV/Posm |
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What effect does anti-diuretic hormone (ADH) have on free water clearance?
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CH2O<0
retention of free water |
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What happens to free water clearance in the absence of ADH?
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CH2O>0
excretion of free water |
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What effect do loop diuretics have on free water clearance?
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They create isotonic urine, making CH2O equal to zero.
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How can the reabsorption rate of a compound be calculated?
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Reabsorption rate = filtered load - excretion rate
= (GFR x Px) - (V x Ux) |
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study
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study
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At a normal plasma level of glucose, what proportion is reabsorbed in the proximal tubule?
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All of it.
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At what plasma glucose concentration does glucosuria begin (threshold)?
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160-200 mg/dL
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What is significant about plasma glucose concentrations of 350 mg/dL
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All of the Na+/glucose transporters in the proximal tubule are saturated.
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What is the clinical significance of glucosuria?
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It is an important clinical clue of diabetes mellitus.
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How are amino acids reabsorbed?
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By sodium-dependent transporters (at least 3) in the proximal tubule.
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What happens in Hartnup's disease?
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A deficiency of neutral amino acid (tryptophan) transporter, resulting in pellegra.
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study
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study
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study
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study
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study
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study
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study
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study
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What happens in the early proximal tubule?
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Brush border enzymes reabsorb most all glucose and amino acids, and most bicarbonate, sodium, chloride, and water. It generates and secretes ammonia which buffers the H+ secretion.
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What happens in the thin descending loop of Henle?
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Passive reabsorption of water due to medullary hypertonicity. This segment is impermeable to sodium.
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What happens in the thick ascending loop of Henle?
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Active reabsorption of sodium, potassium, chloride and paracellular reabsorption of magnessium and calcium. This segment is impermeable to water.
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What happens in the distal convoluted tubule?
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Active reabsorption of sodium and chloride.
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What happens in the collecting tubules?
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Reabsorption of sodium in exhange for secreting potassium and hydrogen ions. Passive secretion of water by aquaporins.
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What effect does PTH have on different segments of the nephron?
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1. Inhibits sodium/phosphate cotransport in the proximal tubule leading to phosphate excretion.
2. Increases calcium/sodium exchange in distal convoluted tubule leading to calcium reabsorption. |
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What effect does Angiotensin II have on the nephron?
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It stimulates sodium/hydrogen exchange in the proximal convoluted tubule leading to sodium and water reabsorption. This permits contraction alkalosis.
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What effect does aldosterone have on the nephron?
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It leads to insertion of sodium channels on luminal side of cells in the collecting tubules. This causes reabsorption of sodium and water.
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What effect does ADH have on the nephron?
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It acts at V2 receptors, increasing aquaporin channels on the luminal side of the collecting tubules.
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How do the concentrations of creatinine and inulin change along the proximal tubule?
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They increase in concentration because of water reabsorption.
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What happens to the chloride concentration in the proximal tubule?
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It increases along the proximal 1/3 and then plateaus along the distal 2/3.
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What drives water reabsorption in the proximal tubule?
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sodium
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What cells detect changes in blood pressure?
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Juxtaglomerular cells.
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What cells detect sodium chloride concentrations in the distal tubule?
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Macula densa cells.
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What three factors regulate renin release from juxtaglomerular cells.
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↓ BP, ↓ sodium delivery, ↑ sympathetic tone (β1 receptors)
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What is the primary function of renin?
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It converts angiotensinogen into angiotensin I.
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Where is angiotensinogen produced?
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In the liver.
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Where is angiotensin converting enzyme do and where is it secreted?
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It is synthesized in the lungs and kidney and It converts angiotensin I to angiotensin II and degrades bradykinin.
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What are six primary functions of angiotensin II?
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1. Acts at AT2 receptors on vascular smooth muscle, causing constriction.
2. Constricts efferent arteriole of glomerulus 3. Stimulates aldosterone secretion from the adrenal gland. 4. Stimulates anti-diuretic hormone secretion from the posterior pituitary gland. 5. Increases proximal tubule Na/H activity 6. Stimulates hypothalamus to cause thirst |
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Why does angiotensin II not result in reflex bradycardia?
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It affects baroceptor function limiting reflex bradycardia.
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How is the heart tied into the renin-angiotensin-aldosterone system?
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Atrial natriuretic peptide is released in response to ↑ BP and relaxes vascular smooth muscle via cGMP causing ↑ GFR and ↓ renin.
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What does antidiuretic hormone respond to?
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It primarily regulates osmolarity but also responds to low blood volume, which takes precedence over osmolarity.
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What does aldosterone do?
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It primarily regulates blood volume.
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What compounds protect blood volume in low-volume states?
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Both ADH and aldosterone.
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What happens following engagement of AT II receptors by angiotensin II?
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Vasoconstriction of arterioles leading to increased BP.
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What do juxtaglomerular cells do?
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They defend GFR via renin-angiotensin-aldosterone system. The secrete renin in response to ↓ renal BP, ↓ Na delivery to distal tubule, and ↑ sympathetic tone.
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What do macula densa cells do?
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The sense sodium in the distal convoluted tubule and signal to juxtaglomerular cells.
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What are the primary endocrine functions of the kidney?
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Erythropoietin, 1,25-(OH)2 vitamin D, renin, prostaglandins.
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What signals erythropoietin release from the kidney?
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hypoxia
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Describe the role of the kidney in calcium and phosphate metabolism.
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PTH leads to ↑ calcium and ↓ phosphate reabsorption in the kidney. It also stimulates 1,25 dihydroxy vitamin D production in proximal tubule cells, which promote intestinal absorption of calcium and phosphate.
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How do prostaglandins synthesized in the kidney function, and what may cause problems with this?
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Prostaglandins function as paracrine hormones to dilate afferent arterioles. NSAIDs may cause acute renal failure by inhibiting this process.
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What kidney enzyme is stimulated by PTH to produce 1,25 dihydroxy vitamin D?
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1α-hydroxylase
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study
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study
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What is the overall effect of ANP?
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Causes increased GFR and sodium filtration with no compensatory sodium reabsorption in distal nephron. This leads to sodium and water loss.
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What three factors stimulate PTH secretion from the posterior pituitary gland?
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↓ plasma calcium, ↑ plasma phosphate, ↓ plasma 1,25 dihydroxy vitamin D
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List six conditions that can lead to potassium shift out of cells (hyperkalemia).
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1. Insulin deficiency (↓ Na/K ATPase)
2. beta-adrenergic antagonists (↓ Na/K ATPase) 3. Acidosis, severe excersize (K/H exchanger) 4. Hyperosmolarity 5. Digitalis (blocks Na/K ATPase) 6. Cell lysis |
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list four conditions that can lead to potassium shift into cells (hypokalemia).
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1. Insulin (↑ Na/K ATPase)
2. beta-adrenergic agonists (↑ Na/K ATPase) 3. alkalosis (K/H exchanger) 4. hypo-osmolarity |
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questions
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bold arrows indicate the primary disturbance
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What are the compensatory responses to metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis?
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1. hyperventilation
2. hypoventilation 3. ↑ renal bicarbonate reabsorption 4. ↓ renal bicarbonate reabsorption |
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Write the Henderson-Hasselbalch equation as it pertains to determining the pH given bicarbonate concentration and CO2 partial pressure.
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pH=pKa + log([bicarbonate]/0.03Pco2)
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What does Winter's formula used for?
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To determine whether a metabolic acidosis is adequately compensated or if the patient also has a primary respiratory acidosis/alkalosis.
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What are the three primary systems that regulate acid concentration in body fluids?
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Lungs (remove CO2=H2CO3), acid/base system, kidneys (remove HCO3)
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What are the relative rates of action of the acid protective systems?
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Buffering action seconds
Respiration minutes Kidney hours to days |
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What does respiratory alkalosis/acidosis refer to?
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Changes in PCO2
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What does metabolic alkalosis/acidosis refer to?
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Changes in bicarbonate production.
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In the kidney, how are bicarbonate and acid eliminated?
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Bicarbonate is eliminated by filtration, where as H+ is actively secreted. Remember that these processes are tied together by brush border carbonic anhydrase.
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If a patient is acidemic, how can you distinguish between metabolic vs. respiratory acidosis?
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Check the PCO2. If higher than 40 mmHg, then respiratory. If lower than 40 mmHg, then metabolic acidosis with compensation.
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If a metabolic acidosis is identified, what is the next step to identify the cause?
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Check the anion gap. AG=Na-(Cl+HCO3)
If high, then MUDPILES. If low, then either diarrhea, renal tubular acidosis, or hyperchloremia. |
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What are possible causes of high anion gap in metabolic acidosis?
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MUDPILES: Methanol, Uremia, Diabetic acidosis, Paraldehyde (Phenoformin), Iron (INH), Lactic acidosis (sepsis), Ethylene glycol, Salicylates
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What are principle causes of respiratory acidosis?
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Hypoventilation: Obstruction, Lung disease, Opiods, Weak respiratory muscles (MG or Guillain Barre).
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How do you distinguish between respiratory or metabolic alkalosis?
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Look at the PCO2, if less than 40 mmHg, then respiratory alkalosis. If greater than 40 mmHg, then metabolic acidosis.
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If metabolic alkalosis is identified, what are the possible causes?
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Diuretic use (losing Cl-), vomiting (most common), antacid use, hyperaldosteronism.
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In metabolic alkalosis, what is the preferable test to do to determine the primary cause?
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Test urine [Cl-]. If low it means volume depletion.
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What are the primary causes of respiratory alkalosis?
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Hyperventilation or aspirin ingestion.
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What can be used to distinguish between diarrhea and renal tubular acidosis in normal anion gap metabolic acidosis?
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Look at the urine anion gap. If negative, kidney function is good, indicating diarrhea.
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What are the three types of renal tubular acidosis?
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Type 1 (distal), Type 2 (proximal), and Type 4 (hyperkalemic).
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What is the major problem in type 1 renal tubular acidosis?
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Defect in the collecting tubule's ability to secrete hydrogen ion. It is associated with hypokalemia and risk for calcium-containing kidney stones.
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What is the major problem in type 2 renal tubular acidosis?
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Defect in proximal tubule bicarbonate reabsorption. Associated with hypokalemia and hypophosphatemic rickets. Fanconi Syndrome causes this.
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What is the major problem in type 4 renal tubular acidosis?
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Hypoaldosteronism or lack of collecting tubule response to aldosterone. Causes hyperkalemia, inhibition of ammonia secretion in proximal tubule. Causes a drop in urine pH due to decreased buffering capacity.
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What is the most common type of renal tubular necrosis?
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Type 4 RTA.
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Study
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Study
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Study
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Study
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What are the major types of casts that may be found in the urine?
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RBC casts, WBC casts, Granular (Muddy brown) casts, Waxy casts, Hyaline casts
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What does the presence of casts indicate?
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Hematuria or pyuria of renal origin.
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What would you expect to see in the urine of patients with bladder cancer or kidney stones?
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RBCs with no casts.
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What would you expect to see in the urine of patients with cystitis?
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WBCs with no casts.
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What disorders commonly present with RBC casts?
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Glomerulonephritis, ischemia, or malignant HTN.
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What disorders commonly present with WBC casts?
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Tubulointerstitial inflammation, acute pyelonephritis, and transplant rejection.
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What disorder presents with granular or muddy brown casts?
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Acute tubular necrosis.
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What would cause the accumulation of waxy casts?
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Advanced renal disease or chronic renal failure.
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What are hyaline casts indicative of?
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They are non-specific.
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What are the three principle categories of glomerular disorders?
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Nephrotic, Nephritic, and Rapidly Progressive Glomerulonephritis (RPGN)
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Study
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Study
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What are the primary modalities for analyzing glomerular disorders?
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Light microscopy, immunofluorescence microscopy, and electron microscopy.
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What types of IF microscopy patterns are there?
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Linear or lumpy bumpy (immune complexes).
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What is the most common cause of a linear IF pattern?
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Goodpasture's syndrome which has anti-basement membrane antibodies.
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What is the definition of Nephritic syndrome?
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An inflammatory process resulting in HOHA: Hematuria and RBC casts, Oliguria, HTN, Azotemia.
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What is the definition of Nephrotic syndrome?
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Massive proteinuria (>3.5 g/day), fatty casts, and edema.
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This is an EM of the glomerulus of a patient. What is the diagnosis?
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Post-streptococcal glomerulonephritis
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Describe the microscopic characteristics of post-streptococcal glomerulonephritis.
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LM: enlarged, hypercellular glomeruli with neutrophils and lumpy bumpy appearance.
EM: subepithelial immune complex humps IF: granular |
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Who usually gets post-streptococcal GN and how do they present, what is prognosis?
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Most frequent in children. Peripheral edema and periorbital edema that resolves spontaneously.
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This is an IF stain showing a rim around the nucleus of a cell. What is the diagnosis?
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Systemic lupus erythematosus.
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Who is responsible for ensuring enlisted persons are aware of their right to appeal?
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Approving athority
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E4-60
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Describe what you see.
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Subendothelial immune complex deposits. These are DNA-anti-DNA complexes.
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Why are immune complexes in SLE subendothelial rather than subepithelial?
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Because they are so large that they can't traverse the basement membrane and get stuck under the endothelial layer.
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Describe what you see and the syndrome.
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Infiltration of parietal cells causing a crescent shape. This is rapidly progressive glomerulonephritis and has a poor prognosis.
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What disease processes may lead to rapidly progressive glomerulonephritis?
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Goodpasture syndrome, Wegener's granulomatosis, and microscopic polyarteritis.
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What is this?
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RBC cast
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What is this?
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White blood cell cast
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What is this?
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Granular (muddy brown) cast
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What is this?
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Calcium oxalate crystal
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What are these?
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Trichomonas vaginalis
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What is this?
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Granular (muddy brown) casts
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What are these?
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Triple phosphate crystals (coffin lids).
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What is this?
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Hyaline cast
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What are these?
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Uric Acid
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What are these?
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Cystine cyrstals
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Describe what you see.
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Squamous epithelial cells and leukocytes.
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Describe the features of Goodpasture syndrome.
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It is a type II hypersensitivity with antibodies specific for the glomerular basement membrane. The IF pattern is linear. It is male-dominant, presents with hemauria/hemoptysis b/c of lung involvement.
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If a patient presents with rapidly progressing glomerulonephritis that is not Goodpasture's syndrome, what test would help distinguish b/n other possibilities?
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c-ANCA would indicate Wegener's granulomatosis, whereas p-ANCA would indicate Microscopic polyarteritis
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What are some characteristics of Berger's disease?
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Increased synthesis of IgA. LM and IF: immune complexes deposit in mesangium. It often presents or flares with URI or acute gastroenteritis.
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Discuss the major findings of Alport's syndrome.
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It is caused by a mutation in type IV collagen resulting in a split basement membrane. Associated with ocular disorders and deafness.
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This patient presented with rapidly progressive glomerulonephritis. Shown here is an IF of a neutrophil. What is the diagnosis.
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Wegener's granulomatosis
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What is this syndrome?
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Rapidly progressive (crescentic) glomerulonephritis
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Describe the slide. If IF revealed IgA complexes, what would be the diagnosis?
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There is mesangial hypercellularity. IgA glomerulopathy (Berger's disease).
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This patient's father and two brothers have kidney problems, but his sisters do not. What is the diagnosis?
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Alport syndrome
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What is it called when a patient has pitting edema all over the body?
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Anasarca
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On an EM, what is always seen in nephrotic syndrome?
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Fusion of the podocytes.
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What is this called, and what syndrome is it associated with?
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Maltese cross, nephrotic syndrome.
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What is this and what syndrome is it associated with?
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Oval fat body (lipid-engorged macrophage), nephrotic syndrome
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What is this called and what is it associated with? If imaged with birefringence, what would be evident?
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Fatty cast, nephrotic syndrome. Maltese cross.
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This is the most common form of nephrotic syndrome in children. What would you expect to see in the urine?
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Elevated albumin because the loss of charge in the basement membrane.
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Describe minimal change (lipoid nephrosis) disease.
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It is the most common form of nephrotic disease in children. There is a selective loss of albumin, not globulins due to GBM polyanion loss.
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What is the most common glomerular disease in HIV patients?
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Focal segmental glomerulosclerosis.
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What changes in the glomerulus are seen in focal glomerulosclerosis?
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Nothing by EM or IF, but LM reveals segmental sclerosis and hyalinosis. May be caused by hyperfiltration.
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An HIV patient comes in with 3.8 g protein lost in a day. Renal biopsy is performed, what is the diagnosis?
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Focal segmental glomerulosclerosis
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What is the most common form of adult nephrotic syndrome?
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Membranous glomerulonephritis (diffuse membranous glomerulopathy).
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What would you expect to see on LM, EM, and IF of membranous glomerulonephritis?
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LM: diffuse capillary and GBM thickening.
EM: spike and dome appearance with subepithelial deposits. IF: granular. SLE's nephrotic presentation |
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This patients comes in to the hospital and has massive proteinuria. What is the most likely diagnosis?
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Membranous glomerulonephritis secondary to SLE.
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What may cause membranous glomerulonephritis?
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Drugs, infections, SLE, solid tumors.
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Why are nephrotic syndromes associated with a higher risk of infection?
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Due to loss of immunoglobulins in the urine.
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This is an H&E with silver stain. What is the diagnosis?
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Membranous glomerulonephritis
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What is the major problem in membranous glomerulonephritis, and how what is its prognosis?
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Immune complexes depositing in the subepithelial region. It generally has a very bad prognosis, second to rapidly progressive glomerulonephritis.
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Describe three abnormal changes and list the likely diagnosis.
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1) large, hypercellular glomerulus
2) mesangial increase 3) PMNs present Membranoproliferative glomerulonephritis |
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Two different forms of MPGN are indicated here, which is which?
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Top, Type I. Bottom, Type II
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What type of membranoproliferative glomerulonephritity is this? Why?
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Type I. Tram track appearance due to splitting of the GBM.
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What are type I and II MPGN associated with?
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Type I, HBV. Type II, C3 nephritic factor.
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What is the diagnosis?
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Diabetic nephropathy (Christmas ball disease).
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What accumulates in the mesangium of patients with diabetic glomerulonephropathy?
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Type IV collagen.
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List two major physiological mechanisms for the development of glomerulonephropathy in diabetics.
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1) Nonenzymatic glycosylation of BM causes loss of charge and proteinuria.
2) NEG of efferent arterioles increases GFR. |
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How can you treat diabetic glomerulonephropathy?
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ACE inhibitor to dilate efferent arterioles (and improve HTN), and better glucose control.
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Diagnosis?
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Based on apple-green birefringence, this is amyloidosis.
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What is this disease, and what kidney disorder may a component of it?
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Henoch-Schonlein disease
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Study
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Study
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What are the major complications of kidney stones?
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Hydronephrosis and pyelonephritis.
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What are the most common types of kidney stones?
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Calcium containing crystals: calcium oxalate and calcium phosphate.
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List four conditions that can cause hypercalcemia.
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Cancer, ↑PTH, ↑Vitamin D, milk-alkali syndrome.
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How may calcium oxalate crystals result?
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Ethylene glycol (antifreeze) or Vitamin C abuse.
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List two additional names for ammonium magnesium phosphate crystals.
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Struvite and triple phosphate.
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What is the second most common kidney stone?
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Triple phosphate crystals.
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What causes triple phosphate crystals?
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Infection with urease-positive bugs (Proteus vulgaris, Staphylococcus, Klebsiella).
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What my triple phosphate crystals form?
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Staghorn calculi which can be a nidus for UTIs.
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What physiological process makes triple phosphate crystals worse?
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Alkaluria
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What is this and what causes it?
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Staghorn calculus caused by triple phosphate crystals.
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What crystals have a strong association with symptoms of gout?
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Uric acid crystals resulting from hyperuricemia.
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What diseases do uric acid crystals often result from?
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Diseases with high cell turnover, such as leukemia and myeloproliferative disorders.
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What are cystine crystals typically secondary to?
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Cystinuria, an autosomal recessive disorder associated with problems in cystine reabsorption.
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How can cystine crystals be treated?
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Alkalization of the urine.
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What is the most common renal malignancy?
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Renal cell carcinoma.
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How are creatinine and urea treated in the kidney?
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Creatinine is filtered, but neither secreted nor reabsorbed. Urea is filtered and reabsorbed.
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What is azotemia?
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High BUN.
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Why does decreased cardiac output lead to azotemia?
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Because decreased CO leads to decreased GFR which allows more time for proximal tubules to reabsorb urea.
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What happens to serum creatinine in decreased cardiac output, and how does this compare to the BUN?
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Decreased GFR will lead to an increase in serum creatinine, but this will not be as severe as for the urea.
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What BUN/Creatinine ratio indicates pre-renal disease?
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>15
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What effect would acute renal failure have on creatinine and BUN?
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Both will increase proportionately (ratio: 10).
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What is the most common cause of acute renal failure in the hospital?
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Acute tubular necrosis.
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What does ATN result from?
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Untreated pre-renal failure (decreased CO) leading to decreased renal perfusion and tubular necrosis.
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Why is ATN fatal if left untreated?
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The epithelial cells detach from the basement membrane and if the BM is damaged, then there is no place for new cells to attach (irreversible).
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What is the diagnosis?
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Acute Tubular Necrosis
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What types of casts would be present in a patient with acute tubular necrosis?
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Granular (muddy brown) casts.
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What are the three stages of ATN?
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1. Inciting event
2. Maintenance (low urine) 3. Recovery (2-3 weeks) |
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What is diffuse cortical necrosis?
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Acute generalized infarction of cortices of both kidneys.
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How does diffuse cortical necrosis arise?
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A combination of vasospasm and disseminated intravascular coagulopathy (DIC), obstetric catastrophes such as abruptio placentae, or septic shock.
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What is drug-induced interstitial nephritis?
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Acute interstitial renal inflammation resulting from hypersensitivity to drugs.
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What is typically found in the urine of patients with drug-induced interstitial nephritis?
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Pyuria (eosinophilia) and azotemia about 1-2 weeks after administration of drug.
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What symptoms are typically seen in patients with drug-induced interstitial nephritis?
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Fever, rash, hematuria, and CVA tenderness.
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What is seen in the urine of patients with acute pyelonephritis?
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White cell casts.
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What is the major pathology associated with acute pyelonphritis?
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It affects the cortex with relative sparing of glomeruli/vessels.
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What symptoms are typically seen in patients with acute pyelonephritis?
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Fever, CVA tenderness, nausea, and vomiting.
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This patient presents with fever, CVA tenderness, nausea, vomiting, and white cell casts. What is the diagnosis?
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Acute pyelonephritis
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What is the diagnosis?
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Chronic pyelonephritis
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Describe findings in chronic pyelonephritis.
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Coarse, asymetric corticomedullary scarring, blunted calyx. Tubules may contain eosinophilic casts (thyroidization of kidney).
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List the three major types of kidney tumors.
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Renal cell carcinoma, Wilm's tumor, and transitional cell carcinoma.
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What is the most common renal malignancy?
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Renal cell carcinoma.
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What is the clinical presentation of renal cell carcinoma?
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Hematuria, palpable mass, and flank pain.
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What chromosomal abnormality is associated with renal cell carcinoma?
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von Hippel-Lindau deletion in chromosome 3.
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What is the typical course of renal cell carcinoma?
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Invades the inferior vena cava and then spreads hematogenously. Metastasizes to the lung and bone.
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What paraneoplastic conditions are associated with renal cell carcinoma?
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Ectopic EPO, ACTH, PTHrP, prolactin
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Describe the abnormalities and diagnosis.
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Renal cell carcinoma. The kidney has been bivalved, revealing a nodular, golden-yellow tumor in the midkidney with areas of hemorrhage and necrosis.
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What are these cells and what is the diagnosis?
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Polygonal clear cells resulting from transformed renal tubule cells. Renal cell carcinoma.
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