Renal Flashcards

Question

Myogenic

Answer 1

Increased constriction if pressure/flow increased

Answer 2

Increased GFR --\> increased flow through tubule and macula dense --\> Paracrine signal from MD to afferent arteriole --\> Constriction --\> Increased resistance --\> decreased hydrostatic pressure --\> Decreased GFR

Answer 3

Intermediate capacity 25%

Answer 4

Low capacity ~8%

Answer 5

Na co-transporters Na/H exchanger

Answer 6

Na-Cl co trasporter

Answer 7

Na/K ATPase

Answer 8

Apical SGLT2 - Low affinity, high capacity Na-glu transport Basolateral - GLUT1

Answer 9

Apical SGLT1 - High affinity, low capacity 2Na-Glu Basolateral GLUT2

Answer 10

Amount of glucose exceeds threshold and Tm = glucose excreted in urine

Answer 11

Familial renal Glucosuria Glucose-Galactose malabsorption syndrome

Answer 12

Mutation in SGLT2 decreases transport capacity --\> decrease Tm --\> glucose excreted Can result in decreased plasma glucose concentration

Answer 13

Mutation of SGLT1 -- decrease transport capacity --\> slight lower Tm --\> mild glucosuria Can effect gut absorption

Answer 14

Urea remains in renal tubules but concentration increases due to water exit --\> travels down concentration gradient to renal venous sytem

Answer 15

PAH is filtered and secreted by renal tubules, not reabsorbed Good measure of Renal plasma flow

Answer 16

Very closely regulated 3.9 \< Normal \< 4.5

Answer 17

Total body content of K (input - output) Distribution between ICF and ECF (Na/K ATPase)

Answer 18

Insulin B agonists Aldosterone Cause increased activation of Na/K ATPase

Answer 19

Lower pH = Decrease K uptake Higher pH = Increased K uptake into cels

Answer 20

Freely filtered

Answer 21

\>90% reabsorbed by proximal tubule and Thick ascending limb

Answer 22

Distal tubule and CCT

Answer 23

Occurs in Distal tubule and CCT Based on levels of K secretion

Answer 24

Passive reabsorption H20 reabsorption --\> increased K concentration --\> K reabsorption down concentration gradient

Answer 25

Thick ascending limb Apical NKCC Basolateral K channel

Answer 26

ICT, CCT, MCD Apical uptake via H/K ATPase Basolateral K channel

Answer 27

ICT and CCT - active secretion K uptake from peritubular interstitium via basolateral Na/K ATPase Passive apical K flux

Answer 28

Increased intracellular K concentration --\> K secretion

Answer 29

Secreted K flushed downstream --\> Low K concentration in lumen --\> Increase K secretion

Answer 30

K secretion due to electrical gradient

Answer 31

Agents that block Na reabsorption by proximal tubule of loop of henle Increased tubular flow in distal tubule and collecting duct = K secretion

Answer 32

Agents that inhibit Na reabsorption in distal nephron Tubular flow secretion effect minimized because of tubular electrical status (more positive)

Answer 33

Increased [K] intake --\> Increased [K] plasma --\> Aldosterone --\> Increased distal nephron K secretion --\> Increased K excretion Increased [K] intake --\> Increased [K] plasma --\> Increased distal nephron K secretion --\> Increased K excretion

Answer 34

AQP1 in apical and basolateral membrane Promotes water leaving tubules and entering interstitium

Answer 35

Descending limb = water reabsorption Ascending limb - Water impermeable DCT - Water impermeable

Answer 36

Cells impermeable to water - no basolateral AQP

Answer 37

AQP-2 channels inserted onto apical membrane, cells are water permeable

Answer 38

Formation of dilute urine Proximal tubule - Isosmotic reabsorption of Na/water Descending limb - Water reabsorption due to increasing medullary osmolarity (via TAL) Turn of Loop - Concentrated tubular fluid that is isosmotic to medullary intersititum Ascending limb - Solute reabsorption and fluid becomes hyposmotic Slight Na reabsorption in distal nephron NET EFFECT: Low osmolarity urine excreted

Answer 39

Requires ADH Formation of dilute urine that reaches distal tubule CCT - Water permeable tubule comes under effect of intersitial osmolarity --\> water reabsorption Medullary collecting duct - Also water permeable, water reabsorbed Highly concentrated urine excreted

Answer 40

Synthesized in supraoptic and paraventricular neurons of hypothalamus Stored in nerve endings in posterior pituitary

Answer 41

increases in plasma osmolarity = ADH release Small plasma changes = large ADH release Most sensitive ADH regulator

Answer 42

Decrease in blood volume sensed by baroreceptors --\> increase ADH release Need large decrease in blood volume

Answer 43

Vomiting Nausea Morphine Nicotine Cyclophosphamide

Answer 44

Alcohol Clonidine Haloperidol

Answer 45

Excessive ADH secretion for given plasma osmolarity Retain water in excess of solute = decreased plasma osmolarity

Answer 46

Patients produce large volume of dilute urine Increased plasma osmolarity Neurogenic - Deficient ADH secretion Nephrogenic - Insensitivity of kidney tubules to ADH

Answer 47

Retention of Na Vasoconstriction Promote acquisition and retention of water

Answer 48

Aldosterone activation --\> Na reabsorption in collecting duct Stimulate Na/H exchange --\> proximal tubular Na reabsorption

Answer 49

Direct effect on vascular smooth muscle Increase TPR to increase systemic arterial pressure

Answer 50

Stimulate thirst --\> acquire water Stimulate ADH release from hypothalamus --\> water retention Decrease medullary blood flow

Answer 51

Stimuli: Increased AngII, decreased plasma [Na], increased plasma [K] Action: Increase Na reabsorption by collecting duct Mechanism: Promote Na entry through apical ENaC and basolateral Na/K ATPase. PRINCIPAL CELL OF COLLECTING DUCT

Answer 52

Stimuli: Activation of SNS Action: Increase Na reabsorption by proximal tubule Mechanism: Activate Na/H exchange

Answer 53

Stimuli: Increased ECF volume Action: Decrease Na reabsorption by all nephron segments Mechanism: Direct effect to inhibit basolateral Na/K ATPase

Answer 54

Proximal tubule reabsorbs constant fraction, 67%, of filtered Na Increased GFR --\> increased oncotic pressure of peritubular capillaries --\> increased reabsorption Reduces impact of increased filtered load on solute/water delivery to distal nephron

Answer 55

Increased GFR Decreased Na reabsorption

Answer 56

Increased Na = Increased ECF = decreased plasma oncotic pressure = Increased GFR via Starling Increased arterial pressure --\> increased capillary hydrostatic pressure --\> increased GFR Decreased AngII --\> decreased arteriolar resistance --\> increased RBF/GFR Increased arterial pressure --\> decreased SNS --\> decreased arterioloar resistance --\> Increased RBF/GFR

Answer 57

Decreased AngII --\> decreased proximal tubule Na reabsorption (Na/H) Decreased aldosterone --\> decreased Na reabsorption in collecting duct Decreased sympathetic tone --\> decreased Na reabsorption in proximal tubule Increased blood volume --\> increased ANP --\> decreased Na reabsorption in collecting duct Increased endogenous digitalis like substance --\> Decreased Na reabsorption

Answer 58

Increase in arterial pressure --\> Increased Na excretion Unknown mechanism IMPAIRED IN HTN Increased Na intake --\> increased ECF volume --\> increased arterial pressure --\> increased Na excretion --\> decreased ECF

Answer 59

1. Low blood volume, JG cells secrete renin into circulation 2. Decrease in perfusion across macula dense, message sent to JG to secrete renin 3. Increased sympathetic activity (B1) via baroreceptors in carotid sinus

Answer 60

Stimuli: Atrial stretch (High ECF) Action: Decrease Na reabsorption by collecting duct Mechanism: ENaC inhibitor

Answer 61

1. Inhibit vasopressin release in hypothalamus 2. Increase GFR a (vasodilation) and decrease Renin 3. Inhibit Aldosterone 4. Decrease BP via medulla oblongata 5. Decrease Na reabsorption via ENaC inhibition

Answer 62

Aldo increases K secretion via compensation for increasing ENaC In collecting duct principal cells

Answer 63

Total solute concentration but comprised mainly of Sodium salts

Answer 64

Effective plasma osmolality Osmolality of solutes that contribute to water distribution

Answer 65

Delivery of water/solutes to nephron dilution sites (TAL, DCT) Proper function of diluting segments (channel function) No ADH

Answer 66

Concentrated medullary interstitium (functioning TAL channels) Presence of ADH Normal response to ADH

Answer 67

Serum osmolality sensed by osmoreceptors in hypothalamus Increase ADH and thirst Increase urine osmolality, water intake

Answer 68

Effective tissue perfusion sensed by baroreceptors and macula densa Activation of RAAS, Aldo, ANP, NE, ADH Urine sodium and thirst affected

Answer 69

Decreased fluid volume due to decreased total body Na

Answer 70

Increased fluid volume due to increased total body sodium

Answer 71

Plasma tonicity - water distribution Volume status - Total body Na

Answer 72

Posm \> 290 PNa \< normal

Answer 73

Increased plasma osmolality with decreased Na concentration Due to other effective osmole causing fluid movement from ICF --\> ECF Hyperglycemia, glycine, mannitol

Answer 74

Remove underlying cause

Answer 75

Lab artifact Increased protein/lipid concentration that is sensed as decreased Na concentration Old lab testing

Answer 76

Immediate effect - water gain (cerebral edema) and altered mental status (low osmolality) Rapid adaptation - Loss of sodium/K/Cl to reduce edema (low osmolality) Slow adaptation - Loss of organic osmolytes (low osmolality) THERAPEUTIC INTERVENTION: Slow correction = brain returns to normal osmolality Rapid correction = Osmotic demyelination - no chill

Answer 77

POsm \< 290 PNa \< 140 Due to excessive water either because of ADH or impaired water excretion Hypovolemic Euvolemic Hypervolemic

Answer 78

True volume depletion (ECF loss, Na and water) ADH stimulation --\> water retention --\> restored ECF volume but NOT Na

Answer 79

Signs of volume depletion Flat neck veins Tachycardia Hypotension Orthostatic hypotension

Answer 80

Volume losses: GI, blood Insensible losses - sweating/burns Renal losses - Loop diuretics, adrenal insufficiency, salt wasting nephropathies

Answer 81

Burns and sweating Low Urine [Na] because RAAS active and Na reabsorption is maximal

Answer 82

High urine [Na] Sodium reabsorption not functioning

Answer 83

Euvolemic on exam SIADH: High urine Osm High urine [Na]: ADH --\> water reabsorption --\> volume increase --\> decrease renin --\> decrease RAAS --\> decrease Na reabsorption

Answer 84

Cause of euvolemic hypotonic hyponatremia Excessive water intake that overwhelms excretory capacity of kidney Urine Osm low due to ADH suppression

Answer 85

ECF volume excess with decreased intravascular volume EDEMATOUS STATES

Answer 86

Heart failure Liver cirrhosis Nephrotic syndrome ADH activated b/c low circulating volume Urine Osm high b/c ADH Urine [Na] low b/c RAAS activation

Answer 87

Advanced renal failure Impaired free water excretion Effective plasma Osm low b/c water retention Total Plasma Osm may be high b/c excessive urea

Answer 88

Correct intravascular volume w/ isotonic fluid

Answer 89

Correct underlying cause SIADH - Water restrict, increase solute intake, V2 antagonist

Answer 90

Diuretics Fluid restriction

Answer 91

DO NOT TREAT QUICKLY Avoid osmotic demyelination syndrome

Answer 92

Serum Na \>145 Loss of free water Occurs in patients who cannot express thirst of don't have access to water

Answer 93

Decreased ADH action - nephrogenic or neurogenic

Answer 94

Neurogenic Insufficient release of ADH in response to increased Na osmolality Lesion in hypothalamic osmoreceptors, supraoptic nuclei, or trauma/surgery

Answer 95

Reduced action of ADH at collecting tubule to due receptor/aquaporin mutation Lithium

Answer 96

Hypotonic fluid loss - Na/water loss but solute concentration is hypotonic to plasma osmolality If free water not replaced --\> hypernatremia Hypertonic sodium gain

Answer 97

K intake through diet GI losses (5-10% absorbed K secreted in GI) Renal losses (90-95% K regulation) Transcellular K shift (ECF vs ICF distribution)

Answer 98

Freely filtered in glomerulus 65-70% reabsorbed in proximal tubule via passive transport

Answer 99

NKCC channel reabsorption of K K pumped into lumen in TAL to enhance K recycling and NKCC function Apical K channel inhibited by ATP - More Na enters cell --\> transported out by Na/K ATPase --\> low ATP --\> apical K activation --\> NKCC function and more Na absorbed

Answer 100

K transported into cell by Na/K ATPase Secreted into tubule via ROMK

Answer 101

1. Luminal electrical charge 2. Luminal concentration gradient 3. K permeability of luminal membrane

Answer 102

1. Aldosterone 2. Plasma [K] 3. Distal flow rate 4. Distal Na delivery

Answer 103

Increases # open Na (ENaC) and K (ROMK) channels Enhances Na/K ATPase activity

Answer 104

Increased plasma K = enhanced Na/K ATPase activity Increased # open K & Na channels

Answer 105

Increased flow = more K washed away = increased K secretion via favorable gradient

Answer 106

Na through ENaC = more negative lumen = K secretion More ENaC absorption = more intracellular Na = enhanced Na/K ATPase = more K secreted

Answer 107

Reabsorption of K via apical H/K ATPase

Answer 108

Transcellular shift GI losses Renal losses Poor intake

Answer 109

Insulin B2 agonists Alkalosis Hypokalemic periodic paralysis

Answer 110

Stimulates Na/K ATPase --\> more K secretion

Answer 111

Increase Na/K ATPase activity --\> K secretion

Answer 112

Alkalosis = high extracellular pH --\> H will leave cell --\> K enters cell to maintain electroneutrality

Answer 113

Acute attacks precipitated by sudden movement of K into cells Lowers plasma K significantly Rest after exercise, stress (catecholamines), high carb meal (insulin) Familial - autosomal dominant mutation Acquired - Thyrotoxicosis

Answer 114

Associated with metabolic alkalosis due to HCL loss --\> K entry into cells b/c H exit Concurrent urinary losses: - Aldosterone activation Plasma Bicarb increase = too much Bicarb that can be absorbed --\> Na pairs with bicarb --\> increased distal delivery of Na --\> K secretion

Answer 115

Metabolic alkalosis Metabolic Acidosis Magnesium

Answer 116

Normo-hypotension Hypertension

Answer 117

Diuretics - Loop/Thiazide Activation of aldosterone by volume depletion Increased distal delivery of Na (blocked absorption more proximally) Salt wasting nephropathies

Answer 118

THINK LOOP DIURETIC Defect in solute reabsorption in TAL NKCC2, Luminal K channel, Basolateral Cl channel can be affected

Answer 119

THINK THIAZIDE DIURETIC Defect in thizide sensitive NaCl cotransporter in DCT

Answer 120

Mineralocorticoid excess: Primary hyperaldosteronism (adrenal tumor, BAH) Glucocorticoid remedial aldosteronism Renal artery stenosis 11BHSD2 deficiency CAH

Answer 121

Gain of function mutation in ENaC Triad: Hypertension - Metabolic alkalosis - Hypokalemia

Answer 122

Renal tubular acidosis Nonreabsorbable anion

Answer 123

Hyperchloremic, non anion gap metabolic acidosis 1. Distal hypokalemic RTA (type I): Impaired distal urine acidification. No protons pumped out = more K secreted 2. Proximal (type II): Reduction in bicarb reabsorptive capacity --\> all bicarb reabsorbed --\> metabolic acidosis that inhibits Na reabsorption --\> hypokalemia

Answer 124

Non reabsorbable anion paired with Na --\> reduced Na --\> Increased distal delivery of Na Diabetic ketoacidosis - Beta hydroxybuterate pairs with Na

Answer 125

Hypokalemia occurs in 40-60% of hypoMg diseases Diseases that waste both K and Mg: Diarrhea, diuretics Correct Mg to restore K

Answer 126

Cardiac arrhythmias: Sinus bradycardia, AV block, Vtach/Vfib Decrease amplitude of T wave, increase U wave amplitude

Answer 127

Weakness and muscle cramps Low K = hyperpolarized skeletal muscle cells = impaired contraction Reduce blood flow by impairing NO release Severe K depletion = respiratory weakness --\> respiratory failure GI muscle weakness = ileus

Answer 128

Impaired insulin release and end organ sensitivity to insulin Worsened glucose control in diabetic patients

Answer 129

Tubulointerstitial and cystic changes in parenchyma Polyuria: Increased thirst and mild nephrogenic DI, concentrating ability impaired HTN: Increased renal vascular resistance

Answer 130

Stool losses

Answer 131

RTA Nonreabsorbable ion

Answer 132

Check BP and volume status Low-normal BP/volume depleted - diuretics, salt wasting nephropathies High BP/volume overload - Mineralocorticoid excess, Liddle's

Answer 133

Transcellular shift Psuedohyperkalemia Renal - Decreased urinary excretion

Answer 134

Elevation in measured serum K due to K movement out of cells during/after blood draw Hemolysis Thrombocytosis Leukocytosis

Answer 135

Metabolic acidosis Hyperglycemia and hyperosmolarity Nonselective B antagonists Exercise Tissue breakdown Digitalis toxicity Hyperkalemic familial periodic paralysis

Answer 136

H will enter cell in order to buffer extracellular pH --\> K will leave and enter ECF/blood vessels

Answer 137

Elevation in serum osmolality = H20 movement from ICF --\> ECF = More K in cell --\> K will move out of cell

Answer 138

Interfere with K uptake by B receptors

Answer 139

Rhabdomyolysis Lysis of large tumor burden after chemo Burns

Answer 140

Block Na/K ATPase

Answer 141

Renal failure Volume depletion with decreased distal Na delivery Functional hypoaldosteronism

Answer 142

Able to maintain K with distal flow rate and aldosterone secretion is maintained Hyperkalemia occurs in patients with decreased flow rate + excess K load/Aldo blocker

Answer 143

Hypovolemia Effective arterial volume depletion with ECF excess Heart failure/liver cirrhosis

Answer 144

Low aldo or resistance to aldo effect Mineralocorticoid deficiency: primary adrenal insufficiency, hyporeninemic hypoaldosteronism (low renin/aldo) Tubulointerstitial disease: Sickle cell and urinary tract obstruction - Distal hyperkalemic RTA - Impaired Na reabsorption reducing K/H secretion

Answer 145

Block aldo activity - ACE-I, ARB, Aldo antagonists Decreased renin release - B blocker, NSAIDs Bind to ENaC - Amiloride, triamterene Calcineurin inhibitors

Answer 146

Severe muscle weakness/paralysis Cardiac arrhythmias/ECG abnormalities: BBB, AV block, sinus bradycardia, sinus arrest, Vtach/fib Early - Tall T waves, short QT Late - prolonged PR/QRS

Answer 147

Adrenal insuffieciency

Answer 148

Type IV RTA Diabetic nephropathy

Answer 149

Aldo resistance Tubuloinsterstitial disease - sickle cell/urinary obstruction

Answer 150

Antagonizing membrane effects of K with Ca Drive ECF K into cells Remove excess K from body

Answer 151

ONLY for patients with ECG changes or acute rise in serum K CaCl2 Hyperkalemia induces membrane depolarization and inactivation of Na channels --\> Ca antagonizes this effect

Answer 152

Insulin + glucose: Insulin will activate Na/K ATPase, glucose prevents hypoglycemia B2 agonist: Stimulate Na/K ATPase

Answer 153

Diuretics: Loop/thizides. Combine with saline to maintain distal Na delivery and distal flow rate

Answer 154

Uptake of K in exchange for cation

Answer 155

Warranted when other measures are ineffective Use when K rises too rapidly

Answer 156

Abrupt loss of kidney function Retention of urea and other nitrogenous waste products Dysregulation of extracellular volume and electrolytes

Answer 157

Pre renal Intrinsic renal Post renal

Answer 158

True volume depletion Decreased effective arterial blood volume

Answer 159

Loss of Na from ECF GI losses, hemorrhagic shock, renal losses, cutaneous losses

Answer 160

Increased ECF but decreased blood volume sensed by baroreceptors --\> edematous states: HF, cirrhosis, sepsis

Answer 161

Renal perfusion decreases --\> homeostatic mechanisms activated Afferent arteriolar vasodilation Efferent arteriolar vasoconstriction Increased filtration fraction = increased post glomerular oncotic pressure = increased salt/water Activation of AngII and ADH = Low urine Na and concentrated urine

Answer 162

Vomiting Diarrhea GI bleed HF, liver disease, sepsis

Answer 163

Orthostatic hypotension, skin tenting, dry mucous membranes Elevated JVP, edema, hypotension

Answer 164

BUN:Creatinine \>20:1 Urine osmolality \> 500 Urine Na \<10 Urine Cl \<10 Urinalysis: No protein/blood/WBC, no casts no cells

Answer 165

Measures percent of filtered Na excreted in urine \<1% = patient will be responsive to volume therapy

Answer 166

Tubulointerstitial Vascular Glomerular

Answer 167

Most common cause of acute intrinsic kidney injury Patch necrosis of proximal tubule and TAL: High metabolic activity so very sensitive to changes in renal perfusion Risk factors: Volume depletion, CKD, NSAIDs, DM

Answer 168

Endothelial/epithelial injury Intratubular obstruction Changes in microvascular blood flow Immunological factors Tubular cells damaged so cannot absorb salt/water --\> increased delivery of salts to macula densa --\> afferent vasoconstriction to reduce salt wasting No TGF = salt wasting and volume depletion = DEATH

Answer 169

Ischemia - Low BP, volume depletion, sepsis Toxin - Radiocontrast media (risk with CKD, DM, hypotension) Toxins

Answer 170

Prolonged hypotension in ICU --\> ischemia Radiocontrast exposure Sepsis (infections) Drugs - aminoglycosides, amphotericin B Crush injuries

Answer 171

BUN:Creatinine = 10-15:1 Urine Na and Cl \>20 FENa \>2% (more filtered Na being excreted) Urine osm \<450 May have low grade proteinuria (deficient protein reabsorption in proximal tubule) Casts and epithelial cells

Answer 172

Inflammatory cell infiltration in kidney interstitium caused by immune response - Medication - Autoimmune - Infection

Answer 173

NSAIDs Penicillins Cephalosporins Sulfonamides Rifampin Cipro PPI

Answer 174

Sjogrens Sarcoidosis Legionella, leptospira, CMV

Answer 175

Rash, fever, eosinophilia Full triad only in ~10% patients

Answer 176

Acute rise in serum creatinine that temporarily correlates with drug administration Peripheral eosinophilia Eosinophiluria Proteinuria WBC and WBC casts

Answer 177

Precipitation of substances in tubules: Immunoglobulins Calcium phosphate Urate Intratubular crystal precipitations from medications Volume depletion and acidic urine

Answer 178

Occurs in multiple myeloma Overproduction of immunoglobulin light chains that get filtered into urine, can block tubule

Answer 179

Occurs following chemotherapy Dead tumor cells release chemicals Intracellular release of uric acid, phosphate, potassium --\> all levels high in blood

Answer 180

Bowel preparation for colonoscopy Acute calcium deposition in tubules with associated interstitial inflammation Highest risk in patients with underlying CKD

Answer 181

Elevated serum uric acid, potassium, phosphorus

Answer 182

High phosphorus Low calcium

Answer 183

Elevated free light chains in serum

Answer 184

Renal atheroembolic disease Vasculitis Thrombotic microangiopathies

Answer 185

Occurs in patients with atherosclerotic disease who undergo aorta/large artery manipulation --\> plaque breaks off and can occlude multiple small arteries Low serum complement, eosinophilia, rash

Answer 186

Inflammation and necrosis of small arteries

Answer 187

Endothelial injury --\> platelet thrombi occluding small vessels --\> ischemia Low platelets, hemolytic anemia - HUS - Thrombotic thrombocytopenia purpura - Malignant HTN Schistocytes (RBC fragments)

Answer 188

Obstruction of the flow of urine anywhere from renal pelvis to urethra Calculi Anatomic abnormalities (children) BPH Urethral stricture Malignancy

Answer 189

Glomerular disease

Answer 190

Acute tubular necrosis

Answer 191

Acute interstitial nephritis

Answer 192

Nausea Vomiting Anorexia Dysguesia Altered cognition Pericarditis

Answer 193

Hyperkalemia (aminoglycosides and cisplatin = hypokalemia via increased flow) Metabolic acidosis ECF volume excess

Answer 194

Renovascular HTN Renal parenchymal HTN

Answer 195

HTN caused by renal artery stenosis Atherosclerosis (75-90%) Fibromuscular dysplasia (10-25%)

Answer 196

Reduced renal perfusion --\> RAAS activation --\> AngII mediated vasoconstriction, ADH, Aldo

Answer 197

Onset in 3-5th decade = FMD \>55yo = Atherosclerotic disease Sudden onset of uncontrolled HTN Malignant HTN Physical: Epigastric bruit Acute unexplained rise in serum creatinine induced Asymmetric renal size

Answer 198

Elevated renin and Aldosterone MRA to asses vessels, contraindicated in high stage CKD

Answer 199

BP meds Lipid lowering meds FMD - ACE-I or ARB --\> percutaneous transluminal angioplasty if ineffective

Answer 200

ACE-I or ARB Lipid lowering meds Anti platelet therapy

Answer 201

Common feature in acute and CKD

Answer 202

Volume overload and suppression of RAAS

Answer 203

Ischemic activation of RAAS

Answer 204

Multifactorial pathogenisis Volume expansion via Na/water retention SNS activation RAAS activation Secondary hyperPTH Endothelial cell dysfunction

Answer 205

ACE-I/ARB slow GFR decline Diuretic for volume removal CCB if neeed

Answer 206

Autonomous production of aldosterone Adrenal adenoma Bilateral adrenal hyperplasia Adrenal carcinoma Triad: HTN, unexplained hypokalemia, metabolic alkalosis

Answer 207

[Plasma aldosterone] : Plasma renin activity Ratio \>35-50 and PAC \>15 = primary hyperaldosteronism Discontinue aldo antagonists for accurate results

Answer 208

Na loading test: If Aldo still high then primary hyperaldosteronism Isotonic saline administration: Aldo should fall \<5

Answer 209

Unilateral adenoma - Laparoscopic surgical removal BAH - Spironolactone/other aldo antagonists

Answer 210

Excess exogenous or endogenous glucocorticoids Exogenous administration Endogenous: Pituitary adenoma, ectopic ACTH production, adrenal adenoma

Answer 211

Centripetal obesity Moon facies Skin atrophy/abdominal striae Acne and hirsutism Proximal muscle weakness HTN Glucose intolerance

Answer 212

24hr urinary cortisol excretion Late evening salivary cortisol Low dose dexamethasone suppression test

Answer 213

Cushings disease/pituitary adenoma - Irradiation or resection Adrenal tumor/ectopic ACTH - Removal

Answer 214

Catecholamine secreting tumor Headache, sweating, palpitations Diagnosis: - Urinary catecholamines - Fractioned plasma metanephrines

Answer 215

Surgical removal of tumor BP control before surgery - Phenoxybenzamine/Phenotlamine - Beta blockers after adequate alpha blockade

Answer 216

Obesity, obstructive sleep apnea and HTN association SNS abnormalities Treatment: Weight loss CPAP Uvulopalatopharyngoplasty

Answer 217

Presence of EITHER: Kidney damage Decreased kidney function for \> 3 months with decreased GFR

Answer 218

Proteinuria - \>150mg protein, \>30mg albumin Glomerular hematuria Imaging - polycystic kidney disease, hydronephrosis, small kidney w/thinned cortices

Answer 219

Metabolism of creatine in skeletal muscle and dietary meat Freely filtered, not absorbed Limitations: Little muscle mass, Secretion by organic pathway in PCT, Does not detect early GFR changes

Answer 220

Stage I: Kidney damage w/normal GFR Stage II: Kidney damage w/ mild decreased GFR Stage III: Moderate GFR decrease (30-59) Stage IV: Severe GFR decrease (15-29) Stage V: Kidney failure. \<15

Answer 221

PKD Autoimmune: Sjogrens, Sarcoidosis Reflux Nephropathy

Answer 222

Autosomal dominant polycystic kidney disease Will progress to kidney failure

Answer 223

Sjogrens Sarcoidosis: Inflammatory infiltrates in tubulointerstitium

Answer 224

Vesicouteral reflux Passage of urine from bladder to upper urinary tract Inadequate closure of ureterovesical junction

Answer 225

Hypertensive vasculopathy - chronic HTN --\> thickening and narrowing of large arteries and glomerular arterioles Renovascular disease - Renal artery stenosis Renal atheroembolic disease - Emboli caused by large artery manipulation

Answer 226

Diabetic nephropathy Nephritic/nephrotic

Answer 227

Obstructive uropathy Prolonged obstruction --\> parenchymal loss Loss of nephron mass due to compression from reflux of urine

Answer 228

Initial damage to kidney (tubulointerstitial, vascular, glomerular, obstructive) --\> renal function maintained by hyperfiltration --\> ongoing hyperfiltration --\> glomerular capillary HTN --\> cytokine activation and podocyte dysfunction --\> proteinuria/glomerular sclerosis/tubulointerstitial fibrosis --\> renal scarring

Answer 229

Glomerulopathy: mesangial expansion, BM thickening, glomerulosclerosis Hyperfiltration and golmerular capillary HTN Microalbuminuria Overt proteinuria

Answer 230

Glomerular hyperfiltration Hyperglycemia and AGE's Elevated prorenin Impaired podocyte-specific insulin signaling

Answer 231

Present in 80-85% CKD Na retention SNS activation RAAS activation Secondary hyperPTH --\> increased Ca --\> vasoconstriction Impaired NO synthesis so reduced vasodilation

Answer 232

Decreased GFR = decreased phosphorus excretion Increased phosphorus = FGF23 increase (to excrete phosphorus) --\> FGF23 inhibits 1a-hydroxylase --\> decreased calcitrol Decreased calcitrol --\> decreased intestinal Ca absorption --\> PTH increase Vascular calcification Renal osteodystrophy

Answer 233

Kidney damage = decreased erythropoetin

Answer 234

Proteinuria HTN Underlying disease AA Male Obesity (increased glomerular capillary pressure) Dyslipidemia SMoking Hyperphosphatemia Metabolic acidosis: Bicarb supplementation = good High protein diet (increased capillary pressure) Hyperuricemia

Answer 235

BP control Renin-angiotensin-aldosterone antagonism - Reduce BP - Decrease glomerular capillary pressure Phosphorus control Treat metabolic acidosis Correct anemia Smoking cessation Statins Low protein diet Treat underlying disease

Answer 236

Connection between artery and vein to arterialize vein and increase blood flow for dialysis needle access Longest lifespan Low infection rate Preferred access

Answer 237

Performed when vasculature not able to permit AVF creation Higher rate of thrombosis and infection

Answer 238

Least desirable Highest infection rate Increased risk of great vessel stenosis

Answer 239

Lines outer aspects of capillary loops Maintains loop shape Provides size and charge barrier to filtrate Maintains GBM

Answer 240

Clinical condition due to DYSFUNCTION OF PODOCYTE 1. Proteinuria \>3.5gm/24hr 2. Hypoalbuminemia 3. Hyperlipidemia with lipiduria 4. Generalized edema

Answer 241

General stain Good for inflammatory cells

Answer 242

Mesangium BM

Answer 243

Fibrosis, necrosis

Answer 244

Ag/Ab complexes form in blood and deposit in renal tissue Circulating Ag deposited in kidney, Ab binds Protein intrinsic to kidney acts as auto antigen, Ab recognizes and binds

Answer 245

Activation of complement --\> cytokines/chemokines, recruitment of inflammatory cells --\> damage to renal tissue

Answer 246

Increased filtration of macromolecules across glomerular capillaries Podocyte abnormality

Answer 247

Urinary albumin loss = decreased blood albumin

Answer 248

Low blood protein = fluid flow to ecf = edema RAAS activation = Na retention, sympathetic stimulation

Answer 249

Decreased oncotic pressure stimulates hepatic lipoprotein synthesis --\> hypercholestrolemia, hypertrigliceridemia Lipid in urine trapped in protein material in renal tubules: Maltese crosses under polarized light

Answer 250

Loss of anticoagulation factors through GC Volume depletion from diuretics --\> decreased oncotic pressure --\> hemoconcentration and increased platelet aggregation Thrombus formation - hemoconcentration in post glomerular circulation

Answer 251

Ig loss in urine

Answer 252

ACE-I or ARB: Reduce intraglomerular pressure, reduce proteinuria Loop diuretics, low Na diet BP control \<130/80 Statin for hyperlipidemia

Answer 253

Most common cause of nephrotic syndrome in children Etiology: Idiopathic, Drugs (NSAIDs), Neoplasm

Answer 254

Exact cause unknown Key feature: Podocyte injury - Systemic T cell dysfunction - Production of glomerular permeability factor --\> podocyte injury --\> effacement of foot processes = proteinuria

Answer 255

Light microscopy: Normal Immunofluorescence: Negative EM: Diffuse effacement of podocyte foot processes

Answer 256

Nephrotic syndrome Untreated MCD associated with mortality due to infection or thromboembolism Good prognosis, no progression

Answer 257

All receive nonspecific Rx: Diuretics, low Na, BP control High dose steroids (prednisone) Cyclophosphamide - steroid dependent patients Cyclosporine - Steroid resistant

Answer 258

Focal segmental glomerulosclerosis Most common cause of nephrotic syndrome in adults Increased incidence in AA and males

Answer 259

Idiopathic Genetic/Familial: Genetic defect in genes that code slit diaphragm proteins in foot processes of podocytes

Answer 260

Heterogenous - Occurs in many forms of renal injury and systemic disease Loss of renal mass, obesity, HIV, sickle cell, drugs Often presents with nephrotic range proteinuria but not full syndrome

Answer 261

Immune dysregulation/T cell function Circulating toxin

Answer 262

Hyperfiltration+increased glomerular capillary pressure: reduced renal mass, obesity, sickle cell Direct podocyte injury from virus/drugs: HIV, pamidronate/heroin

Answer 263

Light microscopy: Focal glomeruli with scarring/sclerosis of glomerular capillary tuft IF: Trapping of C3/IgM in areas of sclerosis EM: Accumulation of matrix material, cells, plasma protein in sclerotic area No immune deposits Primary = diffuse effacement of podocyte foot processes Secondary = patchy effacement of foot processes

Answer 264

Mat present with acute or insidious onset Hematuria in 30% patients, HTN, variable degrees of reduced function No complement abnormalities

Answer 265

Always presents with insidious onset Full nephrotic syndrome NOT always present

Answer 266

Follows progressive course to ESRD

Answer 267

High level proteinuria Reduced renal function Presence of tubulointerstitial fibrosis

Answer 268

ACE-I, ARB, loop, low Na, BP control, statin High dose steroids Cyclophoshamide/cyclosporine No response to therapies = slit diaphragm mutations

Answer 269

ACE-I, ARB, loop, BP control, low Na, statin Treat underlying disease - Weight loss - Anti viral - Discontinue bad drugs

Answer 270

Primary/idiopathic (70%) Secondary (30%) - Drugs/Malignancy/SLE/Infections

Answer 271

Primary - Autoimmune - Circulating IgG antibodies directed against renal tissue (Type M phospholipase A2 receptor on podocyte foot processes) Secondary - Circulating IgG Ab directed against extrinsic antigens (viral proteins, tumor proteins, drug)

Answer 272

Immune complex formation activates complement cascade MAC inserts into podocyte membrance Podocyte foot process effacement Podocyte death and necrosis

Answer 273

Light microscopy: Thick GBM with spikes IF: Diffuse fine granular deposits on capillary walls, IgG/C3 EM: Subepithelial immune deposits, spikes of GBM, effacement of podocyte foot processes

Answer 274

Nephrotic syndrome 40% progress to ESRD if untreated Progression risk factors: - Older age of onset - Male - Increased creatinine - \>8gm proteinuria - Tubulointerstitial fibrosis

Answer 275

ACE-I, ARB, Na low, B control, statin Immune targeted therapy - Cyclophosphamide - Cyclosporine - Rituximab

Answer 276

Most common systemic illness to cause nephrotic syndrome

Answer 277

Metabolic: - Hyperglycemia + pro inflamm molecules --\> biochemical change in glomeruli --\> profibrotic growth factors and increased synthesis of collagen/matrix - Non enzymatic glycosylation of proteins Hemodynamic - Hyperfiltration --\> increased glomerular capillary pressure and hypertrophy --\> injury

Answer 278

LM: Glomerular nodules of matrix material. Thick GBM, thick tubular BM, interstitial fibrosis, vascular sclerosis IF: No immune deposits. Pseudolinear staining of glomerular/tubular BM with IgG and albumin due to sticky BM EM: Diffuse thickening of GBM - Mesangium expansion with increased matrix - No immune deposits - Variable foot process effacement

Answer 279

Proteinuria: Early - microalbuminuria Late - Overt proteinuria and neprotic syndrome Progression: Depends on BP and glycemic control

Answer 280

ACE-I/ARB (important to reduce capillary pressure), Low Na, BP control Strict blood sugar control Kidney pancreas transplant

Answer 281

Cause of proteinuria/nephrotic syndrome in adults Extracellular deposition of abnormally folded proteins Poor prognosis

Answer 282

Multiple myeloma - neoplasm of plasma cells Amyloid made of monoclonal Ig light chains

Answer 283

Chronic inflammatory disease Amyloid made of serum amyloid A protein

Answer 284

LM: Congo red stain positive IF: Variable EM: Haphazardly arranged fibrils

Answer 285

Poor prognosis, ESRD common Treatment: ACE-i, ARB, Low Na, Lop, BP control, statin Primary - chemo, stem cell transplant Secondary - Treat underlying disease

Answer 286

Inflammation of urinary bladder, usually due to infection

Answer 287

1. Frequency of urination 2. Lower abdominal pain 3. Dysuria

Answer 288

E. Coli \>\> Proteus, Klebsiella, Enterobacter

Answer 289

Bladder calculi Urinary obstruction DM Instrumentation Immune deficiency Cytotoxic drugs Radiation

Answer 290

Cyclophosphamide Hemorrhagic cystitis

Answer 291

Hyperemia (redding) of mucosa Exudate Large amounts of hemorrhage = hemorrhagic cystitis

Answer 292

Neutrophilic infiltrate Hemorrhage Ulceration of mucosa Large areas of ulceration = ulcerative cystitis

Answer 293

Acute cystitis

Answer 294

Hemorrhagic cystitis

Answer 295

Acute cystitis

Answer 296

Acute cystitis

Answer 297

Longer duration of infection Chronic infiltrate - lymphocytes/plasma cells Heaped up and reactive urothelium Fibrous thickening of muscularis propria

Answer 298

Chronic cystitis

Answer 299

Follicular Eosinophilic Interstitial Malacoplakia Polypoid Emphysematous Cystitis cystica

Answer 300

Chronic follicular cystitis Germinal center

Answer 301

Eosinophilic cystitis

Answer 302

Most frequent in women Inflammation and fibrosis in all layers of bladder wall, often with ulceration Highliy incapacitating and difficult to treat

Answer 303

Intermittent and severe suprapubic pain Frequency Urgency Hematuria Dysuria

Answer 304

Unique form of chronic cystitis, chronic E coli infection Immunosuppressed patients

Answer 305

Multiple yellowish plaques in mucosa and submucosa

Answer 306

Malacoplakia

Answer 307

Large foamy macrophages, multinucleate giant cells, lymphocytes Michaelis Gutmann bodies: Round intracytoplasmic concretions within macrophages and between cells

Answer 308

Michaelis Gutmann bodies

Answer 309

Results from mucosal irritation - bladder catheter Broad polypoid projections due to submucosal edema

Answer 310

Polypoid cystitis

Answer 311

Polypoid cystitis

Answer 312

Emphysematous cystitis

Answer 313

Cystitis cystica

Answer 314

Majority (\>95%) are ascending bladder infections Most are bacterial infections: 85% gram(-) rods from intestinal tract E. COLI

Answer 315

Hospital acquired Due to indwelling bladder catheters, patients on antibiotics Most are due to E coli

Answer 316

Associated with virulent organisms Staph aureus, salmonella

Answer 317

Urinary tract obstruction Catheters Vesicouteral reflux Pregnancy Pre existing renal disease DM Immunosuppression

Answer 318

Colonization of urethra then bladder - Usually by intestinal flora - Bacterial adhesion molecules interact with urothelium receptors --\> promote migration to kidney and persistent infection Multiplication of organisms in bladder: Outflow obstruction/bladder dysfunction --\> STASIS --\> bacterial growth Bacteria gain access to upper tract: Catheter. Vesicoureteral reflux (back flow) Intrarenal reflux

Answer 319

Active peristalsis of ureters Ureterovesical valves Complete voiding of bladder Turbulent flow of urine exiting urethra

Answer 320

Fever, chills Flank pain, CVA tenderness Constitutional symptoms: malaise, anorexia, vomiting, diarrhea, headache Cystitis symptomsL Urgency, frequency, dysuria

Answer 321

Leukocytosis - Left shift increase WBC Urinalysis - Pyuria (\>5WBC/HPF), WBC casts Urine culture - colony formation Positive blood culture - 15-30% cases

Answer 322

Focal abscesses, wedge shaped areas of suppuration, hemmorhage

Answer 323

Early: PMN infiltrate in interstitium and within tubule, abscess, tubule destruction Later: Mixed inflamm infiltrate, PMN/lymphocytes/plasma cells

Answer 324

Acute pyelonephritis

Answer 325

Acute pyelonephritis

Answer 326

Acute pyelonephritis

Answer 327

Acute pyelonephritis

Answer 328

Most cases follow benign course - antibiotics and supportive care Adults with normal urinary tract = no rogressive disease Bacteruria may persist after therapy

Answer 329

Bacteremia/sepsis - 15-30% Papillary necrosis - necrosis of distal medullary tips, diabetics Pyonephrosis - Exudate filling renal pelvis and ureters. Severe obstruction Perinephric abscess - Extension of inflmmation through renal capsule into perinephric fat

Answer 330

Severe papillary necrosis

Answer 331

Cause of acute ciral pyelonephritis in renal allografts Immunosuppression --\> latent virus activation --\> inflammation of tubules and interstitium Treatment: Reduce immunosuppression

Answer 332

Polyoma virus nephropathy

Answer 333

Chronic disorder characterized by chronic tubulointerstitial inflammation and progresive scarring Causes: 1. Chronic reflux (reflux nephropathy): Usually in childhood 2. Chronic obstruction: Recurrent infection superimposed on obstruction Abnormal urinary tract --\> repeated infections --\> progressive injury

Answer 334

Vague/nonspecific symptoms: Flank pain, low grade fever. History of UTI's. ESRD w/out prior history Common cause of HTN in children (via CKD) Nocturia, polyuria - tubular dysfunction and loss of ability to concentrate urine Secondary FSGS

Answer 335

Chronic pyelonephritis

Answer 336

Chronic pyelonephritis

Answer 337

Chronic interstitial inflammation with fibrosis Tubular atrophy and dilation with hyaline casts Glomeruli vary from normal to ischemic to obsolescent

Answer 338

Chronic pyelonephritis

Answer 339

Special form of chronic pyelonephritis Proteus infections, obstruction Mixed inflammation with large amouns of foamy macrophages

Answer 340

Xanthomatous pyelonephritis

Answer 341

Xanthogranulomatous pyelonephritis

Answer 342

Associated with chronic infections due to urea splitting bacteria Proteus Klebsiella Ureaplasma Struvite crystals --\> Stones Difficult to treat

Answer 343

Staghorn calculi

Answer 344

Staghorn calculi

Answer 345

Caught early: Surgical correction of abnormal urinary tract allows normal function, prevents progressive scarring End stage: No effective therapy

Answer 346

Inflammatory disorder involving interstitium and tubules - non infectious, hypersensitivity reaction Penicillins, NSAIDs, antibiotics, thiazdes

Answer 347

Fever Skin rash Eosinophilia

Answer 348

Mixed inflammation within interstitium: Eosinophils, lymphocytes, PMN, plasma Tubular inflammation, tubular injury Early - interstitial edema Late - interstitial fibrosis, tubular atrophy

Answer 349

Allergic interstitial nephritis

Answer 350

Allergic interstitial nephritis

Answer 351

Allergic interstitial nephritis Chronicity with fibrosis

Answer 352

Discontinue offending drug ASAP Corticosteroids Supportive care

Answer 353

Myeloma cast nephropathy Intratubular cast

Answer 354

Glomerular hematuria: Dysmorphic RBC's, RBC casts Proteinuria: Can be nephrotic range Azotemia: Elevated BUN Oliguria HTN: Volume overload via Na retention - RAAS suppression and icnreased Na/K ATPase

Answer 355

Idiopathic/autoimmune Infectious: - Hep C - Chronic bacterial infection Neoplasia - Mulitple myeloma - CML

Answer 356

Immune complex mediated disease Idiopathic: Antibody directed at unknown antigen Secondary: Antibody directed at viral/bacterial Deposition of Ab/Ag complex in glomerulus OR formation of complex in situ Immune complex formation --\> complement activation --\> MAC

Answer 357

Low C3, C4, total complement

Answer 358

MPGN Global hypercellularity and lobular formation

Answer 359

MPGN Silver stain GBM duplication

Answer 360

MPGN IgM deposits Smooth BM because deposits are subendothelial

Answer 361

MPGN Subendothelial deposits

Answer 362

LM: Hypercellular, lobulated glomeruli. Duplication of GBM IF: IgG, IgM, C3 in mesangium or inner aspect of GBM EM: Immune deposits in mesangium, subendothelium locations. GBM duplication

Answer 363

Idiopathic/autoimmune: Prolonged course with slow rate of progression Secondary: Good prognosis if underlying disease treated

Answer 364

Idiopathic/autoimmune: Steroids Secondary: Treat underlying condition

Answer 365

Rare Excessive activation of alternatic complement pathway

Answer 366

Circulating autoantibody: C3 Nephritic Factor Deficient regulatory protein: Factor H/Factor I Leads to persistent degradation of C3 and constitutive activation of alternative pathway LOW C3 ONLY

Answer 367

Low C3, C4, total complement Assay for C3 nephritic factor, Factor H, Factor I

Answer 368

LM: Similar to MPGN IF: Mesangial and capillary wall C3 EM: Linear deposition of electron dense material along GBM (ribbon like)

Answer 369

Poor prognosis 70% --\> ESRD at 9 years

Answer 370

Non specific therapy if nephrotic Plasmapharesis - Patients with C3 nephritic factor Plasma infusion - Factor H/I deficiency patients Eculizumab - antibody to C5 protein, prevents MAC formation, expensive

Answer 371

Mucosal infection triggered by environmental antigens --\> pathogenic IgA complexes Antigens: Viral, bacterial, food Genetic predisposition: Polygenic

Answer 372

Increased synthesis of abnormal IgA/IgG Abnormally glycosylated IgA produced --\> immune complexes don't clear --\> IgG antibodies directed against abnormal IgA --\> Large fucker of a macromolecule --\> Deposition in mesangium and complement activation

Answer 373

IgA Nephropathy Increased size of mesangium

Answer 374

IgA nephropathy

Answer 375

LM: Variable, increased mesangium IF: Mesangial IgA, C3 EM: Immune deposits in mesangium, increased mesangial matrix and cellularity

Answer 376

40% present with gross hematuria following URI (Synpharyngitic hematuria) 30% present with microscopic hematuria and mild proteinuria 5-10% with acute nephritic syndrome Associated abnormalities: - Skin lesions - GI (celiac, cirrhosis) - IgA vasculitis

Answer 377

No treatment if normal renal function and low proteinuria ACE-I/ARB if \>1gm proteinuria Fish oil Prednisone - Patients with proteinuria even with ACE-I/ARB, progressive disease

Answer 378

Most common cause of acute nephritic syndrome Children 5-12 and adults \>60

Answer 379

Develops in response to infection Acute nephritis 1-6 weeks following infectious illness Strep pharyngitis/impetigo

Answer 380

Immune complex disease caused by specific nephritogenic strains of bacteria - Group A beta hemolytic Strep - Elevated strep titers Hypotheses: 1. Circulating immune complexes comprised of Strep antigen and antibody deposit within glomeruli and activate complement 2. Infection causes alterations of intrinsic GBM proteins, Ab bind and activate complement

Answer 381

Variable Range from asymptomatic with microscopic hematuria to full blown nephritic syndrome

Answer 382

Active urine sediment: Dysmorphic RBC, RBC casts, WBC, WBC casts Low C3, CH50, normal C4 Elevated Strep antibody titers - Streptozyme test

Answer 383

PIGN Hypercellular with numerous PMN

Answer 384

LM: Hypercellular glomerulus with abundant PMN IF: Large granular deposits of IgG, C3 EM: Large, hump like subepithelial deposits

Answer 385

Good prognosis - most recover Children - 95% recover without complications Adults - More insidious, slow progression to chronic GN Treatment - Supportive Care - Treat underlying infection - Manage HTN, edema, proteinuria

Answer 386

50% ionized 10% complexed to phosphate, citrate, carbonate, other ions 40% bound to protein

Answer 387

PCT - 65%. Mostly passive via gradients TAL - 20%. Mainly passive, driven by lumen charge DCT - 10%. Transcellular transport, active

Answer 388

Increases serum calcium 1. Ca release from bone 2. Ca reabsorption from kidney 3. Conversion of vit D to calcitrol by stimulating 1-a-hydroxylase --\> increase Gi absorption

Answer 389

Increase intestinal Ca absorption

Answer 390

1. Sodium - saline infusion increases Ca excretion 2. Ca - Dietary Ca increases excretion 3. Phosphate - Dietary of IV phosphate increases excretion 4. Proton - acidosis increases excretion 5. PTH and Calcitrol

Answer 391

12% filtered phosphate is excreted, remainder reabsorbed PCT: Enter apical membrane via Na dependent transporter (type II, I) --\> cross basolateral membrane via Na dependent transport (type III)

Answer 392

Principal regulator of phosphate reabsorption Inhibits Type II Na dependent phosphate transporter --\> reduces reabsorption Increases phosphate release from bone

Answer 393

Principal phosphate regulator in GI Increases intestinal reabsorption Increases renal reabsorption

Answer 394

FGF 23 Inhibits calcitrol synthesis and NaPi2a synthesis Calcitrol and high phosphate increase FGF23 --\> reduce calcitrol and phosphate

Answer 395

Sodium - saline infusion = excretion Calcium - Hypercalcemia = excretion Proton - Acidosis = excretion PTH/calcitrol/phosphatonin - major regulators Decreased GFR = hyperphosphatemia

Answer 396

Decreased kidney f(x) = decreased Vit D = phosphate retention/Ca decline Decreased Ca = PTH activation

Answer 397

CKD CV risk factors can accelerate vascular calcification - PTH, calcitrol, advanced AGE's, lipoproteins Relationship between CKD and abnormal phosphate/Ca, PTH levels, and vascular calcification

Answer 398

Severe organ dysfunction Heart valve dysfunction Calciphylaxis - necrotizing skin caused by calcific uremic arteriolopathy Large vessel stiffening

Answer 399

High turnover bone disease Osteomalacia Mixed uremic bone disease Adynamic bone disease

Answer 400

High PTH Increased osteoclasts and osteoblasts Bone structure disruption

Answer 401

Low PTH Low turnover Decrease osteoblasts/clasts No mineralization defect Low rate of bone formation

Answer 402

Adynamic bone disease with mineralization defect

Answer 403

Histologic features of ostetitis fibrosa and osteomalacia

Answer 404

Bone pain Muscle weakness Skeletal deformities Growth retardation in children

Answer 405

Early prevention Control hyperphosphatemia: Diet, phosphate binders, dialysis Control Ca: Supplements for Low Ca, Low Ca dialysate for high Ca Vit D analogs: Inhibit PTH synthesis and secretion Calcimimetic agent: Blocks PTH secretion

Answer 406

Stage III: \<70 Stage IV: \<110 Stage V: 150-300

Answer 407

Infection Kidney stones Cancer Glomerular disease

Answer 408

Calcium oxalate stones - increased Ca Sturvite stones - Urea splitting organisms. High NH4 and high uring pH Uric acid stones - Low urine pH Cystine stones - Defect is cystine transporter

Answer 409

IgA nephropathy Familial hematuria/Thin BM disease - GBM collagen defect Alports syndrome - Hereditary nephritis, collagen defect. Basket weave GBM

Answer 410

Uric acid crystals

Answer 411

Calcium oxalate crystals

Answer 412

Cystine crystals

Answer 413

Cholesterol crystals

Answer 414

Waxy cast - chronic disease

Answer 415

Occurs in 50% SLE patients Genetic Environmental - Lower SES, viral antigens Genetic - Loss of tolerance

Answer 416

Immune complex mediated disease Antibody target - nucleosome Cells undergoing apoptosis/necrosis fail to exit circulation --\> intracellular contents exposed to immune system

Answer 417

Circulating nucleosome Ag/Ab complex deposits in kidney Anti nucleosome Ab cross reacts with intrinsic renal antigen Nucleosome antigen deposits first --\> Ab binds antigen

Answer 418

Serology: Anti ds DNA, ANA Low complement: C3, C4, total Active urine sediment

Answer 419

Class I: Minimal LN Class II: Mesangial Prolferative LN Class III: Focal LN Class IV: Diffuse LN Class V: Membranous LN Class VI: Advanced sclerosing LN

Answer 420

LM: Hypercellularity involving capillary loops Necrosis, crescent formation Immune complexes visible, wire loop capillaries (thickened)

Answer 421

Lupus Nephritis: Wire loops Intra capillary immune deposits Hypercellular areas with capillary loop destruction

Answer 422

Full house IF Lupus Nephritis

Answer 423

Lupus Nephritis Global immune deposits Subepithelial, subendothelial, mesangial

Answer 424

Immune complexes in all compartments: Subendothelial, subepithelial, mesangial

Answer 425

Variable, depends on pattern of injury Relapsing and remitting disease symptoms

Answer 426

Depends on clinical presentation and biopsy results Class III-V treated aggressively Active lesions - Cyclophosphamide, steroids --\> induce remission Maintenence therapy - Cellcept, azathioprine, steroids Alternative agents: Rituximab

Answer 427

Rapidly progressive glomerulonephritis Sever acute nephritic syndrome, progressive loss of renal function over days-weeks --\> ESRD if untreated

Answer 428

Type I: Anti GBM Type II: Immune complex mediated Type III: Pauci immune

Answer 429

Anti GBM - Goodpastures Formation of autoantibodies against Type IV collagen Immune deposits in GBM and pulmonary BM

Answer 430

Immune complex mediated IgA nephropathy PIGN Lupus Nephritis

Answer 431

Pauci Immune type ANCA C-ANCA: Proteinase3 target antigen. Renal limited or associated with granulomatosis with polyangitis P-ANCA: MPO target antigen. Renal limited or associated with microscopic polyangitis

Answer 432

Serologic tests: Anti GBM P/C-ANCA

Answer 433

LM: Necrosis of glomerular capillaries. Crescent formation, proliferation of cells in urinary space Anti GBM/Pauci: Non involved glomeruli look normal IF: Type I - Linear IgG along capillary walls Type II - Positive, depends on cause Type III - NEgative EM: Immune deposits only in Type II

Answer 434

High dose steroids Cyclophosphamide Rituximab Azathioprine Plasmapharesis - Anti GBM

Answer 435

RPGN Note crescent

Answer 436

RPGN Note crescent

Answer 437

RPGN Fibrinogen crescent

Answer 438

Type I RPGN Linear IgG deposits

Answer 439

End result of many forms of GN Clinical presentation: Renal failure with elevated creatinine Uremia Proteinuria and/or hematuria

Answer 440

LM: Globally sclerosed glomeruli, interstitial fibrosis, arteriolosclerosis, arteriolar hyalinosis IF: Variable EM: Variable

Answer 441

Common neoplasm Benign Papillary/tubular architecture Bland nuclei, no atypia No fibrous capsule or desmoplastic response

Answer 442

Renal papillary adenoma

Answer 443

Benign, rare Association with tuberous sclerosis Microscopic path: Blood vessels, smooth muscle, adipose tissue

Answer 444

Angiomyolipoma - adipose tissue

Answer 445

Angiomyolipoma Smooth muscle

Answer 446

Angiomyolipoma Blood vessels

Answer 447

Angiomyolipoma

Answer 448

Benign neoplasm Nest arrangement of cells Eosinophilic granular cytoplasm Bland, round central nuclei

Answer 449

Oncocytoma

Answer 450

Oncocytoma

Answer 451

85% of all primary renal malignancies Behavior related to: Size Stage: Involvement of surrounding fat, vascular invasion, lymph node mets Grade

Answer 452

Adults, male \> female Triad of symptoms: Costovertebral angle pain Palpable mass Hematuria Polycythemia: Paraneoplastic syndrome, erythropoietin secretion

Answer 453

Partial nephrectomy Radical nephrectomy: Whole kidney Adjunct chemotherapy

Answer 454

Clear Cell Papillary Chromophobe

Answer 455

Deletion of chromosome 3p Loss of VHL Promote tumor angiogenesis through VEGF

Answer 456

Trisomy 7 MET mutation (proto-oncogene)

Answer 457

Renal Cell Carcinoma

Answer 458

Renal Cell carcinoma

Answer 459

Renal Cell carcinoma

Answer 460

Cells arranged in nests/sheets Delicate fibrovascular network CLEAR CYTOPLASM

Answer 461

Clear Cell RCC

Answer 462

Clear Cell RCC

Answer 463

Cuboidal/low columnar epithelial tumor cells Papillary formation of cells with fibrovascular core Papillae may contain prominent macrophages

Answer 464

Papillary RCC

Answer 465

Papillary RCC

Answer 466

Eosinophilic cytoplasm with plant like cell borders Greater nuclear atypia

Answer 467

Chromophobe RCC

Answer 468

Invasion through renal capsule into perinephric fat Invasion into renal vein, proximal spread along IVC Lymph nodes - Renal hilum/para-aortic Distant mets - Adrenal, liver, brain, lungs, bone

Answer 469

Malignant renal tumor of chilfren Mutation of WT-1 gene on chromosome 11 WAGR syndroms: Wilms, Aniridia, Genital anomalies, retardation Denys-Drash syndrome: Wilms, gonadal dysgenesis, early onset nephropathy w/ renal failure

Answer 470

Abdominal mass Ab pain, hematuria, intestinal obstruciton, HTN

Answer 471

Wilms Tumor

Answer 472

Triphasic Pattern 1. Primitive blastema 2. Epithelial component - abortive tubules/glomeruli 3. Stroma - Fibrous or myxoid patters

Answer 473

Wilms Tumor

Answer 474

Wilms tumor Epithelial elements

Answer 475

Anaplasia of tumor cells Correlates with more aggressive behavior

Answer 476

Wilms tumor - Anaplasia

Answer 477

Combined therapy Surgical nephrectomy, radiation, chemo

Answer 478

Origin in urothelium lining the renal pelvis Clinical features: Associated with urothelial carcinoma elswhere in urinary tract Hematuria, urinary obstruction, hydronephrosis, flank pain

Answer 479

Urothelial cell carcinoma

Answer 480

Urothelial cell carcinoma

Answer 481

Papillary: Papillae with vascular cores, lined by malignant urothelial cells Flat: no papillary growth, disordered polarity/maturity of cells

Answer 482

Normal Urothelium

Answer 483

Papillary urothelial cell carcinoma

Answer 484

Low grade papillary urothelial cell carcinoma

Answer 485

High grade urothelial cell carcinoma - papillary

Answer 486

Flat urothelial cell carcinoma

Answer 487

Presence/absence of invasion High grade = invasion Tumor infiltrates adjacent tissue into renal parenchyma

Answer 488

Invasive urothelial cell carcinoma

Answer 489

High grade invasive urothelial cell carcinoma

Answer 490

Cigarette smoking - most important Chemical carcinogens Infectious agent - Schistosoma haematobium (Bladder SCC) Radiation, cyclophosphamide

Answer 491

Hematuria Dysuria

Answer 492

Urine Cytology - Less invasive, detect high grade. Less specific for low grade Cytoscopy with biopsy

Answer 493

Leiomyoma Urothelial papilloma

Answer 494

Urothelial cell carcinoma SCC

Answer 495

Papillary urothelial cell carcinoma

Answer 496

Invasive urothelial cell carcinoma - bladder

Answer 497

Background: Often due to chronic irritation/inflammation Association with schistosomiasis Appearance: Intercellular bridges, keratinazation of single cells, keratin pearls Radical cystectomy

Answer 498

Squamous cell carcinoma

Answer 499

Gland forming tumor, mucin production May arise from urachal remnant Treat: Radical cystectomy +/- radiation

Answer 500

Poorly differentiated appearance Treatment: Chemo+cystectomy+radiation if localized Chemo if systemic

Answer 501

T1 - invasion into lamina proprial T2 - Invasion into muscularis T3 - Invasion into soft tissue outside bladder

Answer 502

Clinical course: 60% tumors single, 70% confined to bladder New tumors after excision ==\> higher grade Prognosis: Depends on grade and stage

Answer 503

Transuretheral resection - Low grade, non invasive papillary lesions Bacillus Calmette Guerin - Attenuated TB. USed for high grade non invasive lesions. Incites granulomatous response against tumor Radical cystectomy - T2 or higher tumors Chemotherapy - Advanced disease

Answer 504

Diabetic ketoacidosis Lactic acidosis Renal failure Toxins (Aspirin)

Answer 505

Diarrhea RTA Carbonic anhydrase inhibitors

Answer 506

Acetazolamide Carbonic Anhydrase inhibitor Not good for HTN because solutes delivered to TAL and can be reabsorbed Used for epilepsy, glaucoma, altitude sickness

Answer 507

Loop diuretics, Furosemide NKCC2 inhibitor Not the best for HTN Increased excretion of Ca, Mg, K, H Use for hypervolemic states: HF, cirrhosis

Answer 508

Thiazide drugs (HCTZ, chlorthalidone) Na/Cl symporter blocker FIrst line HTN Not as good as loop for edematous states

Answer 509

Amilorde/Triamterene ENaC blockers Prevents K and H secretion Use adjunct with Loop/thiazide to prevent hypokalemia Can cause hyperkalemia Not great diuretics

Answer 510

DCT Na/Cl symporter blocker First line HTN drug Can increase K and H secretion via collecting tubule mechanisms

Answer 511

Na/Cl symporter blocker First line HTN drug

Answer 512

Loop Diuretic NKCC2 blocker Use for treating hypervolemic states (HF, cirrhosis) Increase excretion of Ca, Mg via electrostatic mechanisms Not best diuretic for HTN treatment

Answer 513

Osmotic laxative Helps treat cerebral edema

Answer 514

Mineralocorticoid receptor blocker Prevent Aldosterone action - No ENaC uptake Potassium sparing diuretic b/c no K secretion - Even with increased Na, charge restriction prevents K secretion

Answer 515

Carbonic Anhydrase inhibitor Acts in PCT Affects acid/base status without disrupting ion balance

Answer 516

ENaC inhibitors Can result in hyperkalemia (no K secretion) Use adjunct with thiazides/Loop to prevent hypokalemia

Answer 517

The devil incarnate for kidneys Causes arteriolar vasoconstriction and decreased GFR

Answer 518

Immunosuppressant Can be used in inflammatory nephrotic syndromes MCD, FSGS, Membranous nephropathy

Answer 519

Immunosupressant Can be used to treat inflammatory nephrotic syndromes: MCD, MN

Answer 520

Non selective irreversible alpha blocker Use for Pheochromocytoma

Answer 521

Antibiotic Can cause AIN

Answer 522

Bipolar medication Can cause DI

Answer 523

Use in hyperkalemia ONLY if ECG changes Short term drug

Answer 524

Cation exchange resin Hyperkalemia

Answer 525

Non functional in humans

Answer 526

Most degenerates, small structure remains Becomes ducts of reproductive system: Wolffian, mesonephric

Answer 527

Final and definitive kidney and ureter

Answer 528

Derived from intermediate mesoderm Lateral folding results in dorsolateral ridges that run along length of embryo (urogenital ridge)

Answer 529

Begins to form and regresses at week 4

Answer 530

4th week - mesonephric tubules form in IM, cranial --\> caudal Mesonephric duct forms (solid rod of cells) and fuses with cloaca Mesonephric tubules fuse with duct, create passage from mesonepchric excretory unit to cloaca

Answer 531

Arises from ureteric bud and metanephric blastema

Answer 532

Buds off mesonephric duct Induces IM to form metanephric blastema

Answer 533

Urine collecting elements Collecting tubules, major/minor calyces, ureters Undergoes repeated branching

Answer 534

Portion of kidney between glomerular capillaries and collecting duct Bowmans capsule, PCT, Loop of Henle, DCT

Answer 535

Reciprocal induction of ureteric bud and metanephric blastema are required for normalbranching and tubulation Mutations anywhere in pathway cause problems

Answer 536

Metanephric kidney originates deep in pelvic region Shift towards abdominal region (week 6-8) 90 degree medial rotation, face inward

Answer 537

Base of allantois and attachment to urogenital sinus expands and forms urinary bladder Urachus closes and becomes median umbilical ligament

Answer 538

Growth of bladder incorporates mesonephric duct and ureteric bud into bladder wall Remaining ureteric bud = ureters Trigone (smooth part of bladder) formed from entry of mesonephric duct and ureters

Answer 539

Forms when bilateral metanephric blastema fuse Get suck under IMA during ascention

Answer 540

Kidney epithelia overexressing PAX2 --\> atretic ureter

Answer 541

Renal dysplasia characterized by multiple cysts and dysplastic kidney tissue POTTER Pulmonary hypoplasia Oligohydraminos Twisted face Twisted skin Extremity defects Renal failure in utero

Answer 542

External urethral spincter (Rhabdosphincter)

Answer 543

Bladder neck/prostate --\> membranous urethra --\> bulbar urethra --\> Pendulous urethra Membranous urethra is site of incontinence

Answer 544

Shorter than males, fused to anterior vaginal wall Incontinence can be caused by: 1. Childbirth that damages pudendal nerve --\> external sphincter 2. Childbirth --\> anterior vaginal wall damage 3. Menopause --\> low estrogen --\> atrophy or urethra

Answer 545

Rich in M3 receptors M3 activation --\> detrusor contraction --\> relaxed bladder outlet --\> void urine

Answer 546

Beta adrenergic receptors (B3) NE release --\> detrusor relaxation --\> urine storage

Answer 547

Alpha receptors NE --\> constriction --. Storage

Answer 548

S2-S4 Detrusor contraction, urethral relaxation Detrusor contracts via Ach relsease Urethra probably through NO

Answer 549

NE release B3 receptors on bladder --\> relaxation via cAMP Constrict urethra (alpha receptors)

Answer 550

Somatic cholinergic Ach release on nicotinic receptors on rhabdosphincter --\> contraction --\> stop void

Answer 551

A delta fibers in detrusor - Sense wall stretch/tension C fibers in bladder mucosa - Stretch and nociception

Answer 552

Irritation = afferent fibers firing with decreased filling --\> frequency/urgency

Answer 553

Storage reflex - based on spinal pathways Filling --\> afferents fire --\> reflex firing from hypogastric nerve --\> NE release = Inhibit detrusor contraction Contract bladder neck/proximal urethra Block PS transmission Pudendal nerve also fires = contracted rhabdosphincter

Answer 554

Filling sends signal to PMC --\> PMC only fires when threshold is reached If threshold reached and PMC disinhibited --\> Stimulate PS transmission - detrusor contraction/urethral relaxation Inhibit Pudendal nerve mediated rhabdosphincter contraction Inhibit Guarding reflex via hypogastric nerve - No NE release

Answer 555

Urine flow through urethra --\> facilitates bladder contraction and more voiding

Answer 556

Excessive bladder contraction --\> involuntary urine losses Urge incontinence - Immediate need to urinate that cannot be suppressed Urgency and frequency

Answer 557

Loss of normal function of bladder outlet Stress incontinence - Laugh/cough etc Can result after surgery --\> damage to nerves

Answer 558

Primary problem is failure to empty bladder fully Results in buildup of urine --\> overflow trickles out into urethra Etiology: Unable to contract bladder Retention due to blockage (enlarged prostate)

Answer 559

Detrusor overactivity --\> overactive bladder Impaired PMC inhibition

Answer 560

Detrusor Sphincter Dyssynergia No connection with PMC so no relaxed sphincter

Answer 561

Detrusor areflexia, fixed external sphincter No bladder contraction Sphincter retains residual tone Urinary retention and overflow incontinence