Diseases

Question 0

Nephrogenic Diabetes Insipidus

Answer 0

Kidneys are unable to conserve water
Due to: lack of response of collecting ducts to ADH
Unresponsive to injected ADH

Question 1

Neurogenic Diabetes insipidus

Answer 1

Kidneys unable to conserve water
Due to: lack of production or release of ADH
responsive to injected ADH

Question 2

Syndrome of Inappropriate ADH

Answer 2

Excessive water retention
Hyponatremia with continued urinary Na+ secretion
Urine osmolarity > serum osmolarity

Body responds to water retention with decreased aldosterone (hyponateremia) to maintain near-normal volume status

Can lead to cerebral edema and seizures
Correct slowly to prevent central pontine meylinolysis

Causes: ectopic ADH (small cell lung cancer)
CNS disorders/head trauma
Pulmonary disease
Drugs

Treatment: fluid restriction, IV hypertonic saline, conivaptan, tolvaptan, demeclocycline

Question 3

Autosomal Dominant Polycystic Kidney Disease

Answer 3

Due to PKD1 gene mutations on Chromosome 16 (most)
PKD2 gene mutations on chromosome 4
Requires second hit genetic mutation
Both involed in tubular cell proliferation and fluid secretion

Both regulate nephron epithelial cell developent and apoptosis, vascular development in kidneys, liver brain, heart and pancrease

Cysts develop in collecting ducts most
Cysts: thickens and changes of adhesion of basement membrane
epithelial cell proliferation stimulated by increased ICF
increased cAMP leads to increased CL channel and increased aquaporin channel conductance in apical membrane leading to fluid accumulation

Presents with: flank pain, hematuira, hypertension urinary infection and progressive renal failure

Death from chronic kidney disease or hypertension (atrophy and fibrosis of renal parenchyma)

Associated with berry aneurysms, mitral valve prolapse, benign hepatic cysts

Question 4

Pre-renal azotemia

Answer 4

Functional response to renal hypoperfusion not associated with renal injury

Can lead to irreversible renal injury

Response to Volume Depletion (trying to maintain GFR)
Decreased renal perfusion leads to activation of SNS and RAAS
Increased AII levels leads to vasoconstriction of efferent arteriole
Increased AII levels and Increased SNS lead to increased proximal tubular Na+ and H2O absorption
Decreased renal perfusion also leads to aldosterone and ADH secretion leading to increased Na+, BUN and water reabsorption

LABS: Increased BUN:creatinine ratio (Increased BUN reabsorption due to Increased Na and H2O reabsorption) greater than 20
Increased Urine osmolality (Increased Na and H2O reabsorption)
higher than 500
Decreased urinary Na+ and FeNa (Increased Na reabosption)
less than 20 and less than 1%

Causes: hypovolemia, Decreased perceived blood volume (CHF, Cirrhosis, nephrotic syndrome), intrarenal vasoconstriction (NSAIDS, hepatorenal syndrome)

Question 5

Post-renal Acute Kidney injury

Answer 5

Obstruction of urinary collecting system
Patients with normal renal function and 2 kidneys you need bilateral obstruction of urinary tracts

Causes: prostate disease, retroperitoneal and pelvic malignancies, bladder or pelvic disease, neurogenic bladder, ureteral obstruction-stones, clots papillary necrsosis

Rapidly and fully reversible if diagnosed early

Urine osmolarity less than 350
Urine Na+ greater than 40
FeNa greater than 1% if mild, greater than 2% if severe
BUN/Cr greater than 15

Question 6

Acute tubular necrosis

Answer 6

Ischemic or Nephrotoxic (7-21 day duration)

Drugs that cause ATN: aminoglycosides, radiocontrast, lead and cisplatin

Risk factors: pre-existing CKD, atherosclerosis, Diabetes, poor nutrional status, cardiac surgery and AAA repair

Denuding of epithelial cells (proximal tubules and thick ascending loop of Henle), loss of brush border enzyme
Occlusion of lumens by cellular debris and casts

Presents: 3 stages
1. inciting event
2. maintenance phase: oliguric; lasts 1-3 weeks, risk of hyperkalemia (arrythmias), metabolic acidosis (retention of H+ anions)
increased ECF-weight gain, edema, pulmonary vascular congestion
Decreased Na and Ca
Increased PO4 and Mg
3. Recovery phase-polyuric; BUN and creatinine fall, risk of hypokalemic
Tubular re-epithelization and regain renal function

Dramatically decreased GFR
Dirty or muddy brown casts
Specific gravity is low
Una is high

Ischemic event: proximal tubule and thick ascending limb most susceptible
Nephrotoxic event: proximal tubule most susceptible

Treatment: maintain perfusion pressure in glomerulus
Correct electrolyte and metabolic disturbances
Dialysis if indicated

Question 7

Acute intersitial nephritis

Answer 7

Drug induced intersitial nephritis or Hypersensitivity nephritis
Not dose related-immune reaction related

Significant edema and mononuclear (lymphocytic and macrophage) infiltration in intersitium

Glomerulus spared

Serum IgE and eosinophilslevels elevated

Clinical triad: fever, eosinophilia and rash with renal dysfunction
CVA tenderness
not painful urination

UA: pyruia, WBC casts, little proteinuria, RBCs and eosinophilia

Common drugs (15 days after): penicillins, cephalosporins, sulfonamides, phenytoin, rifampin, diuretics
Months after NSAIDs
Drugs act as hapten inducing hypersensitivity

Treatment: remove offending drug +/- steroids

Question 8

Acute Pyelonephritis

Answer 8

Acute supourative inflammation of kidney
Affects intersitium, tubules and renal pelvis

Caused by: vesicouretral reflux, UTI and hematogenous spread to kidney

Hallmarks: interstitial suppurative inflammation
Intratubular aggregates of PMNs
Can result in tubular necrosis

Complications include papillary necrosis, pyonephrosis, perinephric abscess

UA: WBCs, WBC casts, mild proteinuria
Presents as fever, dysuria, costovertebral angle tenderness, nausea and vomiting

Non pathogenic flora prevent colonization by pathogenic strains

Question 9

Papillary Necrosis

Answer 9

necrosis of tips or distal 2/3 of pyramids-gray white or yellow of tips

Due to poor blood supply to papilla versus the rest of the kidney

usually chronic and bilateral
Presents with: colicky flank pain gross hematuria, proteinuria

Acute: sloughing of necrotic tissue and diagnosis made by finding tissue in urine

Associated with:
urinary tract obstruction,
analgesic abuse (phenacetin acetominphen derivative)-decreased prostaglandin synthesis inhibits renal flow,
sickle cell anemia and trait: obstruction of small kidney vessels
pyelonephritis: edematous insterstitium compresses medullary vasculature
diabetes mellitus: non-enzymatic glycosylation leads to vascular damage that compromises renal vasculature

Question 10

Vascular Disease: instrinsic injury to the kidney

Answer 10

Large vessel disease: renal thromboembolism, renal artery dissection, renal vein thrombosis
Results in renal infarction

Presents with flank pain, hematuria, increased LDH
Needs to be bilateral to cause increased creatinine

Question 11

Renal atheroembolism

“cholesterol emboli syndrome”

Answer 11

Spontaneous or iatrogenic showering of cholesterol crystals from atheromatous plaques

Onset can be days to weeks after procedure

Emboli result in skin, GI, renal, cutaneous hepatic abnormalities

Clinical: purple mesh rash or blue toes
Can have eosinophilia, eosinophiluria, decreased complement

Treatment is supportive

Question 12

Intratubular obstruction

Answer 12

Light chains in myeloma
Calcium in hypercalcemia
Uric acid in tumor lysis syndrome (treat with by alkalanizing urine) 
Acyclovir crystals
Myoglobin in rhabodmylolysis

Question 13

Rhabodmyolysis

Answer 13

Causes: cocaine, seizures, statin drugs, crush injuries

Injury to tubules: direct tubular toxicity at acidic pH
Vasoconstriction

Question 14

Diabetic Nephropathy

Answer 14

#1 cause of ESRD
Patients with GFR 25-50% greater than normal are more likely to get DM renal disease 

Earliest clinical finding is microalbuminuria

Once dipstick is + for protenuria there is already a 30-50% decline in GFR

Question 15

End stage renal disease

Answer 15

Progressive loss of kidney function is the result of the compensatory glomerular hemodynamic changes in response to nephron loss
-remaining nephrons are injured as a result of the compensatory mechanisms that take place in response to an injured nephron
Kidney adapts by increasing the filtration rate in remaining nephrons
Initially helps but results in long term damage

Mechanisms: loss or renal mass leads to hemodynamic adaptation, single nephron hyperfiltration, activation of RAAS, systemic hypertension, and hyperlipidemia

leads to increased inflammation and oxidative stress: up-regulation of TGF-B, EGF, VEGF, IGF-1, and PDGF
Decrease in NO

Results in: mesangial cell and podocyte atrophy/apoptosis
Endothelial cells decreasing NO production
Tubular epithelial cells: hypertrophy/atrophy, cytokine and chemokine production
Interstitial cells: infiltration and proliferation

All lead to matrix elaboration causing glomerulosclerosis and intersitial fibrosis.

Slowing progresssion: treatmetn of HTN, reduction of proteinuria, improve glycemic control

Question 16

Anemia as complication of CKD

Answer 16

Main factor: Inability to produce enough erythropoietin

Other factors:
Decreased responsiveness to erythorpoietin
Decreased RBC lifespan
Fe deficiency, B12 deficiency, or folate deficiency
Chronic infection or inflammation

Hct begins to fall when GFR is 30% of normal or when creatinine is between 2 and 4

Normochromic, normocytic anemia

Causes: fatigue, impaired sleep, impaired cognitive function
Directly related to development of LVH
Treat with erythropoietin

Question 17

Renal osteodystrophy as complication of CKD

Answer 17

alterations in bone morphology and bone pathology associated with CKD

Asymptomatic to bone pain to pathologic fractures

Subtypes:

1. osteitis fibrosa cystica: increased bone turnover, end result of secondary hyperparathyroidism
2. adynamic bone disease: excess suppression of PTH, main lesion in dialysis patients
3. osteomalacia: low bone turnover,
4. Mixed uremic osteodystrophy

Question 18

Renal osteodystrophy: Secondary Hyperparathyroidism

Answer 18

Phosphate retention when GFR falls

Question 19

Uremia

Answer 19

Signs and symptoms of advanced kidney failure
Indicates need for dialysis

Mechanisms:
1. Altered fluid and electrolyte excretion
Little to no urine excretion
Stage 3 and beyond there is decreased H+ excretion leading to chronic metabolic acidosis -treated with bicarbonate or lead to worse bone disease or muscle breakdown
2. accumulation of uremic toxins (decreased excretion of organic solutes)
Uremic encephalopathy: insomnia, altered cognitive function, confusion, hiccups, anxiety, depression. May lead to seizures, coma or death
Peripheral neuropathy: restless or burning legs/feet
GI symptoms: anorexia, nausea, vomiting, breath smells funny (uremic fetor)
Hematologic: anemia, impaired WBC and immune function, abnormal platelet (bruising)
Dermatologic: uremic frost, pruritis, ecchymosis
Cardiac: uremic pericarditis
3. decreased renal hormone synthesis
(decreased renin, decreased calcitriol, decreased erythorpoietin)

Question 20

Nephritic Syndrome

Answer 20

Inflammatory process
Hematuria and RBC casts in urine
Associated with azotemia, oliguria, hypertension and proteniuria

Question 21

Acute Proliferative Glomerulonephritis

Answer 21

Ex: post streptococcal glomerulonephritis
1-4 weeks after group A beta-hemolytic streptococal infection of the skin or pharynx

Coca-Cola Colored urine (hematuria)-dysmorphic RBCs and RBC casts
Periorbial edema
Increase in ASO titers, anti DNAase B and anti cationic proteinase
Decreased C3 in serum

Primarily affects children-recover completely

Pathogenesis: immune complex mediated

LM: hypercelular, enlarged glomeruli many neutrophils and monocytes
IF: granular lumpy bumpy due to IgG, IgM and C3 deposition along GBM and mesangium
EM: subepithileal hump-like immune complex deposits

Type III hypersensitivity
Resolves spontaneously

Question 22

Rapidly progressive Glomerulonephritis

Answer 22

Severe and rapidly progressive glomerular injury

Oliguria, azotemia, hematuria and variable proteinuria found

Untreated leads to death within weeks or months

LM: Crescents: breaks in GBM leads to leaks of fibrinogen converted to fibrin. IgG and C3b also present.
Parietal epithelial cells proliferate and fill up Bowman’s space
Monocytes and macrophages migrate to urinary space
IF: Type I-linear (anti-GBM)
Type II-Immune complex-granular
Type III-Pauci immune-Little to no deposition
EM: severe injury with GBM break
Immune complex deposits

Question 23

RPGN Type I

Answer 23

Anti-GBM disease

Goodpastures syndrome: RPGN plus pulmonary hemorrhage
Ab to type IV collagen in GBM cross reacts with pulmonary alveolar basement membranes (hemoptysis)

Linear glomerular basement membrane deposits of IgG and C3

Treatment: plasmapheresis, cytotoxic therapy

Question 24

RPGN Type II

Answer 24

Immune complex idiopathic, post infectious(Strep gomerulonephritis) , lupus nephritis, Henoch-Shonlein purpura (IgA nephropathy) Lumpy-bumpy granular pattern on IF Plasmapheresis does not help

Question 25

RPGN Type III

Answer 25

ANCA associated Patietns have circulating anti-neutrophil cytoplasmic Ab in blood part of systemic vasculitis: Wegener graulomatosis-C-ANCA test positive Microscopic polyagniitis: P-ANCA test positive NO IgG or complement deposits on BM Patients present with renal failure, pulmonary symptoms (cough, dyspnea, hemoptysis) and upper respiratory tract symptoms (epitaxis, mucosal ulceration, chronic sinnusitis) Treatment: cyclophosphamide therapy High incidence of irreversible renal failure

Question 26

Nephrotic Syndrome

Answer 26

Massive proteinuria Leakage from damaged GBM, increased permeability to plasma proteins Hypoalbuminemia Generalized edema (oncotic pressure change) Sodium and water retention (perceived loss of water) Hyperlipidemia-liver compensates by increasing lipid synthesis Hypercoagulability-thromboembolism due to loss of AT III in urine Vulnerable to infection (loss of Igs) Fatty casts

Question 27

Membranous Glomerulopathy

Answer 27

Idiopathic Secondary to: drugs (penicillamine, captopril, gold, NSAIDs) lung and colon cancer, melanoa, SLE, hep B and C, syphilis, scistosomiasis, and malaria Slowly progressive course LM: diffuse capillary and GBM thickening (no increase in cellularity) looks thick and fuzzy or spiked IF: granular deposits of IgG along the GBM (dot to dot) EM: Diffuse subepithileal immune-complex deposits (IgG and C3) -spikes and domes Poor response to steroid therapy and may progress to chronic renal disease

Question 28

Minimal Change disease

Answer 28

Most common in children May be triggered by recent infection, immunization, or immune stimulus or Hodgkin lymphoma LM and IF: normal EM: foot processes of epithelial cells are flattened/effaced (podocytes) Albuminuria Responds well to steroids

Question 29

Focal Segemental Glomerulosclerosis

Answer 29

Most common cause of nephrotic syndrome in adults in the US Idiopathic Secondary: HIV, heroin addiction, sickle cell disease, morbid obesity, interferon treatment, adaptive response from other renal diseases Inherited forms LM: focal=some glomeruli, segmental=part of the glomerulus, sclerosis=scarring Segmental sclerosis and hyalinosis IF: negative EM: effacement of foot processes (similar to minimal change disease) most progress to renal failure; recurs in kidney transplants Variable response to steroids

Question 30

Type I: Membranoproliferative Glomerulonephritis

Answer 30

Slowly progressive, unremitting course can remit in kidney transplants Can present with nephritic or nephrotic syndrome LM: hypercellular Mesangial proliferation gives lobular appearance Wire-loop local accumulations of subendothelial deposits Thickening and duplication GBM-tram-track double contour GBM pattern IF: C3 granular pattern sometimes deposits of C1q and C4 EM: Subendothelial deposits (BAD) Associated with HBV, HCV, or idiopathic Secondary to SLE Nephrotic and nephritic

Question 31

Type II: membranoproliferative Glomerulonephritis

Answer 31

Slowly progressive, unremitting course can remit in kidney transplants Can present with nephritic or nephrotic syndrome Intramembranous deposits LM: hypercellular Mesangial proliferation gives lobular appearance Wire-loop local accumulations of subendothelial deposits Thickening and duplication GBM-tram-track double contour GBM pattern IF: C3 irregular granular or linear foci in GBM and in mesagnial rings (intramembranous dense deposits) EM: Ribbon like dense deposits in the basement membrane Associated with C3 nephritic factor (stabilizes C3 convertase and decreases serum C3 levels) Secondary to SLE Nephrotic and nephritic

Question 32

IgA nephropathy (Berger disease)

Answer 32

Most common type of GN worldwide Recurrent gross or microscopic EPISODIC hematuria with RBC casts , mild proteinuria LM: mesangial proliferation IF: IgA immune complex deposits in mesangium EM: Immune complex deposits in mesangium Pathogenesis: increased IgA synthesis in response to environmental agents, flares after infection (URI) or gastroenteritis Slowly progressive Can recur after transplants

Question 33

Henoch Schonlein Purpura

Answer 33

Variant IgA nephropathy with systemic symptoms Tetrad: skin purpura (arms legs and buttocks), abdominal pain or intestinal bleeding, intussecpetion, arthralgias (necrotizing vasculitis of dermal vessels and subepidermal hemorrhage), nephritic syndrome Common in children Secondary to: liver disease and gluten enteropathy/celiac disease

Question 34

Alport Syndrome

Answer 34

Defective GBM type IV collagen synthesis-thinning and splitting of GBM Hematuria, Chronic renal failure, nerve deafness, eye defects X-linked recessive Presents with hematuria, progresses to proteinuria and overt renal failure EM: basket weave-thinning and splitting of GBM

Question 35

Thin Basement membrane disease (benign familial hematuria)

Answer 35

Defective collagen type IV NO deafness or eye abnormalities Most patietns heterozygous Renal function normal/prognosis excellent Kidney biopsy: diffuse thinning of the GBM on EM

Question 36

Diabetic glomerulonephropathy

Answer 36

Renal failure one of leading causes of death Nephrotic syndrome Glycosylation of proteins in small vessels occurs in glomerulus leading to GBM leakage with earliest sign being microabluminuria LM: thickening of basement membrane Increase in matrix (sclerosis) Nodular glomerulosclerosis (Kimmelstiel-Wilson disease-PAS+ and eosinophilic) mesangial expansion IF: negative EM: Non-specific Diffuse thickening of GBM and increased mesangial matrix Course: slowly progresssive decline in renal function, recurs in transplants ACE-inhibitors and ARBs slow progression (Glycosylation of efferent arterioles increased GFR leads to Mesangial expansion) Hyperglycemia induces ANP leading to increased hydrostatic pressure, increased GFR and increased glomerular hypertrophy

Question 37

Lupus Nephritis

Answer 37

Immune complex mediated Proliferative form is the worst major cause of morbidity and mortality Wire loop glomerular capillary appearance on LM subendothelial deposits

Question 38

Amyloidosis

Answer 38

LM-congo red stain show apple-green birefringence under polarized light Associated with chronic conditions-TB, multiple myeloma and RA)

Question 39

Urge incontinence

Answer 39

Urge: frequent abrupt and strong desire to void even without normal pressure Detrusor over activity, neuropathic detrusor over activity Infection, bladder cancer, BPH, prostatitis

Question 40

Stress incontinence

Answer 40

Involuntary loss of urine during physical activities during physical activities that increase intra abdominal pressure Deplacement of the bladder neck or insufficient strength of pelvic floor muscles Multiple births, prostatectomy, menopause (lower estrogen lowers muscular pressure around urethra) Sacral trauma leading to decreased EUS contraction

Question 41

Overflow incontinence

Answer 41

Overdistension of the bladder Outlet obstruction: BPH Sacral trauma leading to decreased detrusor contraction

Question 42

Functional incontinence

Answer 42

Physical or mental impairment that prevents one from reaching the facilities in time Ex: arthritis preventing one from undoing their pants in time

Question 43

Overall Kidney stone symptoms and complications

Answer 43

Complications: hydronephrosis and pyelonephritis Presents with: unilateral flank tenderness, colicky pain radiating to groin and hematuria Encourage fluid intake

Question 44

Calcium kidney stone

Answer 44

Precipitates at increase pH=calcium phosphate Precipitates at decrease pH=calcium oxalate Crystal: envelope or dubbell shaped Promoted by hypercalciuria (idiopathic or secondary to hypercalcemia such as cancer or high PTH) Oxalate crystals result from ethylene glycol, vitamin C abuse, or Crohn disease Treatment: thiazides and citrate Most common kidney stone Hypercalciuria and normocalcemia

Question 45

Ammonium magnesium phosphate kidney stone

Answer 45

Precipitates at increased pH Crystal: coffin lid Also known as struvite Caused by infection of urease + bacteria: proteus, saphylcoccus, Klebsiella) Hydrolyze urea to ammonia leading to urine alkalinization Can form staghorn calculi Treatment: eradication of underlying infection and surgical removal of stone

Question 46

Uric acid kidney stone

Answer 46

Precipitates at decreased pH RADIOLUCENT ON X-RAY use CT or ultrasound Crystal: rhomboid or rosettes Risk factors: decreased urine volume, acidic pH, gout, myeloproliferative disorders, increased protein diet, and decreased fluid intake Associated with hyperuricemia Treatment: alkalinization of urine

Question 47

Cystine kidney stone

Answer 47

Precipitates at decreased pH Crystal: Composed of sulfur, hexagonal Mostly seen in children secondary to cytinuria Due to AR disorder leading to defect in proximal tubule reabsorption of cystine Can form staghorn calculi Sodium nitroprusside test is postive Treatment: alkalinization of urine and hydration

Question 48

Acute infectious cystitis

Answer 48

Inflammation of urinary bladder Presents as suprapubic pain, dysuria, urinary frequency and urgency Systemic signs of fever and chills are usually absent postiive for leukocyte esterase (+), nittrites appear for gram-negative organisms Sterile pyuria

Question 49

Diffuse proliferative glomerulonephritis

Answer 49

Due to SLE or Membranoproliferative glomerulonephritis LM: wire looping of capillaries EM: subednothelial and sometimes intramembranous IgG based Immune complexes often with C3 deposition IF: granular Most common cause of death in SLE Nephrotic and nephritic

Question 50

Discoid (pancake) kidney

Answer 50

Both kidneys do not ascend | Fuse within true pelvic cavity

Question 51

Crossed and fused kidney

Answer 51

one kidney initially crosses midline and fuses with other while both are in true pelvis Combination undergoes relative ascent

Question 52

Benign Prostatic hyperplasia

Answer 52

Common in men >50 Prostate has rubbery consistency Hyperplasia of prostate gland in periurethral and transitional zones-smooth elastic firm nodular enlargment Not considered pre-malignant Presents with: increased frequency of urination, nocturia, difficulty starting and stopping stream of urine, and dysuria May lead to distenstion and hypertrophy of bladder (increases contractility), hydronephrosis and UTIs renal scarring and atrophy, overflow incontinence Increased PSA Treatment: alpha 1 blockers (terazosin, tamsulosin), finasteride

Question 53

Renal artery stenosis

Answer 53

Common cause of obstruction by an atheromatous plaque at origin of the renal artery Ischemic kidney secretes renin leading to hypertension Atrophy ensues due to oxygen and nutrient deprivation Atrophic kidney shows crowded glomeruli, tubulointerstitial atrophy and fibrosis can be caused by fibromuscular dysplasia -narrowing of multiple segments of renal artery Abdominal and flank bruits may be present

Question 54

Hartnup disease

Answer 54

AR Defieciency of neutral amino acid (trpytophan) transporters in proximal renal tubular cells and on enterocytes Leads to neutral aminoaciduria and decreased absorption from gut Results in pellagra like symptoms-photosensitivity, skin rashes, ataxia (wax and wane) Treat with high protein diet and nicotinic acid

Question 55

Gitelman syndrome

Answer 55

Reabsorptive defect of NaCl in DCT AR Less severe than Bartter syndroem Leads to hypokalemia and metabolic alkalosis (saline unresponsive) but no hypercalciuria

Question 56

Liddle Syndrome

Answer 56

Increased Na reabsorption in distal and collecting tubules (increased activity of epithelial Na channels) AD Results in hypertension, hypokalemia, metabolic alkalosis and decreased aldosterone Treatment: amiloride

Question 57

Hyper vs Hyponatremia

Answer 57

Hypo: nausea and malaise stupor, coma, muscle weakness, convulsion, confusion Hyper: irritability, stupor coma, muscle spasticity, seizures

Question 58

Hyper vs Hypokalemia

Answer 58

Hypo: u waves on ECG, flattened T waves, arrhythmias, muscle weakness Hyper: wide QRS peaked T waves on ECG, arrhythmias, muscle weakness

Question 59

Hyper vs Hypocalcemia

Answer 59

Hypo: tetany, seizures, QT prolongation Hyper: stones, bones, groans, psych overtones

Question 60

Hypo vs HyperMagnesia

Answer 60

Hypo: tetany, torsades de pointes Hyper: decreased deep tendon reflexes, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia

Question 61

Hyper vs HypoPhosphatemia

Answer 61

Hypo: bone loss, osteomalacia Hyper: renal stones, metastatic calcifications, hypocalcemia

Question 62

Respiratory Acidosis

Answer 62

pCO2 greater than 40 (renal compensation within 48 hours) ``` Airway obstruction Acute lung disease Chronic lung disease Opioids Weakening of respiratory muscles ``` HCO3 less than 30=acute HCO3 greater than 30=chronic

Question 63

Metabolic acidosis with increased anion gap

Answer 63

``` anion gap is greater than 12 MUDPILES MSUD Methanol (formic acid) Uremia Diabetic ketoacidosis Propylene glycol Iron tablets/INH Lactic acidosis Ethylene glycol (oxalic acid) Salicylates (late) Starvatiion ```

Question 64

Metabolic acidosis without increased anion gap

Answer 64

``` Cl- compensates for decreased HCO3 HARD-ASS Hyperalimentation (artificial supply of nutrients) Addison disease (adrenal insufficiency) renal tubular acidosis Diarrhea Acetazolamide Spironolactone Saline infusion ```

Question 65

Respiratory alkalosis

Answer 65

``` Hyperventilation (renal compensation within 48 hours) Hysteria Hypoxemia Salicylates early Tumor Pulmonary embolism ```

Question 66

Metabolic alkalosis with low urine Cl-

Answer 66

Vomiting Prior thiazide or loop diuretic use Saline responsive

Question 67

metabolic alkalosis wit high urine Cl- and hypovolemia

Answer 67

Current loop or thiazide diuretic use (saline responsive) Barter and Gitelman syndromes-saline unresponsive

Question 68

metabolic alkalosis with high Cl- and hypervolemia

Answer 68

Increased mineralcorticoid activity Primary aldosteronism, cushing syndrome, ectopic ACTH Saline unresponsive

Question 69

Salicylate poisoning acidosis/alkalosis response

Answer 69

Respiratory alkalosis early: medulla increases respirations | Metabolic acidosis late: predominates after 4-5 horuos

Question 70

Bartter Syndrome

Answer 70

Reabsorptive defect in thick ascending loop of Henle AR Affects Na/K/Cl cotransporter Results in hypokalemia and metabolic alkalosis (saline unpresponsive) with hypercalciuria

Question 71

Fanconi Syndrome

Answer 71

Reabsorbtive defect in PCT Associated with increased excretion of nearly all amino acids, glucose, HCO3- and PO4 May result in metabolic acidosis Causes: hereditary defects (wilson disease), ischemia, and nephrotoxins/drugs

Question 72

Type 4 renal tubular acidosis

Answer 72

hyperkalemia, ph less than 5.5 Hyperaldosteronism, aldosterone resistance or K+ sparing diuretics Hyperkalemia impairs ammoniagenesis in the proximal tubule leading to decreased buffering capacity and decreased H+ secretion into urine

Question 73

Type 1 renal tubular acidosis

Answer 73

Distal ph greater than 5.5 Defect in a intercalated cells to secrete H+ No new HCO3 is generated leading to metabolic acidosis Associated with HYPOKALEMIA increaesd risk for phosphate kidney stones (increased urine pH and increased bone turnover)

Question 73

Type 2 renal tubular acidosis

Answer 73

Proximal pH less than 5.5 Defect in proximal tubule HCO3 reabsorption resulting in increased excretion of HCO3 in urine and metabolic acidosis urine is acidified by a intercalated cells in collecting tubule Associated with HYPOKALEMIA Increased risk for hypophosphatemic rickets Causes: fanconi syndrome, chemicals toxic to proximal tubule and carbonic anyhdrase inhibtors

Question 73

Selective proteinuria

Answer 73

Albumin loss with little loss to more bulky tumors

Question 73

Tubular proteinuria

Answer 73

Low MW proteins normally filtered and reabsorbed in PCT Appearance means PCT dysfunction

Question 74

Overload proteinuria

Answer 74

Reabsorbed proteins overload tubular reabsorption capacity (multiple myeloma)

Question 75

Functional proteinuria

Answer 75

Change in blood flow through glomerulus Excessive high fever, emotional stress or cold

Question 76

Orthostatic proteinuria

Answer 76

Older, tall thin adolescent Increase protein excretion upon standing upright Overnight collection reveals normal albumin excretion

Question 77

Isolated proteinuria

Answer 77

Incidental finding, asymptomatic

Question 78

IgA nephropathy

Answer 78

LM-mesangial proliferation EM-mesangial IC deposits IF-IgA based IC deposits in mesangium (Dense on EM) Often presents with a URI or acute gastroenteritis Episodic hematuria (painless) with RBC casts

Question 79

Hydronephrosis

Answer 79

Distention/dilaton of renal pelvis and calyces usually caused by urinary tract obstruction (renal stones, BPH, cervical cancer, injury to ureter-hystorectomy and pelvic lymphadenopathy) Retroperitoneal fibrosis and vesicoureteral reflux Dilation occur proximal to site of pathology Leads to compression atrophy of renal cortex and medulla Kidney shows atrophy and scarring of renal parenchyma Only impairs function if bilateral or patients only has one kidney Presentation: flank pain that radiates to groin and palpable mass on deep abdominal exam LM: interstitial fibrosis with mononuclear infiltration and tubular atrophy

Question 80

Acute infectious cystitis

Answer 80

Inflammation of urinary bladder Presents: suprapubic pain, dysuria, urinary frequency, and urgency Systemic signs are absent Risk factors: female, sexual intercourse and indwelling catheters Causes: E. Coli, Staph sapro, Klebsiella, proteus mirablilis, adenovirus Bladder defense mechanisms: mucosa doesn't allow for bacterial attachment Normal urine is bacterocidal-increased urea and osmolarity Urea flow washes bacteria downstream Labs: positivve for leukocyte esterase Nitrites for gram- organisms sterile pyuria and - urine cultures suggest urethritis

Question 81

Chronic pyelonephritis

Answer 81

Result of recurrent episodes of acute pyelonephritis Requires predisposition such as vesicoureteral reflux or chornically obstructing kidney stones Coarse, asymmetric corticomedullary scarring, blunted calyx Tubules contain eosinophilic casts resembling thyroid tissue

Question 82

Chronic interstitial nephritis

Answer 82

Long term NSAID use or COX-2 inhibitors Reversible NSAIDs concentrate in renal medulla leads to increased levels in papilla than cortex Decreased prostangladins leads to constriction of vasa recta leading to ischemia which can go to papillary necrosis Also uncouple oxidative phosphorylation in renal mitochondria with direct cell damage patchy interstitial inflammation with necrosis, fibrosis, and scarring of papillae Distenstion of caliceal architecture and tubular atrophy seen in light microscopy

Question 83

Diffuse cortical necrosis

Answer 83

Acute generalized cortical infarction of both kidneys Likely due to combination of vasospasm and DIC Associated with obstetric catastrophes and septic shock

Question 84

Intrinsic renal failure

Answer 84

Due to ATN, ischemia toxins possibly RPGN Patchy necrosis leads to debris in obstructing tubule and fluid backflow across necrotic tubule decreasing GFR Urine has epithelial/granular casts BUN/Cr ratio is decreased below 15 Urine osmolarity is less than 350 Urine Na+ is greater than 40 FeNa is greater than 2%

Question 85

Autosomal recessive polycystc kidney disease

Answer 85

INfantile Associated with congenital hepatic firbrosis Significant renal failure in utero can lead to potter sequence Concerns beyond neonatal period include hypertension, portal hypertension, and progressive renal insufficiency cysts found in distal tubules and collecting ducts

Question 86

Medullary cystic disease

Answer 86

Inherited disease causing tubulointerstitial fibrosis and progressive renal insufficiency inability to concentrate urine Medullar cysts not visualized by shrunken kidneys on ultrasound Poor prognosis