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CPR II > Week 7 (Exam 3) > Flashcards

Week 7 (Exam 3) Flashcards

1
Q

Pathogenesis of Primary Membranous Glomerulo-Nephropathy

A

In-situ immune complex formations involving Phospholipase A2 Receptor on Podocytes
Involves in MAC and IgG4
Usually presents as Nephrotic Syndrome

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2
Q

Acute Proliferative Glomerulonephritis presentation in children

A

Malaise, fever, nausea, oliguria and hematuria 1-2 weeks after recovery from sore throat
Dysmorphic red cells or abc casts, mild proteinuria, periorbital edema and mild-moderate HTN

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3
Q

Whats the etiological difference between Cystitis Cystic and Cystitis Glandulars (CC and CG)?

A

Utothelium metaplasia into buds (nests of von Brunn), then invades the lamina propria. In CC it then differentiates into cystic deposits. In GC, it differentiates into intestinal columnar mucin-secreting glands

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4
Q

Clinical presentation of Renal Cell Carcinoma

A

Classic Triad: Hematuria, Costovertebral pain, palpable flank mass
Clear cells are from Glycolgen and Lipid accumulation

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5
Q

Main Renal Loss mechanisms of hypokalemia

A 
Diuretics
Increased Mineralocorticoid (aldosterone, ENaC)
Hypomagnesemia
Increased Distal Delivery of Na and H2O
RTA type 1 or 2
Intrinsic renal defect
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6
Q

Clinical presentation of WAGR

A

Genitourinary malformation: males have undescended testes and females have streak gonads or uterine malformations

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7
Q

Sx of Hypokalemia

A 
Cardiac Arrhythmias
Skeletal Muscle (esp Diaphragm) weakness
Rhabdomyolysis
Metabolic Alkalosis
Nephrogenic Diabetes Insipidus
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8
Q

Pathophysiology of Gitelman Syndrome

A

AR mutations of NaCl co-Transporter (NCCT)
NaCl wasting, Hypovolemia, RAAS (increased collecting duct Na reabsorption, H and K secretion)
Increased Ca reabsorption
Hypomagnesemia from down regulating TRPM6 in DCT

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9
Q

Calcium and cardiac AP

A

Increased Ca raises the threshold (makes it harder)

Lowered Ca lowers the threshold (makes it easier)

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10
Q

glomerular pathology of chronic glomerulonephritis

A

normal, lipid in tubules

loss of foot processes, no deposits

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11
Q

Glomerular Pathology of Membranous Glomerulo-Nephropathy

A

Diffuse Capillary Wall Thickening without increased cells
Spikes of Silver Staining Matrix from BM to urinary space
Supepithelial deposits of dense IgG and G3 with overlying obliterated foot processes

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12
Q

How to replace a potassium deficit

A

Potassium Chloride: K increases by 0.1 for every 10 given

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13
Q

Most common benign renal neoplasia

A

Renal papillary adenoma (benign), less than 1cm

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14
Q

Rapidly Progressive Glomerulonephritis Type I

A

Anti-GBM Ab

Renal Limited, Goodpasture syndrome

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15
Q

Patterns of tubular damage in Toxic injury

A

Continuous necrosis in PCT and PST

Patchy necrosis in Ascending LOH

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16
Q

Criteria of Malignant HTN

A

180/120 BP
Papilledema, Retinal hemorrhages, encephalopathy, CV abnormalities, renal failure
Early sx are from increased intracranial pressure

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17
Q

Pathophysiology of Minimal change disease

A

Unknown, loss of glomerular polyanion, podocyte injury
Its a nephrotic syndrome
Proteinuria and effacement of glomerular foot processes without Ab deposits. Responds well to steroids
Prensents as Edema and FPF on Bx

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18
Q

Pathophysiology of Liddle Syndrome

A

Mutated ENaC channel in collecting duct
Prevents degradation of them from luminal surface of principle cells via ubiquitin (too many!)
Increases Na reabsorption and urine K and H hypokalemia and metabolic alkalosis)

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19
Q

Clinical manifestations of Liddle Syndrome

A

Resistant Hypertension
Hypokalemia
Metabolic Acidosis (saline non-responsive)

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20
Q

Glomerular Pathology of Post-infectious Glomerulonephritis

A

Endocapillary Proliferation, leukocyte infiltration
Granular IgG and C3 in GMB, maybe IgA
Supepithelial humps, sub endothelial deposits

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21
Q

Amiloride

A

Blocks luminal Na Channels in collecting duct

Spironolactone blocks aldosterone receptor in collecting duct

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22
Q

First line treatment for stage 2/moderate hyponatremia

A

Vaptan or Hypertonic NaCl

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23
Q

Clinical Applications of Spironolactone

A

counteracts K loss induced by other diuretics in the treatment of HTN
off-label for reducing fibrosis post-MI heart failure

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24
Q

Toxicities of HCTZ

A

Sulfonamide etc

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25
Q

Clinical manifestations of Chronic Kidney Disease

A

Starts silent, develops uremia
Persistently diminished GFR (below 60 3+ months)
Persistent albuminuria
Generally Irreversible

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26
Q

What happens with ethylene glycol damage to the kidney?

A

Virtually all PCT epithelial cells show swelling and vacuolization

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27
Q

Pathophysiology of IgA nephropathy

A

Unknown, recurrent hematuria or proteinuria

Isolated (or can be nephritic)

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28
Q

Clinical manifestations of AKI

A

Rapid decline in GFR
Severe can have oliguria or anuria
Maybe from Glomerular, interstitial, vascular, or ATN
Can be reversible or become CDK

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29
Q

Triamterene

A

Similar to amiloride for edema and off-label for HTN, rapidly absorbed, 6-9 hours, eliminated as drug metabolized

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30
Q

Criteria for End Stage Renal Disease

A

GFR blow 5% normal

End stage of uremia

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31
Q

Insulin and K

A

Drives K into the cell (decreases serum k)

Alkalemia, ICF donates H+ to the ECF

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32
Q

Benign Nephrosclerosis

A

Pattern of hyaline sclerosis of renal arterioles, small a

multi-focal ischemia of kidney parenchyma supplied by sclerotic vessels

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33
Q

Characterizations of Acute Proliferative Glomerulonephritis

A

Marked Hypercellularity
Leukocyte infiltration: exudative within glomerular tuft
Granular deposits of IgG, IgM, C3

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34
Q

Where do renal oncocytoma arise from?

A

Type A intercalated cells of cortical collecting ducts
(acid-base homeostasis)
Mahogany-brown and well-circumscribed with central stellate scar. Packed with Mitochondria

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35
Q

Goodpasture Ag

A

Peptide within noncollagenous regions of collagen IV

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36
Q

Acute pyelonephritis

A 
Acute bacterial infection of the kidney
95% from the bladder with pre-existing defect
Vesicoureteral Reflux (back-flow up ureter)
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37
Q

Pathophysiology of Postinfectious Glomerulonephritis

A

Immune complex mediated, circulating or planted Ag

Usually Nephritic Syndrome

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38
Q

Clinical Applications of Conivaptan

A

Treats euvolemic and hypervolemic hyponatremia
For Hospitalized, symptomatic pts unresponsive to fluid restriction
Watch out for too rapid of serum sodium correction

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39
Q

Cardiac Arrhythmias associated with Hypokalemia

A

Premature Atrial Contractions
Premature Ventricular Contractions
Tachycardia, Bradycardia, V Fib

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40
Q

Renal Angiomyolipoma

A

AD, Lesions of brain, skin, kidney, heart, lungs, eyes

Strong association with Tuberous Sclerosis/TSC

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41
Q

Chlorothiazide

A

Similar to HCTZ but poor oral absorption

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42
Q

Uremia

A

Azotemia + constellation of findings of renal damage

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43
Q

3 main reasons for hypokalemia

A 
Transcellular Shift (Insulin, b2 agonist, m. alkalosis)
Extrarenal Loss (GI: vomiting, diarrhea, Sweating)
Renal Loss
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44
Q

Toxicities of Desmopressin

A

Black Box Hyponatremia

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45
Q

Differentiate Central vs Nephrogenic Diabetes Insipidus

A

Central: lack of ADH (tx with ADH agonist / dDAVP)
Nephrogenic: Unresponsive to ADH (tx with water and thiazide unless its from lithium: give amiloride instead)

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46
Q

Vaptan MOA

A

block ADH receptors at the collecting duct

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47
Q

Etiology of RTA 2

A

Most common in children is Cystinosis

Most common in adults with Fanconi is MM

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48
Q

Clinical applications of HCTZ

A

HTN, Not effective in patients with low GFR

Calcium nephrolithiasis

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49
Q

Negative Urine Anion Gap

A

Appropriate distal nephron urinary acidification

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50
Q

Symptoms of Uremia

A

CV: HTN, Atherosclerosis, Stenosis, CGF
GI: Occult bleeding, N/v, Uremic Fetor
Neuro: Uremic Encephalopathy, Amyloidosis
Skin: Fluid retention, CaP deposits, Nail Atrophy

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51
Q

Respiratory acidosis and K

A

Increaes serum K

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52
Q

RTA type 1 most common secondary causes

A

Auto-immune disorders

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53
Q

RTA type 2 most common secondary causes

A

Fanconi’s syndrome, MM, drugs

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54
Q

Medullary Sponge Kidney

A

Non-Hertiable, Benign
Medullary Cysts on Excretory Urography
Hematuria, UTI, Recurrent Renal Stones

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55
Q

3 groups of predisposing to Wilms Tumors patients

A

WAGR (wilms-aniridia-genital-retardation)
Denys-Drash Syndrome (gonadal and renal tumors)
Beckwith-Wiedemann syndrome (non-WT1, IGF 2)

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56
Q

Chronic Hypernatremia

A

Greater than 48 hours or unknown duration

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57
Q

Pathophysiology of Goodpasture

A

Anti-GBM COL4-A3 Ag

Rapidly Progressive Glomerulonephritis

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58
Q

Diagnosis of RTA 2

A

Urine pH can be high or low

Urine Anion gap is Negative

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59
Q

a-Intercalated cells transporters

A

H-ATPase

H/K-ATPase

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60
Q

Nephritic Syndrome

A

Glomerular Disease dominated by acute onset hematuria, proteinuria, HTN, Oliguria with Azotemia
Usually immune mediated glomerular injury

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61
Q

What bladder cancer staging is optimistic vs very bad?

A

Ta, Tis, T1 are low stage. Isn’t cured, but not deadly

T2 - T4, highly muscle invasive, is very bad

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62
Q

Visceral Epithelial Cell (podocyte) Injury

A

Abs causing foot process effacement (fusion).

Associated with Detachment of epithelial cells and protein leakage through defective GBM and filtration slits

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63
Q

Diagnosis of RTA 1

A

Unable to acidify urine pH below 5.5
Hypokalemia (urinary k wasting)
UAG is Positive

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64
Q

Advanced Renal Hyaline Arteriolosclerosis

A

Often found in diabetes
Thickened, tortuous afferent arteriole
Amorphous (thickened) vascular wall

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65
Q

Pathophysiology of Chronic Glomerulonephritis

A

Variable, usually presents as chronic renal failure

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66
Q

Metolazone

A

Long acting thiazide diuretic like HCTZ

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67
Q

Clinical manifestations of Gitelman Syndrome

A

Hypokalemia
Metabolic acidosis (non-saline responsive)
Low to normal blood pressure
HYPOCALCIURIA (opposite bartter), like w/ Thiazides
Hypomagnesemia

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68
Q

Normal Osmolality Gap

A

10

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69
Q

Where does urothelial carcinoma of the kidney originate

A

Urothelium of the Renal Pelvis

Presents with Hematuria, may block urinary outflow and lead to palpable hydronephrosis and flank pain

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70
Q

Clinical Applications of Conivaptan

A

Treats euvolemic and hypervolemic hyponatremia
For Hospitalized, symptomatic pts unresponsive to fluid restriction
Watch out for too rapid of serum sodium correction

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71
Q

Black box warnings of amiloride

A

hyperkalemia

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72
Q

Vaptan MOA

A

Prevents ADH-mediated insertion of the aquaporin water channels into luminal membrane of principal cells in collecting duct (prevents water reabsorption)

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73
Q

Rapidly Progressive Glomerulonephritis Type III

A

Pauci-Immune. NO anti-GBM Abs!
ANCA-Associated, Idiopathic
Granulomatosis with Polyangiitis, Microscopic Polyangiitis

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74
Q

Toxicities of Furosemide

A

Sulfonamide
Ototoxicity
Hyper-Glycemia, -uremia
Hypo-kalemia, -natremia, -calcemia, -magnesemia, etc

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75
Q

Papillary necrosis pattern of analgesic nephropathy

A

Red-brown necrotic papillae sloughed into calyces

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76
Q

Adult Polycystic Kidney Disease

A

AD PKD (polycystin) 1 / 2, always bilateral
Large multi cystic kidney, liver cysts, berry aneurysms
Hematuria, flank pain, UTI, renal stones, HTN

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77
Q

Where do sodium channel blockers work?

A

Cortical Collecting Duct

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78
Q

Glomerular Pathology of Goodpasture

A

Extracapillary Proliferation with crescents, necrosis
Linear IgG and C3, Fibrin in crescents
No Deposits, GBM disruptions, fibrin

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79
Q

How to Identify Acute Kidney Injury

A

Rapid Decline in GFR
Severe forms can have oliguria and Anuria
Maybe from glomerular, interstitial, vascular, tubular injury
Can be reversible or progress to CKD

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80
Q

Where do loop diuretics work?

A

Thin Ascending Loop

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81
Q

PKD 1 vs PKD 2

A

PKD1: 16p13.3, Polycstin-1, Cell-Cell/Cell-Matrix interaction
PKD2: 4q13-p23, Polycsytin-2, Ca2+ channel

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82
Q

RTA Type 4

A

Hyperkalemic RTA
Decreased Aldosterone Secretion or Aldosterone Resistance
Leads to decreased net H and K secretion in collecting duct

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83
Q

Crescentic Glomerulonephritis

A

Collapsed, compacted, glomerular tufts
Crescent shaped mass of proliferating visceral and parietal epithelial. Wrinkling of GBM, fragmenting and disruption
Rapid Obliteration of urinary space
Infiltrates of Macrophages and Leukocytes

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84
Q

Major pathological finding of Papillary urothelial neoplasms of low malignant potential

A

Thickened epithelium covering papillary projections

minimal cellular atypia

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85
Q

Exchange Resins

A 
Sodium Polystyrene Sulfonate / Kayexalate (exchanges Na_ ions for K mostly in the colon)
Zirconium Cycloslicate (exchanges Na and H ions for K throughout intestines)
Patiromer (exchanges Ca+ for K primarily in colon)
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86
Q

How to treat Hyperkalemia via K removal

A

Loop Diuretics or Thiazide
Exchange Resins
Hemodialysis

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87
Q

Etiology of malacoplakia

A

Defective phagosome function and related to chronic infection (E coli, usually)

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88
Q

Where does Renal Cell Carcinoma arise from?

A

Renal Tubular Epithelium (adenocarcinoma)

Happens a lot with smoking

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89
Q

Multicystic renal dysplasia

A

non-heritable absence of ureter, cauasing obstruction
Irregular kidneys with cysts of various size
Bilateral= renal failure, surgically cured if unilateral

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90
Q

Rapidly Progressive Glomerulonephritis

A

Nephritic syndrome with rapid decline in GFR

Implies Glomerular Injury

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91
Q

Chlorthalidone

A

Similar to HCTZ but half life of 40-60 hours

Prolonged/stable response with proven benefits

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92
Q

Why are urinary diverticulae commonly acquired?

A

Persistent urethral obstruction (like prostatic enlargement)

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93
Q

1 neoplastic SIADH cause

A

Oat cell carcinoma

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94
Q

Classic phases of AKI/ARF

A

Initiation: 36 hours, oliguria
Maintenance: HyperKalemia
Recovery: HypoKalemia from urine loss, infection

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95
Q

Loop Diuretics MOA

A

Blocks NaK2Cl cotransporter in TAL

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96
Q

Glomerular pathology of chronic glomerulonephritis

A

Hyalinized glomeruli, replacement of virtually all

Granular or negative on fluorescence microscopy

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97
Q

Glomerular pathology of Dense-Deposit Disease aka MPGN II

A

Mesangial proliferative or membranoproliferazive patterns of proliferation, GBM thickening, splitting
C3, no C1q or C4
Dense deposits

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98
Q

Bartter Syndrome Type 3 Mutation

A

All are AR

CLC-Kb

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99
Q

Most common tumor of men

A

Testicular Germ Cell Tumors

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100
Q

IV K replacement

A

K Chloride, K Acetate (usually just for severe)

10 - 20 mEq/hour

101
Q

Simple (renal) cysts

A

Non-heritable, benign
Single or several cysts, normal-sized kidneys
Microscopic hematuria

102
Q

Clear cell carcinoma

A

Most common renal cell carcinoma
Non-papillary, sporadic 95%
When familial, chromosome 3 short arm deletions/translocations (VHL ts gene)

103
Q

Treatment of Liddle Syndrome

A

Amiloride or Triamterene (blocks sodium channel)

Low salt diet

104
Q

Clinical Manifestations of Bartter syndrome

A

Hypokalemia
Metabolic Alkalosis (saline non-responsive)
Low to normal BP
Hypercalciuria and Nephrocalcinosis

105
Q

RTA Type 2

A

Proximal RTA

Decreased HCO3- reabsorption in PCT. Lost in urine, low in serum. Eventually stabilizes

106
Q

K Homeostasis cells in the distal nephron

A

Principle cells for secretion

a-intercalated cells for reabsorption

107
Q

Basement membrane is moth-eaten, or frayed

A

Alport Syndrome

108
Q

Vaptan MOA

A

Prevents ADH-mediated insertion of the aquaporin water channels into luminal membrane of principal cells in collecting duct (prevents water reabsorption)

109
Q

Primary vs Secondary Nephrotic Syndrome

A

Primary: Renal Only, primary kidney disease is most common in children
Secondary: Systemic, more common in adults (DM, SLE)

110
Q

Amiloride

A

Blocks luminal Na Channels in collecting duct (ENaC)

Spironolactone blocks aldosterone receptor in collecting duct

111
Q

Normal HCO3-

A

24

112
Q

Adult-onset Nephronophthisis

A

AD
Corticomedullary cysts, shrunken kidneys
Salt wasting, polyuria

113
Q

Tolvaptan

A

Selective AVP V2 receptor antagonist administered Orally
Hotta use it less than 30 days for hyponatremia (hepatotoxic)
It can also slow progression of adult PKD

114
Q

Osmotic Demyelination Syndrome

A

Happens in Pontine and Extrapontine Neurons
Delayed 2 - 6 days
Can develop Locked in syndrome

115
Q

Three major causes of decreased renal K secretion Hyperkalemia

A 
Low Aldosterone Secretion 
Aldosterone Resistance (K sparing Diuretics)
AKI or CKD (low GFR)
116
Q

Best method for assessing renal K+ excretion

A

24 hour urine potassium

117
Q

Licorice

A

Has glycyrrhizic acid, potentiates aldosterone effects in kidney and dose-dependently increases systolic BP

118
Q

Bartter Syndrome Type 4 Mutation

A

All are AR

Barttin Mutation

119
Q

3 circulating Auto-Abs in DMI

A

Anti-Insulin, -GAD, -ICA512

120
Q

Xanthogranulomatous Pyelonephritis association

A

Proteus sp.

121
Q

What would you order to assess the volume status of a hypotonic hyponatremic patient?

A

Random Urine Sodium Level
Urine Osmolarity
(serum Uric Acid if considering SIADH: high in urine)

122
Q

Thiazide MOA

A

Block NaCl cotransporter in DCT

Mg is reabsorbed in primarily in TALH/distal nephron

123
Q

Immune complexes in Subepithelial Humps

A

Acute Glomerulonephritis

124
Q

How to treat Transcellular Shift Hyperkalemia

A

Insulin and Dextrose
B2 Agonist (albuterol)
Bicarb (likely not effective)

125
Q

Risk of too rapid of sodium correction in chronic hyponatremia case

A

Osmotic Demyelination Syndrome (ODS) from brain swelling and rapid shrinking

126
Q

Actue vs Chronic Hyponatremia criteria

A

Acute: Less than 48 hours
Chronic: Longer than 48 hours or unknown

127
Q

Beckwith Widemann Syndrome clinical presentation

A

Hemihypertrophy, macroglossia

128
Q

Major pathogenesis of Transcellular Shift Hyperkalemia

A 
Pseudohyperkalemia
Metabolic Acidosis
Insulin deficiency, hyperglycemia, hyperolsmolarity
Increased Tissue Catabolism
Meds, Exercise, Blood Transfusion
129
Q

Microscopy findings in Diffulse Proliferative Lupus Nephritis

A

Glomerulus really biggened, looks stuffed into Bowmans

Resultant decrease in urinary space

130
Q

Anion Gap above 20

A

Suspect Alcohol ingestion

131
Q

Sarcoma botryoides

A

Embryonal Rhabdomyosarcoma, Cambium layer of tumor cells right below the epithelium results in nevoid appearance

132
Q

Most common malignancy associated with ectopic ADH production

A

Small Cell Lung Cancer

133
Q

Focal Segmental Glomerulosclerosis Collapsing Variant

A

in HIV and mores in Black patients

134
Q

Where do thiazide diuretics work?

A

DCT

135
Q

Pediatric Polycystic Kidney Disease

A

AR
Enlarged, cystic kidneys at birth
Hepatic Fibrosis

136
Q

Hereditary Segmental Glomerulosclerosis

A

Mutations in cell adhesion coding genes NPHS1 and 2
Those coding for Nephrin, Podocin, a-actinin 4 (AD)
TRPC6 (transient receptor potential calcium channel 6)
APOL-1 on Chr 22 in Black patients (related to resistance to trypanosomal infection)

137
Q

Ethacrynic acid

A

Non-sulfonamide loop diuretic reserved for those with sulfa allergy

138
Q

Bence-Jones proteins and the kidney

A

Causes or is indicative of a tubulointerstitial nephritis

139
Q

Thin basement membrane lesion

A

Benign clinical course, like Alport syndrome involves mutations in genes coding for GBM type IV collagen
In spectrum of diseases that includes hereditary nephritis
Asymptomatic Hematuria, most are heterozygous

140
Q

Eplerenone

A

More selective aldosterone antagonist than spironolactone

Approved for post-MI heart failure and alone for HTN

141
Q

Toxicities of Desmopressin

A

Black Box Hyponatremia

142
Q

Most common causes of End Stage Renal Disease

A

DM (primarily glomerular)

HTN (primarily vascular / arteriolar / tubulointerstitial)

143
Q

Ddx of NAGMA

A 
DURHAAM:
DIARRHEA
Ureteral Diversion
RENAL TUBULAR ACIDOSIS
Hyperalimentation
Acetazolamide
Addison's disease
Misc
144
Q

Mutations of invasive and bad bladder cancer vs superficial and non-invasive

A

TP53 (chr 17p) and RB is invasive

Chr 9 monosomy or deletions are usually fine

145
Q

Oral K

A

K chloride, K phosphate, K bicarb (precursors citrate, gluconate)

146
Q

Common Etiologies of RTA 1

A

Glue Sniffing and Sjogrens

Can manifest with nephrolithiasis or nephrocalcinosis

147
Q

Malignant arteriolosclerosis

A

Injury associated with malignant / accelerated HTN
Ischemic kidneys, elevated renin
“flea-Bitten” appearance of renal hemorrhages

148
Q

Polar Scarring of the kidney

A

Often from VUR with Chronic Pyelonephritis

149
Q

Painless Hematuria

A 
Think Urothelial (transitional cell) Carcinoma!
Theres usually multiple tumors at initial diagnosis
150
Q

glomerular pathology of focal segmental glomerulosclerosis

A

focal and segmental sclerosis and hyalinosis

“increasingly, a category of disease”

151
Q

Mesangial Immune Deposits

A

IgA nephropathy

152
Q

Normal Anion Gap

A

12

153
Q

How would you identify a tubulointerstitial nephritis?

A

Inability to concentrate urine: polyuria (acute or chronic)

154
Q

Metabolic alkalosis and K

A

Decreases serum K

155
Q

Diagnosis and treatment of Pyroglutamic (5-oxoproline) acidosis

A

Urinary Organic Acid Screen

Tx: discontinue acetaminophen, IVF, N-Acetylcysteine

156
Q

Eosiniphilic Cystitis

A

Infiltration of submucosal eosinophils, can also represent nonspecific subacute inflammation etc

157
Q

Pathophysiology of focal segmental glomeruloscerosis

A

Primary: Podocyte injury by unknown mechanisms
Secondary: ex. by prior glomerulonephtriytis, HTN, HIV…
Usually presents as nephrotic syndrome

158
Q

Most common causes of Hypokalemic Transcelluar Shift

A

Insulin
b2 Agonist
Metabolic Alkalosis

159
Q

Nephritic vs nephrotic presentations

A

Nephritic has greater hematuria

Nephrotic has greater Proteinuria

160
Q

Etiology of RTA 4

A

Deficiency of circulating Aldosterone (DM, drugs)
Aldosterone Resistance in collecting ducts
Both cause impaired Na reabsorption by principle cells
Hyperkalemia
Worsens Acidosis by preventing ammoniagenesis

161
Q

Clinical applications for desmopressin

A

Central Diabetes Insipidus

Primary Nocturnal Enuresis

162
Q

Glomerular pathology of IgA nephropathy

A

Focal mesangial proliferative glomerulonephritis, mesangial widening
IgA +/- IgG, IgM, and C3 in mesangium
Mesangial and paramesangial dense deposits

163
Q

Bartter Syndrome Type 2 Mutation

A

All are AR

ROMK

164
Q

How to treat Hyperkalemia with Peaked T waves

A

Calcium glutinate (stabilizes cardiac membrane)

165
Q

Microscopy of malacoplakia

A

Foamy macrophages, multinuclear giant cells, some granulomas

Laminated mineralized concretions, Michaelis-Gutmann bodies, in the macrophages

166
Q

Licorice

A

Has glycyrrhizic acid, potentiates aldosterone effects in kidney and dose-dependently increases systolic BP

167
Q

Patterns of tubular damage in Ischemic injury

A

Patchy necrosis of PCT, PST, Ascending LOH

168
Q

Nephrotic Syndrome (there’s 5 of them)

A

Glomerular Disease w/ severe proteinuria, hypoalbuminemia, edema, hyperlipidemia
Includes Membranous Nephropathy + Minimal Change Disease + Focal Segmental Glomerulosclerosis + Membranoproliferative Glomerulonephritis + Dense Deposit Disease (MPGN II)
Basically Leaky GBM (esp to albumin), RBCs don’t enter urine

169
Q

Clinical presentation of malacoplakia

A

Bladder inflammation with 3-4 cm soft yellow, plaques

170
Q

K sparing diuretics

A 
Na channel blockers (triamterene, amiloride)
Aldosterone Antagonists (spironolactone)
171
Q

Metabolic Alkalosis ddx

A 
Hypokalemia
Vomiting or NG tube
Diuretics
Volume Depletion
Mineralocorticoid Excess
172
Q

Normal Arterial pH

A

Normal: 7.35 - 7.45

173
Q

Prominent U wave

A

Hypokalemia

174
Q

PAS Type IV Collagen Stain findings in Diabetic Glomerulosclerosis

A

Diffuse Capillary Basement Membrane Thickening
Diffuse Mesangial matrix increase
Acellular PAS+ nodules

175
Q

Barium Toxicity

A

Blocks K+ channel and prevents efflux from cells

Causes hypokalemia

176
Q

5% albumin

A

Expands the plasma volume compartment

177
Q

Labs of Azotemia

A

Elevated BUN, Decreased GFR

178
Q

Sx of GC and CC

A

Chronic irritation, frequency, dysuria, urgency, hematuria

179
Q

Anatomical sites of kidney stone lodging

A

UPJ and UVJ (not thought to be at the ureteral crossing of the iliac vessels as much)

180
Q

Subendothelial Immune Deposits

A

Lupus Nephritis

Membranoproliferative Glomerulonephritis

181
Q

Bartter Syndrome Type 1 Mutation

A

All are AR

NKCC2

182
Q

Hypokalemia Criteria

A

Serum K below 3.5

183
Q

Histology of Papillary Renal Cell Carcinoma

A

Papillae and foamy macrophages in stalk

184
Q

How does metabolic acidosis work in hyperkalemia

A

K enters the cells so H exits them

Decreased ammoniagenesis and ammonium chloride excretion in the kidneys

185
Q

Acute Hypernatremia

A

Less than 48 hours

186
Q

RTA Type 1

A

Distal RTA: unable to acidify urine

Decreased net H+ ion secretion in DCT, collecting duct

187
Q

Glomerular pathology of Membranoproliferazive glomerulonephritis Type 1

A

Mesangial proliferative or membranoproliferazive patterns of proliferation, GBM thickening, splitting
IgG++ C3, C1q++ C4
Subendothelial Deposits

188
Q

Loop Diuretics MOA

A

Blocks NaK2Cl cotransporter in TAL

189
Q

Clinical presentation of interstitial cystitis (Hunner ulcer)

A

Chronic, persistent, painful, 30-40 yo women

Intermittent suprapubic pain, urinar frequency, urgency, hematuria, dysuria, Culture Negative

190
Q

Most common defect associated with acute pyelonephritis

A

Defective Vesicoureteral Junction (children with UTIs)

Bladder Outlet Obstruction (prostatic hypertrophy)

191
Q

3% and 5% NaCl

A

Expands the ECF while shrinking the ICF

192
Q

ADAMTS13

A

Protease regulating vWF

Mutations founding TTP (prominent neuro sx)

193
Q

Acute Post-Infectious Glomerulonephritis

A

Nephritic syndrome
Usually after Strep infection in children and young adults
Deposition of immune complexes, mainly sub epithelial
Neutrophils and glomerular cell proliferation. Good Px

194
Q

Criterion for Hypernatremia

A

Serum Sodium above 145

195
Q

Acute proliferative glomerulonephritis

A

Immune complex injury from exogenous Ag
Presents in adults with edema, elevated BUN, etc
Historical antecedent infection by b-hemolytic strep-specific nephritogenic strains of Lancefield Group A

196
Q

Pathophysiology of membranoproliferazive glomerulonephritis (MPGN) type 1

A

Nephrotic when primary, nephritic when secondary

Immune complex mediated

197
Q

What is usually the cause of bacterial urethritis

A

Gonorrhea, Chlamydia, HPV

198
Q

Cardiac changes in hyperkalemia

A

V Fib
Bradycardia form AV block
Asystole

199
Q

Bumetanide

A

Sulfonamide like furosemide but more predictable oral absorption

200
Q

Spironolactone MOA

A

Competitive antagonist aldosterone receptors
Partial agonist at androgen receptors
K+ sparing diuretic

201
Q

K losing diuretics

A

Thiazides (NaCl cotransporter blockers)
Loop Diuretics (Na K 2Cl Cotransporter blockers)
Carbonic Anhydrase inhibitors
Osmotic diuretics (nonreabsorbable solutes)

202
Q

Why does Metabolic Alkalosis happen with Hypokalemia

A

K moves from inside to outside cell to maintain [K+]

Leads to H+ going inside from outside cell for electric reasons

203
Q

Presentation of Alport Syndrome

A

Hematuria progressing to chronic renal failure
Nerve deafness and eye disorder (cataracts, etc)
X-Linked 85% of the time

204
Q

Papillary necrosis pattern of DM

A

Pale Grayish necrosis

Limited to papillae

205
Q

Alport Syndrome

A

Form of Hereditary Nephritis (homozygous)
Mutated genes encoding GBM type IV collagen
Manifests as Hematuria and slow progressing proteinuria and declining renal function
Glomeruli are normal until late in disease course

206
Q

HAGMA ddx

A

GOLD MARK

Glycols, Oxoproline (acetaminophen), L- and D- Lactic Acidosis, Methanol, Aspirin, Renal Failure, Ketoacidosis

207
Q

Renal Tubular Defects that can lead to RTA

A

Impaired H ion Secretion

Impaired HCO3- Reabsorption

208
Q

HCTZ MOA

A

Blockade of NaCl cotransporter

K-Losing

209
Q

Pathophysiology of Heymann Glomerulonephritis

A

Immune complex deposition on foot processes

210
Q

Rapidly progressive Glomerulonephritis Type II

A

Immune Complex
Idiopathic, Post-Infectious Glomerulonephritis
Lupus nephritis, Henoch-Schonlein, IgA Nephropathy

211
Q

Clinical presentation of Denys Drash

A

Gonadal Tumors

212
Q

Pathophysiology of Bartter Syndrome

A

Transporter mutations at Thick Ascending Loop
NaCl loss, volume depletion, 2nd hyperaldosteronism
Cl- loss in macula dense causes PGE2 increase: renin (more aldosterone, hypokalemia, met alkalosis)
“Net result is like Loop Diuretics”

213
Q

Frequent misdiagnosis of Polypoid cystitis

A

Papillary carcinoma. Look for this in in-dwelling catheters as this irritates the bladder mucosa

214
Q

Diagnostics of Liddle Syndrome

A

Genetic testing, Low Aldosterone levels and renin levels

215
Q

Two eponymic diseases associated with IgA Nephropathy

A 
Berger Disease (renal, not systemic)
Henoch-Schönlein Purpura
216
Q

Normal PCO2

A

40

217
Q

Acquired Renal Cystic Disease

A

Non-heritable, dialysis-dependent
Cystic degeneration in end-stage kidney disease
Hemorrhage, erythrocytosis, neoplasia

218
Q

Clinical applications of Furosemide

A

Management of edema
Decreases preload, EC volume, Rapid dyspnea
Treatment of HTN (works with low GFR, unlike thiazides)

219
Q

Where is NH4 produced?

A

From Glutamine metabolism in PCT

220
Q

Ddx of increased Serum Osmolality Gap

A 
Methanol
Ethanol
Diethylene glycol (diuretic mannitol)
Isopropyl alcohol (rubbing alcohol)
Ethylene Glycol
221
Q

Insulin and K

A

Drives K into the cell

Alkalemia, ICF donates H+ to the ECF

222
Q

Principle Cell Transporters

A

Na channel: creates net luminal negative charge

Indirectly favors tubular H secretion

223
Q

Wire loops on light microscopy

A

Renal Glomerular capillary basement membrane with sub endothelial dense deposits (also in mesangium)
Found in SLE

224
Q

Metabolic acidosis and K

A

Increases serum K

225
Q

0.45% NaCl

A

Expands ICF and ECF, but mostly the ECF

226
Q

Hyperkalemia criteria

A

Serum K over 5.0 or 5.5

227
Q

Pathophysiology of Dense Deposit Disease (MPGN type II)

A

Auto-Ab, alternative complement pathway via C3NeF (nephritic factor) binding C3 convertase
“unique permeation of glomerular basement membranes by electron dense material”
Usually presents as Hematuria and chronic renal failure

228
Q

RTA type 2 most common secondary causes

A

Fanconi’s syndrome, MM, drugs

229
Q

Histology of Interstitial cystitis (Hunner ulcer)

A

Mast cells, lymphocytes

Inflammation and fibrosis of the bladder wall, fissures

230
Q

Oral K

A

K chloride, K phosphate, K bicarb (precursors citrate, gluconate)

231
Q

Three sources of Pseudohyperkalemia

A

Transcellular shift:
RBC hemolysis (during venipuncture)
Serum Blood samples (clotted blood samples)
Leukocytosis

232
Q

K losing diuretics

A

Thiazides (NaCl cotransporter blockers)
Loop Diuretics (Na K 2Cl Cotransporter blockers)
Carbonic Anhydrase inhibitors
Osmotic diuretics (nonreabsorbable solutes)

233
Q

Emergency management of hyperkalemia

A 
IV calcium (antagonize cardiac effects)
Redistribute K into cells (insulin, glucose, bicarb, b2)
K elimination (K-losing diuretic, mineralocorticoid, etc)
Monitor Intake
234
Q

Sickle Cell Nephropathy

A

generally hematuria and hyposthenuria
Patchy papillary necrosis
Sometimes proteinuria, rarely nephrotic

235
Q

Post-renal azotemia

A

Seen when urine flow is obstructed distal to calyces and renal pelvis

236
Q

Eplerenone

A

More selective aldosterone antagonist than spironolactone

Approved for post-MI heart failure and alone for HTN

237
Q

Familial Juvenile Nephronophthisis

A

AR MCKD1 and 2 mutations
Corticomedullary Cysts, Shrunken Kidney
Salt Wasting, Polyuria, Polydipsia, Growth Retardation

238
Q

Epimembranous Immune Deposits

A

Membranous Nephropathy

Heymann Glomerulonephritis

239
Q

Osmotic pressure of glucose (or any non-dissociating solute) at 1mmol/L

A

19.3 mmHg

240
Q

Positive Urine Anion Gap

A

Inappropriate Distal Nephron Urinary Acidification

241
Q

Differentiate Central vs Nephrogenic Diabetes Insipidus

A

Central: lack of ADH (tx with ADH agonist / dDAVP)
Nephrogenic: Unresponsive to ADH (tx with water and thiazide unless its from lithium: give amiloride instead)

242
Q

Wilms tumor Histopathology

A

Often have precursor Nephrogenic Rests
triphasic (favorable): Blastemal, epithelial, stroll
anaplastic (unfavorable): Diffuse (always bad) or Focal

243
Q

Follicular Cystitis

A

Aggregation of lymphocytes in lymphoid follicles in the mucosa and underlying wall. Usually associated with Chronic Infection

244
Q

Triamterene

A

Similar to amiloride for edema and off-label for HTN, rapidly absorbed, 6-9 hours, eliminated as drug metabolites

245
Q

Pre-renal azotemia

A

From Hypoperfusion of the kidneys in the absence of primary renal parenchymal damage
Ex. Hemorrhage, shock, CHF, volume depletion

246
Q

Thiazide MOA

A

Block NaCl cotransporter in DCT

Mg is reabsorbed in primarily in TALH/distal nephron

247
Q

Delta Delta Gap

A

Used in patients with HAGMA to determine if there is a coexistent NAGMA or Metabolic Alkalosis

248
Q

Typical vs Atypical HUS

A

Typical: from E Coli O157:H7 or Shigella
Atypical: Inherited complement mut, endothelial injury (chemo / immunosuppression), other

249
Q

Black box warnings of amiloride

A

hyperkalemia

CPR II (8 decks)

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