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*First Aid in Brainscape* > Steve O's Ridiculous Renal Realities > Flashcards

Steve O's Ridiculous Renal Realities Flashcards

1
Q

Mesonephros

A

functions as the interim kidney for 1st trimester;

later contributes to the male genital system

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2
Q

Metanephros

A

permanent;
first appears in 5th week of gestation;
nephrogenesis continues through 32-26 weeks of gestation;
Contains ureteric bud, metanephric mesenchyme,

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3
Q

Ureteric bud

A

derived from caudal end of mesonephric duct;
gives rise to ureter, pelvises, calyces, and collecting ducts;
fully canalized by 10th week

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4
Q

metanephric mesenchyme

A

ureteric bud interacts with this tissue;

interaction induces differentiation and formation of glomerulus through the distal convoluted tubule

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5
Q

Ureteropelvic junction

A

last to canalize and the most common site of obstruction (hydronephrosis) in fetus

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6
Q

Potter’s sequence

A

Oligohydramnios causing compression of developing fetus leading to limb deformities, facial anomalies (low set ears, and retrognathia) and and compression of chest leading to pulmonary hypoplasia (cause of death);
causes include ARPKD, posterior urethral valves, bilateral renal agenesis

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7
Q

Horseshoe kidney

A

Inferior poles of both kidneys fuse;
as they ascend from pelvis, get trapped under inferior mesenteric artery and remain low in the abdomen;
kidney function is normal;
increased risk for ureteropelvic junction obstruction, hydronephrosis, renal stones, and rarely renal cancer (wilms tumor);
associated with Turner Syndrome

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8
Q

Multicystic dysplastic kidney

A

Due to abnormal interaction between ureteric bud and metanephric mesenchyme;
this leads to a nonfunctional kidney consisting of cysts and connective tissue;
if unilateral (most common), generally asymptomatic with compensatory hypertrophy of contralateral kidney;
often diagnosed prenatally via ultrasound;
not inherited, cysts are in renal parenchyma

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9
Q

Why is the left kidney taken during living donor transplant?

A

Because the renal vein is longer

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10
Q

Ureters: what is the course from kidney to bladder

A

pass under uterine artery and under ductus deferens (retroperitoneal);
Water under bridges;
Gynecologic procedures involving ligation of the uterine vessels may damage the ureter leading to ureteral obstruction or ureteral leak

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11
Q

Glomerular filtration barrier

A

Filters based on charge and on size;
Composed of- Fenestrated capillary endothelium (size barrier), Fused basement membrane with heparan sulfate (negatively charged barrier), Epithelial layer consisting of podocyte foot processes;

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12
Q

When is the charge barrier lost in the GF barrier

A

Lost in nephrotic syndrome, resulting in albuminuria, hypoproteinemia, generalized edema, and hyperlipidemia

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13
Q

How to measure effective renal plasma flow

A

estimated using para-aminohuppuric acid (PAH) clearance because it is both filtered and actively secreted in the proximal tubule;
nearly all PAH entering the kidney is excreted

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14
Q

Glucose clearance

A

Glucose reabsorbed in PCT;

anything over ~200 not reabsorbed;

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15
Q

Amino acid clearance

A

Sodium dependent transporters in proximal tubule reabsorb amino acids;

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16
Q

Hartnup disease

A

autosomal recessive;
deficiency of neutral amino acid (e.g. tryptophan) transporters in proximal renal tubular cells and on enterocytes;
leads to neutral aminoaciduria and decreased absorption from the gut;
results in pellagra like symptoms;
treat with high protein diet and nicotinic acid

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17
Q

Fluid compartments and their size

A

60% is total body water;
40% total body weight is intracellular;
20% of total body weight is extracellular;
5% of total body weight is plasma volume;
15% of total body weight is interstitial volume

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18
Q

Notable components of PCT

A

contains brush border;
reabsorbs all glucose and amino acids and most of the bicarb, Na, Cl, Phosphate, K+, and H2O;
isotonic absorption;
generates and secretes NH3, which acts as a buffer for secreted H+;
PTH inhibits Na/Phosphate cotransport leading to secretion of Phosphate;
ATII stimulates Na/H+ exchange causing increased Na, H2O, and bicard reabsorption (permitting contraction alkalosis);
65-80% Na reabsorbed here

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19
Q

Thin descending loop of henle

A

Passively reabsorbs H2O via medullary hypertonicity (impermeable to Na+);
concentrating segment;
Makes urine hypertonic

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20
Q

Important components of the Loop of Henle

A

Actively reabsorbs Na, K, and Cl-;
indirectly induces the parallel reabsorption of Mg2+ and Ca2+ through + lumen potential generated by K+ backleak;
impermeable to H20;
makes urine less concentrated as it ascends;
10-20% Na reabsorbed

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21
Q

important components of the Distal Convoluted Tubule

A

Actively reabsorbs Na and Cl;
makes urine hypotonic;
PTH increases Ca/Na exchange leading to Ca reabsorption;
5-10% of Na reabsorbed

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22
Q

Important components of the collecting tubule

A

Reabsorbs Na in exchange for secreting K and H (regulated by aldosterone);
aldosterone acts on mineralcorticoid receptor which inserts Na channel on luminal side;
ADH acts on V2 receptor inserting aquaporin channel;
3-5% Na reabsorbed here

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23
Q

Fanconi syndrome

A

Reabsorptive defect in PCT;
assoc. w/ increased excretion of nearly all amino acids, glucose, bicarb, and phosphate;
may result in metabolic acidosis (proximal renal tubular acidosis);
causes include hereditary defects (e.g. wilson disease), ischemia, and nephrotoxins/drugs;
FABulous Glittering Liquid

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24
Q

Bartter syndrome

A

Reabsorptive defect in thick ascending loop of henle;
autosomal recessive, affects Na/K/2Cl cotransporter;
results in hypokalemia, and metabolic alkalosis with hypercalciuria;
FABulous Glittering Liquid

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25
Q

Gitelman syndrome

A 
Reabsorptive defect of NaCl in DCT;
Autosomal recessive;
less severe than Bartter syndrome;
leads to hypokalemia and metabolic alkalosis, but no hypercalciuria;
FABulous Glittering Liquid
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26
Q

Liddle syndrome

A

Increased Na reabsorption in distal and collecting tubules (increased activity of epithelial Na channel);
autosomal dominant;
results in HTN, hypokalemia, metabolic alkalosis, decreased aldosterone;
treat with amiloride

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27
Q

Where does Angiotensin II go to have an effect

A

1) acts on AT I receptors on smooth muscle causing vasoconstriction and increased BP;
2) constricts efferent arteriole causing increased FF to preserve GFR in low volume states;
3) activates aldosterone;
4) activates ADH release from posterior pituitary;
5) Stimulates hypothalamus causing thirst

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28
Q

ANP

A

released from atria in response to increased volume;
may act as a check on RAAS;
relaxes smooth muscle via cGMP causing increased GFR and decreased renin

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29
Q

ADH: what does it respond to

A

primarily regulates osmolarity;

also responds to low blood volume

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30
Q

Aldosterone: what does it regulate

A

Primarily regulates ECF Na+ content and volume;

responds to low blood volume states as well

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31
Q

Juxtaglomerular apparatus

A

consists of JG cells (modified smooth muscle of afferent arteriole) and the macula densa (NaCl sensor, part of the distal convoluted);
JG cells secrete renin in response to decreased renal blood pressure, decreased NaCl deliver to distal tubule and increased sympathetic tone (B1);
note that beta blockers work here as well as heart

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32
Q

Erythropoietin

A

released by interstitial cells in the peritubular capillary bed in response to hypoxia;

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33
Q

Kidney function on Vit. D

A

Proximal tubule cells convert 25-OH vit. D to 1,25-(OH)2 vitamin D;
Via 1alpha-hydroxylase (increased by PTH)

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34
Q

Renin secreted by

A

JG cells in response to decreased renal arterial pressure and increased renal sympathetic discharge via beta1

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35
Q

Prostaglandins and their effect on kidneys

A

Paracrine secretion vasodilates the afferent arterioles to increase RBF;
NSAIDs block this leading to constriction of the afferent arteriole and decreased GFR;
this may result in acute renal failure

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36
Q

Potassium shift due to digitalis

A

K shift out of cells

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37
Q

Potassium shift due to hyperosmolarity

A

K+ shifts out of cell

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38
Q

Potassium shift due to hypo-osmolarity

A

K+ shifts into cell

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39
Q

Potassium shift due to insulin deficiency

A

K+ shifts out of cell

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40
Q

Potassium shift due to insulin activity

A

K+ shifts into cell (increased Na/K ATPase)

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41
Q

Potassium shift due to lysis of cells

A

K+ shifts out of cell

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42
Q

Potassium shift due to acidosis

A

K+ shifts out of cell

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43
Q

Potassium shift due to alkalosis

A

K+ shifts into cell

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44
Q

Potassium shift due to beta adrenergic antagonist

A

K+ shifts out of cell

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45
Q

Potassium shift due to beta adrenergic agonist

A

K+ shifts into cell (increased Na/K ATPase)

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46
Q

Symptoms of low Na level

A

Nausea, malaise, stupor, coma

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47
Q

symptoms of high Na level

A

Irritability, stupor, coma

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48
Q

Symptoms of Low K level

A

U wave on ECG, flattened t waves, arrhythmias;

muscle weakness

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49
Q

Symptoms of High K level

A

Wide QRS and peaked T waves on ECG, arrhythmias;

muscle weakness

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50
Q

Symptoms of low Ca2+ levels

A

Tetany, seizure, QT prolongation

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51
Q

Symptoms of high Ca2+ levels

A

stones (renal), bones (pain), groans (abdominal pain), psychiatric overtones (anxiety, altered mental status), but not necessarily calciuria

52
Q

Symptoms of low Mg2+ levels

A

tetany, torsades de pointes

53
Q

Symptoms of high Mg2+ levels

A

Decreased DTRs, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia

54
Q

Metabolic Acidosis with increased anion gap (>12)

A

MUDPILES;

Methanol, Uremia, Diabetic ketoacidosis, Propylene glycol, Iron or INH, Lactic acidosis, Ethylene glycol, Salicylates

55
Q

Metabolic acidosis with normal anion gap (8-12)

A

HARDASS;

Hyperalimentation, Addison disease, Renal tubular acidosis, Diarrhea, Acetazolamide, Spironolactone, Saline infusion

56
Q

Renal tubular acidosis in general

A

a disorder of the renal tubules which leads to non-anion gap hyperchloremic metabolic acidosis

57
Q

Renal tubular acidosis: type 1

A

Distal, pH >5.5;
Defect in ability of alpha intercalated cells to secrete H+, thus new bicarb is not generate leading to metabolic acidosis;
associated with hypokalemia, increased risk for calcium phosphate kidney stones (due to increased pH and increased bone turnover);
Caused by amphotericin B toxicity, analgesic nephropathy, multiple myeloma (light chains), and congenital anomalies (obstruction) of the urinary tract

58
Q

Renal tubular acidosis: type 2

A

Proximal, pH

59
Q

Renal tubular acidosis: Type 4

A

Hyperkalemic, pH

60
Q

What are the causes of RBC casts

A

glomerulonephritis, ischemia, or malignant HTN;

61
Q

What are the causes of WBC casts

A

tubulointerstitial inflammation, acute pyelonephritis, transplant rejection

62
Q

What are the causes of Fatty casts

A

oval fat bodies;

nephrotic syndrome

63
Q

What are the causes of Granular casts

A

muddy casts;

Acute tubular necrosis

64
Q

What are the causes of Waxy casts

A

advanced renal disease/chronic renal failure

65
Q

What are the causes of hyaline casts

A

Nonspecific, can be a normal finding, often seen in concentrated urine samples

66
Q

Nomenclature for glomerular disorders: Focal

A
67
Q

Nomenclature for glomerular disorders: diffuse

A

> 50% of glomeruli are involved;

e.g. diffuse proliferative glomerulonephritis

68
Q

Nomenclature for glomerular disorders: Proliferative

A

Hypercellular glomeruli;

e.g. Mesangial proliferation

69
Q

Nomenclature for glomerular disorders: membranous

A

thickening of glomerular basement membrane;

e.g. membranous nephropathy

70
Q

Nomenclature for glomerular disorders: primary glomerular disease

A

Involve only glomeruli;
this a primary disease of the kidney;
e.g. minimal change disease

71
Q

Nomenclature for glomerular disorders: Secondary glomerular disease

A

Involves glomeruli and other organs, this a disaese of another organ system, or a systemic disease that has impact on the kidney;
e.g. SLE, diabetic nephropathy

72
Q

Glomerular diseases that cause Nephritic syndrome

A

Berger (IgA glomerulonephropathy);
Acute Poststreptococcal glomerulonephritis;
Alport syndrome;
Rapidly progressive glomerulonephritis

73
Q

Glomerular diseases that cause Nephrotic syndrome

A 
Focal segmental glomerulosclerosis;
Membranous nephropathy;
Minimal change disease;
amyloidosis;
Diabetic glomerulonephropathy
74
Q

Glomerular diseases that cause both nephritic and nephrotic

A

Diffuse proliferative glomerulonephritis;

membranoproliferative glomerulonphritis

75
Q

Nephrotic syndromes in general cause what

A

nephrOtic syndrome presents with massive prOteinuria (>3.5 g/day, forthy urine), hyperlipidemia, fatty casts, edema;
Assoc. w/ thromboembolism (hypercoagulable state due to AT III loss in urine);
increased risk of infection (loss of immunoglobulins)

76
Q

Focal segmental glomerulosclerosis

A

LM-segmental sclerosis and hyalinosis;
IF is negative;
EM effacement of foot process similar to minimal change disease;
Most common cause of nephrotic syndrome in blacks and hispanics;
can be assoc. w/ HIV, sickle cell, interferon treatment, and chronic kidney disease due to congenital absence or removal;
inconsistent response to steroid therapy;
may progress to chronic renal disease

77
Q

Membranous nephropathy

A

LM- diffuse capillary and GBM thickening;
IF-Granular as a result of immune complex deposition;
EM- Spike and Dome with subepithelial deposits;
most common cause of primary nephrotic syndrome in whites;
can be associated with antibodies to phopholipase A2 receptor, drugs (NSAIDs, penicillamine), infections, SLE or solid tumors;
poor response to steroids;
may progress to chronic renal disease;

78
Q

Minimal change disease

A

LM-normal glomeruli (lipid may be present in PCT cells);
IF is negative;
EM will show effacement of the foot processes;
Nephrotic syndome;
Most common in children;
may be triggered by recent infection, immunization, or immune stimulus;
may be assoc. w/ hodgkin lymphoma (e.g. cytokine mediated damage);
excellent response to corticosteroids

79
Q

Amyloidosis Nephrotic syndome

A

LM- congo red stain shows apple-green birefringence under polarized light;
kidney is the most commonly involved organ;
assoc. with chronic conditions (e.g. Multiple Myeloma, TB, rheumatoid arthritis)

80
Q

Membranoproliferative glomerulonephritis

A

nephritic syndrome that can also present as Nephrotic;
Type 1- subendothelial immune complex deposition with granular IF;
tram track appearance due to GBM splitting caused by mesangial ingrowth;
Associated with HBV, HCV, may be idiopathic
Type 2- Intramembranous IC deposits “dense deposits”;
associated with C3 nephritic factor (stabilizes C3 convertase leading to decreased serum C3 levels

81
Q

Diabetic glomerulonephropathy

A

LM- mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis (kimmelstiel Wilson lesion);
nonenzymatic glycosylation of efferent arterioles leading to increased GFR and increased mesangial expansion

82
Q

Overview of nephritic syndromes

A

nephrItic=Inflammatory;
when it involves glomeruli it leads to hematuria and RBC casts in urine;
associated with azotemia, oliguria, HTN (due to salt retention), and proteinuria (

83
Q

Acute poststreptococcal glomerulonephritis

A

LM-glomeruli enlarged and hypercellular;
IF- (starry sky) granular appearance (lumpy bumpy) due to IgG, IgM, and C3 deposition along GBM and mesangium;
EM- subepithelial immune complex (IC) humps;
Most frequently in children;
occurs ~2 weeks after group A strep infection of pharynx, skin;
resolves spontaneously;
Type III hypersensitivity;
presents with peripheral and periorbital edema, dark urine (cola colored), and HTN;
increased anti-DNase B titers and decreased compliment levels

84
Q

Rapidly progressing glomerulonephritis

A

Can present as nephritic or nephrotic;
LM and IF show crescent moon shape;
crescents consist of fibrin and plasma protein (e.g. C3b) w/ glomerular parietal cells, monocytes, and macrophages;
Associated with goodpastures, granulomatosis w/ polyangitis, microscopic polyangiitis;
Poor prognosis;
rapidly deteriorating renal function (Days to weeks)

85
Q

Goodpasture syndrome

A

type II hypersensitivity;
antibodies to GBM and alveolar basement membrane causing linear IF;
Hematuria/hemoptysis;
against type IV collagen (lungs, kidney, and lens)

86
Q

Diffuse proliferative glomerulonephritis

A 
due to SLE or MPGN;
LM "loop wiring" of capillaries;
EM- subendothelial and sometimes intramembranous IgG-based ICs often with C3 deposition;
IF- granular;
Most common cause of death in SLE;
can be nephritic or nephrotic
87
Q

IgA nephropathy

A 
AKA berger disease;
Nephritic syndrome;
LM- mesangial proliferation;
EM- mesangial IC deposits;
IF- IgA based IC deposits in mesangium;
seen in HSP;
often presents/flares with a URI or acute gastroenteritis;
episodic hematuria with RBC casts
88
Q

Alport syndrome

A

presents as nephritic syndrome;
Mutation in type IV collagen leading to thinning and splitting of the glomerular basement membrane;
Most commonly X-linked;
Glomerulonephritis, deafness, and less commonly eye problems

89
Q

Urine dipstick is positive for RBCs in urine, what does this mean

A

means dipstick reacted to peroxidase reaction of hemoglobin;
if no RBCs seen under microscopy then you have myoglobinurea;
myoglobinurea will cause reactive oxygen species so hydrate and alkalination of urine must be done

90
Q

Calcium renal stones

A

See envelope or dumbbell shaped crystals in urine;
radiopaque;
precipitates in increased pH (calcium phosphate) and decrease pH (calcium oxylate);
Promoted by hypercalciuria (look for diseases that increase Ca levels);
oxalate crystals can come from ethylene glycol (antifreeze), vit C abuse, Crohn disease;
prevent with Thiazide, citrate, and increased fluid;
Most common stone is calcium oxylate

91
Q

Ammonium Magnesium Phosphate renal stones

A

Coffin lid crystals;
Radiopaque;
precipitate at increased pH;
AKA struvite stone;
caused by infection (urease + like proteus, kleb, staph);
can form staghorn calculi that can be nidus for UTIs;
treat with eradication of underlying infection and surgical removal of stone

92
Q

Uric Acid renal stones

A

Rhomboid or rosettes stone;
radiolucent;
precipitate at decreased pH;
Risk factors- decreased urine volume, arid climates, and acidic pH;
visible on CT and ultrasound, not on x-ray;
strong association with hyperuricemia (like gout);
often seen in leukemia (high cell turnover diseases);
treat with alkalization of urine

93
Q

Cystine renal stones

A

Hexagonal stones;
radiopaque;
precipitate in decreased pH;
mostly seen in children, secondary to cystinuria;
can form staghorn calculi;
sodium nitroprusside test +;
treat with alkalinization of urine and increased hydration

94
Q

Hydronephrosis

A

distention/dilation of the renal pelvis and calyces;
usually caused by urinary tract obstruction;
other causes include retroperitoneal fibrosis and vesicoureteral reflux;
dilation occurs proximal to site of pathology;
only impairs renal function if bilateral or patient only has one kidney;
leads to compression atrophy of renal cortex and medulla

95
Q

Renal cell carcinoma

A

originates from proximal tubule cells;
see polygonal clear cells filled with accumulated lipids and carbohydrates;
most common in men 50-70;
increased incidence in smokers and obesity;
manifests clinically with hematuria, palpable mass, secondary polycythemia, flank pain, fever, and weight loss, invades renal vein then IVC and spreads hematogenously;
metastasizes to lung and bone;
associated with defect in chromosome 3 (von-hippel-lindau);
resistant to chemo and radiation;
most common primary renal malignancy

96
Q

Renal oncocytoma

A

Benign epithelial cell tumor;
large eosinophilic cells with abundant mitochondria without perinuclear clearing (vs. chromophobe RCC);
presents with painless hematuria, flank pain, and abdominal mass;
treat with nephrectomy

97
Q

Wilms tumor

A

nephroblastoma;
most common renal malignancy of early childhood (ages 2-4);
contains embryonic glomerular structures;
presents with huge, palpable flank mass and/or hematuria;
Loss of function mutations in tumor suppressor genes WT1 or WT2 on chromosome 11;
may be part of beckwith-Wiedemann syndrome or WAGR complex (Wilms, Aniridia, Genitourinary malformation, mental Retardation)

98
Q

Transitional Cell Carcinoma

A

Most common tumor of urinary tract system;
can occur in renal pelvis, renal calyces, ureters, and bladder;
painless hematuria (no casts) suggests bladder cancer;
associated with problems in your Pee SAC (Phenacetin, Smoking, Aniline dyes, and Cyclophosphamide)

99
Q

Squamous cell carcinoma of the bladder

A

Chronic irritation of urinary bladder leads to squamous metaplasia causing dysplasia and squamous cell carcinoma;
Risk factors include Schistosoma haematobium infection (middle east), chronic cystitis, smoking, chronic nephrolithiasis;
presents as painless hematuria

100
Q

Acute infectious cystitis

A

inflammation of urinary bladder;
presents as suprapubic pain, dysuria, urinary frequency, and urgency;
systemic signs (fever, chills) are usually absent;
Risk factors include female, sexual intercourse, and indwelling catheters;
causes- e coli, staph saprophyticus, klebsiella, proteus mirabilis (ammonia scent), adenovirus (hemorrhagic cystitis);
Lab findings- + leukocyte esterase, nitrites appear for gram - organisms, sterile pyuria and - urine cultures suggests gonorrhoeae or chlamydia

101
Q

Acute pyelonephritis

A

Affects cortex w/ sparing of glomeruli and vessels;
presents with dysuria, fever, CVA tenderness, nausea, and vomiting;
caused by ascending UTI (e coli), vesiculoureteral reflux, and hematogenous spread to kidney;
often presents with WBC casts in urine;
CT shows striated parenchymal enhancement;
risk factors are indwelling urinary catheter, tract obstruction, DM, and pregnancy;
Complications include chronic pyelonephritis, renal papillary necrosis, perinephric abscess;
treat with antibiotics

102
Q

Chronic pyelonephritis

A

the result of recurrent episodes of acute pyelonephritis;
typically requires predisposition to infection such as vesicoureteral reflux or chronic obstructing kidney stones;
Coarse asymmetric corticomedullary scarring, blunted calyx;
tubules can contain eosinophilic casts resembling thyroid tissue (thyroidization of kidney)

103
Q

Drug-induced interstitial nephritis (tubulointerstitial nephritis)

A

Acute interstitial renal inflammation;
pyuria (classically eosinophils) and azotemia occurring after administration of drugs that act as haptens, inducing hypersensitivity;
nephritis typically occurs 1-2 weeks after certain drugs (e.g. diuretics, penicillin derivatives, sulfonamides, rifampin), but can occur months after starting NSAIDs;
associated with fever, rash, hematuria, and CVA tenderness, but can be asymptomatic

104
Q

Diffuse cortical necrosis

A

Acute generalized cortical infarction of both kidneys;
likely due to a combination of vasospasm and DIC;
associated with obstetric catastrophes (e.g. abruptio placentae) and septic shock

105
Q

Avute tubular necrosis: stages and overview

A

most common cause of intrinsic renal failure;
self-reversible in some cases, but can be fatal if not treated;
death most often occurs during initial oliguric phase;
findings- granular (muddy brown) casts;
3 stages- 1) inciting event 2) maintenance phase-oliguric, lasts 1-3 weeks, risk of hyperkalemia, metabolic acidosis 3) recovery phase-polyuric, BUN and creatinine fall, risk of hypokalemia

106
Q

Avute tubular necrosis: 2 types

A

1) Ischemic- secondary to decreased renal blood flow (e.g. hypotension, shock, sepsis, CHF), results in death of tubular cells that may slough into tubular lumen (proximal tubule and thick ascending limb are highly susceptible to injury)
2) Nephrotoxic- secondary to injury resulting from toxic substances (e.g. aminoglycosides, radiocontrast agents, lead, cisplatin), crush injury (myoglobinurea), hemoglobinuria, proximal tubule is particularly susceptible to injury

107
Q

Renal papillary necrosis

A

Sloughing of renal papillae leading to gross hematuria and proteinuria;
may be triggered by a recent infection or immune stimulus;
associated with DM, acute pyelonephritis, chronic phenacetin use (acetaminophen is phenacetin derivative), sickle cell anemia and trait

108
Q

Acute Renal Failure

A

In normal nephron BUN is reabsorbed (for countercurrent multiplication), but creatinine is not;
acute kidney injury is defined as an abrupt decline in renal function with increased creatinine and increased BUN over a period of several days

109
Q

Prerenal azotemia

A

As a result of decreased RBF (e.g. hypotension) causing decreased GFR;
Na/H2O and urea retained by kidney in an attempt to conserve volume, so BUN/creatinine ratio increases;
urine osmolarity > 500;
urine Na 20

110
Q

Intrinsic renal failure

A

Generally due to acute tubular necrosis or ischemia/toxins;
less commonly due to acute glomerulonephritis (e.g. RPGN);
patchy necrosis leads to debris obstructing tubule and fluid backflow across necrotic tubule leading to decreased GFR;
urine has epithelial/granular casts;
BUN reabsorption is impaired leading to decreased BUN/creatinine ratio;
Urine osmolarity 40;
FENa >2%;
Serum BUN/Cr

111
Q

Postrenal azotemia

A

due to outflow obstruction (stones, BPH, neoplasia, congenital anomalies);
develops only with bilateral obstruction;
Urine osmolarity 40;
FENa >1% (mild)-2% (if severe);
Serum BUN/Cr >15

112
Q

Consequences of renal failure

A

inability to make urine and excrete nitrogenous waste;
MAD HUNGER- Metabolic Acidosis, Dyslipidemia (increased tg), Hyperkalemia, Uremia (increased bun and creatinine), Na/h2o retention, Growth retardation, Erythropoietin failure (anemia), Renal osteodystrophy

113
Q

Renal osteodystrophy

A

Failure of Vit D hydroxylation, hypocalcemia, and hyperphosphatemia leading to secondary hyperparathyroidism;
hyperphosphatemia also independently decreased serum Ca by causing tissue calcifications, whereas decreased 1,25-(OH)2 vitamin D leads to decreased intestinal Ca2+ absorption;
causes subperiosteal thinning of bones

114
Q

ADPKD

A

adults;
bilateral enlarged kidneys with tons of cysts;
destroys the kidney parenchyma;
presents with flank pain, hematuria, hypertension, urinary infection, progressive renal failure;
Autosomal dominant defect in PKD1 (85%, chromosome 16) or PKD2 (15%, chromosome 4);
death from chronic kidney disease or HTN (caused by increased renin);
associated with berry aneurysms, mitral valve prolapse, benign hepatic cysts

115
Q

ARPKD

A

Infants;
autosomal recessive;
associated with congenital hepatic fibrosis;
significant in utero renal failure can lead to potter sequence;
future concerns of HTN, portal HTN, progressive renal insufficiency;
no surface cysts like ADPKD, only in parenchyma

116
Q

medullary cystic disease

A

Inherited disease causing tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine;
medullary cysts usually not visualized;
shrunken kidneys on ultrasound;
poor prognosis

117
Q

simple vs complex renal cyst

A

simple cysts usually found in outer cortex filled with ultrafiltrate, very common, and account for majority of all renal masses, found incidentally and typically asymptomatic;
Complex cysts, including those that are septated, enhanced, or have solid components as seen on CT, require follow-up or removal due to risk of renal cell carcinoma

118
Q

Mannitol

A

osmotic diuretic, increased tubular fluid osmolarity, producing increased renal flow, decreased ICP and Intraocular pressure;
used for drug overdose, increased intracranial/ocular pressure;
toxicity-pulmonary edema, dehydration;
contraindicated in anuria, CHF

119
Q

Acetazolamide

A

mechanism- carbonic anhydrase inhibitor, causes self-limited sodium bicarb diuresis and decreased total body bicarb stores;
used for glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness, pseudotumor cerebri;
toxicity-hyperchloremic metabolic acidosis, paresthesias, NH3 toxicity, sulfa allergy

120
Q

Furosemide

A

Mechanism: inhibits Na/K/2Cl of thick ascending limb of loop Henle, abolishes hypertonicity of medulla, preventing concentration of urine, stimulates PGE release (vasodilate afferent arteriole), increased Ca excretion (loops loose Ca);
used for edema, HTN, and hypercalcemia;
toxicity- ototoxicity, hypokalemia, dehydration, allergy (sulfa), Nephritis (interstitial), Gout, OH DANG!

121
Q

Ethacrynic acid

A

Mechanism- phenoxyacetic acid derivative (not a sulfonamide), essentially same action as furosemide;
Use: diuresis in patients allergic to sulfa drugs;
Toxicity: same as furosemide, can cause hyperuricemia, never use to treat gout

122
Q

Hydrochlorothiazide

A

inhibits NaCl reabsorption in early distal tubule, decreasing diluting capacity of the nephron, decreased Ca excretion (increasing plasma Ca, so if increased PTH don’t give);
Uses- HTN, CHF, idiopathic hypercalciuria, nephrogenic diabetes insipidus, osteoporosis;
toxicity- hypokalemic metabolic acidosis, hyponatremia, hyperglycenmia, hyperlipidemia, hyperuricemia, and hypercalcemia, sulfa drug

123
Q

K+ sparing diuretics:

A

Spironolactone and eplerenone are competitive aldosterone receptor antagonists in the cortical collecting tubule;
triamterene and amiloride act at the same part of the tubule by blocking Na channels in CCT;
uses- hyperaldosteronism, K depletion, CHF;
Toxicity- hyperkalemia (can lead to arrhythmias), endocrine effects with spironolactone (gynecomastia, antiandrogen effects)

124
Q

ACE inhibitors: mechanism

A

captopril, enalapril, lisinopril;
inhibit ACE, decreasing ATII causing decreased GFR by preventing constriction of efferent arterioles;
levels of renin increase as result of loss of feedback inhibition;
inhibition of ACE also prevents inactivation of bradykinin, a potent vasodilator;

125
Q

ACE inhibitors: uses

A

captopril, enalapril, lisinopril;

HTN, CHF, proteinuria, diabetic nephropathy, prevent unfavorable heart remodeling as a result of chronic HTN;

126
Q

ACE inhibitors: toxicity

A

CATCHH;
Cough, Angioedema (contraindicated in Cl esterase inhibitor deficiency), Teratogenic (fetal renal malformations), increased Creatinine (decreased GFR), Hyperkalemia, and Hypotension;
avoid in bilateral renal artery stenosis because it will cause further GFR decrease

127
Q

Angiotensin II receptor blockers

A

ARBS;
-sartans;
similar to ACE inhibitors but do not increased bradykinin so less chance of cough;
Competitively inhibits ATII at angiotensin I receptor;
AT II is the most powerful Na retention hormone

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