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USLME Kiss my ass and pray > Renal DIT > Flashcards

Renal DIT Flashcards

1
Q

3 parts of the embryological kidney

Which gives rise to the ureteric bud?
Which gives rise to the audlut kidney

A 
Pronephros
Mesonephros
-caudal end -> ureteric bud
Metanephros
-adult kidney
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2
Q

Ureteric bud arises from? Gives rise to (4)

A

arises from the caudal end of the mesonephros -> induces metanephric mesenchyme to induce into nephrons and form glomerluli

the bud -> renal calyx, ureters, collection duct, pelvis

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3
Q

Most common site of obstruction in a fetus

A

ureteropelvic junction -> last to canalize

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4
Q

What does the mesenephros give rise to? (2)

A

ureteric bud (caudal end)

male genital system (in males)

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5
Q

Potters syndrome presents as?

Due to

A

Due to oligohydraminos (classically renal a genesis; also ARPKD and posterior urethral valves)

POTTER

Pulmonary hypoplasia
Oligohydraminos
Twisted face 
Twisted skin
Extremities malfunction
Renal agenesis
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6
Q

Horseshoe kidney is associated w/

A

turners syndrome

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7
Q

Renin is released from what cell under what 3 conditions

A

Released from Juxtaglomerular cells (next to the afferent artery) in response to

Low afferent BP (JG cells sense)
Low Na concentration in efferent arteriorl (Macula densa sense)
Beta 1 stimulation

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8
Q

Glomeruli filtration barrier is made of (3)

A

fenestrated endothelium
negatively charged basement membrane
podocytes (viseral layer)

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9
Q

Ureters course in relation to major anatomy?

Retroperitoneal or paritoneal?

A

retroparitoneal course

Ureters flow under the the uterine arteries in females and vas defer ins in males

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10
Q

% of the body that is water
-EC vs IC
W/in EC
–plasma vs intertitial

A

60% of the body is water
-1/3 extra cell and 2/3 intracellular

1/4 of extracellular fluid is plasma
3/4 extracellular fluid is interstitial

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11
Q

Renal clearance formula

A

UV/P

U- urine concent
V - urine flow rate
P - plasma concentration

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12
Q

Clearnance and relation to GFR

A

Cl< GFR = absorbtion
Cl> GFR = excretion
Cl =GFR = no ∆ ~ inulin

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13
Q

GFR calculation and estimation

A

calculate using inulin and the Clearance formula
[U(urine concent inulin) V] / (Plasma concent of inulin)

Can estimate w/ creatine which slightly over estimates GFR w/ mild secretion

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14
Q

Normal GFR =

A

100 mL/min

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15
Q

Effective renal plasma flow concept and formula

A

Effective renal plasma flow is ALL of the blood flow through the kidney, not just what is measured with clearance

Use PAH (para aminohiipuric acid) to calculate due to active secretion AND filtration at the proximal tubule

RPF~ Cl formula = clearance of PAH
[U (PAH) x V] / P (PAH)

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16
Q

Filtration Fraction formula and concept

A

filtration fraction is a comparisons of how much is being filtered at a given time compared to total flow

FF = GFR/RPF (or renal plasma flow)

normally 20%

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17
Q

Filtered load formula

A

GFR x plasma concentration

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18
Q

Excretion rate in renal?

A

U x V

the top part of the clearance formula ( flow rate x conncentration in the urine)

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19
Q

Prostaglandins and effect on the filtration

A

dialate afferent arteriole

  • Increase GFR
  • Increase RPF
  • No ∆ in FF
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20
Q

NSAIDs effect on glomeruli filtration

A

blocks prostaglandins afferent dialation ->

Decrease GFR
Decrease in RPF
-No ∆ in FF

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21
Q

angiotension II role of on glomeruli filtration

A

preferentially constricts the efferent arteriole

Increases GFR
Decrease in RPF
-> Increase in FF

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22
Q

ACE inhibitors and role on glomeruli filtration

A

blocks angiotensions II preferential constricion on the efferent arteriole

Decreases GFR
Increases RPR
Decreases FF

explains why creatine increases w/ ACE inhibitors

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23
Q

Ureter stone and effect on glomerlui filtration

A

blocks the flow downstream -> back pressure

Decreases GFR
No change in RPF
Decrease in FF

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24
Q

Increase in plasma globulin and effect on glomeruli filtration

A

increase osmotic pressure w/in the blood vessel

Decreases GFR
No change in RPF
Decrease in FF

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25
Q

Glucose clearance minimized due to?

  • point of saturation
A

Na/Glucose cotransporters in the proximal tubule reabsorb ALL glucose up to 160 mg/dL; then have some spill in the urine

Transporters saturated at 350 mg/dL

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26
Q

AA clearance and reabsorbtion

A

3 cotransporters that use Na absorb : acidic, basic and neutral AA in the proximal tubule

Neutral AA reabsorbtion dysfunciton = Hartnup’s disease
- Tryptophan deficiency -> niacin deficiency -> pellagra

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27
Q

Hartnup’s disease

A

deficiency in neutral AA/Na co-transporter in the kidney -> excessive loss of reabsorption of tryptophan

Can’t make Niacin (B3) -> pellagra

  • diarrhea
  • dermatitis
  • dementia
  • death
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28
Q

Pellegra can be due deficiency of what in the kidney

Presents as?(4)

A

neutral AA/Na co-transporter (no tryptophan -> B3/niacin)
-Hartnup’s disease

Dementia
Dermatitis
Diarrhea
Death

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29
Q

Part of the nephron responsible for collection of 2/3 of fluids and electrolytes

A

proximal

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30
Q

First half Proximal tubule collects? (6)

A

Bicarb (converted -> H2O and CO2 in lumen -> cell and converted back to bicarb)

glucose
AA
inorganic phosphate
lactate
electrolytes (isotonically, meaning water follows)
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31
Q

2nd half of proximal tubule collects?

A

Cl

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32
Q

Where does organic anions and cations get excreted in the nephron?

Due to?

A

in the proximal tubule
-alpha ketoglutarate gradient set up by Na/K atpase drives out organic anions into the lumen

organic cations are excreted by the electrochemical gradient set up with 3 Na out for every 2 in ATPase
- H is reabsorbed w/ lose of cation

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33
Q

thin ascending loop responsible for

A

reabsorbing water

impermeable to Na

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34
Q

Thick ascending loop responsible for (2)

A

actively reabsorbing Na/K/2Cl
->induces Mg and Ca to pass pericellular

Impermeable to water -> dilutes urine

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35
Q

Early distal tubule is responsible for (2)

A

Na/Cl actively being reabsorbed
Responding to PTH by placing Ca/Na exchangers on the basolateral side to reabsorb Ca

Impermeable to H2O

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36
Q

PTH has 3 functions w/ Ca(3)

A

Induces Ca reabsorption from bone
Stimulates Vitamin D conversion in the kidney by activating 1 hydroxylase
Places Na/Ca exchanges to reabsorb Ca in the kidney

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37
Q

2 types of cells in the collecting duct and their respectful roles

A 
principle cells
-responds to 
Aldosterone 
- ENaC and EK channels
ADH
-V2 and aquaporins

intercalcalated cells

  • A cell (alpha) -> secrete H
  • B cell (beta) - > secrete HCO3
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38
Q

Aldosterone acts where and has what function (3)

A

acts on the principle cell in the collecting duct to place Na channels to reabsorb Na and have H2O follow.
-Also places K channels which is thus lost to the lumen

In the alpha intercalated cell -> excretion of H

Epleronone and Spironolactone block

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39
Q

ADH/vasopressin act where and has what function

A

acts in the collecting duct on V2 and leads to the placement of aquaporins in the lumen to reabsorb water

Interfered w/ by lithium

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40
Q

Uses of mannitol

A

Drug overdose
elevated intracranial pressure
shock
glaucoma (acute angle closure)

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41
Q

What electrolyte is slightly elevated w/ the use of mannitol

A

Na in the serum due to the loss of free water

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42
Q

Glaucoma diuretics

A

Mannitol - acute closed angle

Acetazolamide - chronic

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43
Q

How does acetazolamide help in altitude sickness?

A

Blocks carbonic anhydrase in the lumen of the kidney thus leading to excretion instead of reabsorption in proximal tubule

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44
Q

Toxicity associated w. acetazolamide use

A

hyperchloremic metabolic acidosis

do not use w/ any hypokalemia, hyponatremic or hyper chorolate

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45
Q

Uses of acetazolamide

A

glaucoma- chronic
urinary alkalization
metabolic alkalosis -> piss away excess bicarb
altitude sickness

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46
Q

Dieuretics to stay away from if sulfa allergy(3)

A

acetazolamide

Loops
-furosimide

hydrochorothizide

Use ethacrynic acid

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47
Q

Need to use a loop but the patient is allergic to sulfa drugs use

A

ethacrynic acid

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48
Q

Which diuretics lose Ca and which retain

A

Loops lose Ca (may exacerbate a kidney stone problem)

Thiazides retain ( maybe use in idiopathic hypercalciuria)

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49
Q

Toxicity w/ loop diuretics(6)

be wary combing w/ what drug class

A

Ototoxic and nephrotoxic
-aminoglycosides

hypokalemia
dehydration
allergy
gout

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50
Q

Thiazide toxicity (7)

A 
hypokalemic metabolic alkalosis
hyponatremia
hyperglycemia
hyperlipidemia
hyperuicemia -> gout
hypercalcemia
-allergy - sulfa
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51
Q

Drugs used to increased morbidity and mortality in CHF patients (3)

A

Beta blockers
K sparing dieuretics
ACE inhib/ARBs

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52
Q

Hydrocholorthiazides ex (4)

A

hydrocholothiazide
chlorothiazide
chorthalidone
metolazone

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53
Q

K sparing dieuretics (4)

A

SEAT

Spiranolactone
Epleronone

Amiloride
Triamterene

may used in combination w/ Loops or thiazides to retain some K

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54
Q

Toxicity of K sparing diuretics (2)

A

Hyperkalemia -> arrhythmia

Antiandrogen -> gynectomastia in men / menstural problems in females

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55
Q

diuretics causing acidosis(2)

A

carbonic anhydrase inhibitor (acetazolamide)

K sparing (spares H excretion as well in the intercalated A cell)

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56
Q

diuretics causing alkalosis (2)

A

loops and thiazides

the loss of Cl leads to less bicarb being excreted and

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57
Q

anemia in a pateint due to renal failure

A

lack of erythropoeitin

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58
Q

enzyme in kidney that converts Vit D into its most active form

A

1 alpha hydroxylase

unregulated by PTH

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59
Q

what does the kidney secrete to vasodialate afferent arterioles to increase GFR

A

prostaglandins

NSAIDs can precipitate acute renal failure

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60
Q

ANPs action on the kidney

A

causes increase in GFR and Na filtration w/ no compensatory Na reabsorption in the distal tubule

opposite of aldosterone

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61
Q

SIADH can be caused (5)

A 
Ectopic ADH - small cell lung CA
CNS disorder/head truama/ infection
Pulmonary disease
Drugs - cyclosporine
Idiopathic
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62
Q

Presentation of SIADH(3)

Rx?

A

excessive water retention

hyponatremia w/ continued Na excretion
-low aldosterone due to hypercolemia (net Na loss)

urine osmolarity is low

Need to correct low Na very slowly (central pontine myelinolysis)

Rx -Demeclocycline, flid restricion, conivaptana nd tolvaptan

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63
Q

Central Diabetes insepitis causes (3) and presentation

A

pituitary tumor
trauma
surgery

intense thirst and polyuria - increased serum osmolarity, low specific gravity of urine (very dilute)

partial - some ADH
complete - No ADH

responds to desmopressin

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64
Q

Nephrogenic diabetes insepitis causes(4) and presentation

A

hereditary
secondary to hypercalcemia
lithium *
demeclocylcine

intense thirst and polyuria - increased serum osmolarity, low specific gravity of urine (very dilute);

Does not respond to desmopressin

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65
Q

Rx for SIADH (4)

A

Demopressin if central

Nephrogenic

  • Hydrochlorathiazide - induces proximal tube reabsorbstion
  • indomethacin - decrease renal blood floe
  • amiloride - stops Lithium from getting in the ENaC if causal
66
Q

Na imbalance

High (4)

Low (3)

A

Low

  • malaise/stupor
  • Siezures
  • coma
  • mental status change

High

  • irritability
  • stupor
  • coma
67
Q

K imbalance

High (4)

Low(5)

A

High

  • Wide QRS
  • Peaked t waves
  • muscle weakness
  • arrhythmia - v tach

Low

  • flat T waves
  • maybe U waves
  • arrhythmia - v tach
  • torsades
  • muscle weakness

K and Mg run together

68
Q

Ca imbalance

High (4)

Low (2)

A

High

  • Stones - kidney
  • Bones - pain
  • Groans - ab pain
  • psychiatric overtones - anxiet change in mental status confusion

Low

  • Tetany
  • siezure
69
Q

Mg inbalance

High (3)

Low(2)

A

High

  • decreased DTRs,
  • lethargy,
  • bradycardia

Low

  • arrythmia - torsasdes
  • tetany
70
Q

Shifts K out of the cell causing hyperkalemia (5)

A 
Digitalis
Cell Lysis
insulin deficiency
beta blockers
acidosis

Drugs that may cause

  • k sparing
  • Ace inhibitors
71
Q

Shifts K into the cell causing hypokalemia (4)

A

Insulin (increase Na/K ATPase)
alkalosis
Beta agonists ( increase Na/K ATPase)

Drugs that may cause
- thiazides and loops

72
Q

Rx for acute hyperkalemia (3)

A

beta agonists
induced alkalosis
insulin - give dextrose 1st

73
Q

Causes of respiratory acidosis

A 
Hypoventilation
respiratory muscle weakness
Lung obstruction
Air trapping
Opiods -> resp depression
Acute/chronic lung disease
74
Q

Causes of metabolic acidosis

-increased anion gap (9)

A

MUDPILES - gaining H

Methanol
Uremia
DKA
Propylene glycol
Iron tablets/ Isoniazid
Lactic acidosis - coding and not perfusing
Ethylene glycol
Saliclates -late
75
Q

Calculate anion gap

A

Na - (Cl - HCO3)

76
Q

Respiratory alkalosis causes (3)

A

Hyperventilation

  • high altitude
  • psychogenetic

Salicylates - early

Acute hypoxemia - PE

77
Q

metabolic alkalosis causes (4)

A

loop dieuretics
vomiting
antacid use
hyperaldosterone (hypokalemia, hypertension also)

78
Q

Metabolic acidosis w/o anion gap(4)

A

losing bicarb

Renal tubule acidosis (3 types)
Diarrhea
acetazolamide
spironolactone

hypealimentation
addisons
saline infusion as well

79
Q

Renal tubular acidosis Type I - defect and presentation?

urine pH?

A

defect in H secretion by alpha inceralated cells in the collecting tubule

urine pH of 5.5

hypokalemia w/ increased risk of CaPhosphate stones due to neutralization
metabolic acidosis w/out anion gap

80
Q

Renal tubular acidosis type 4 - defect and presentation ?

urine pH

A

defect in the hypoaldosterone or perceived hypoaldosterone -> hyperkalemia

hyperkalemia impairs collecting tubules from generating NH4 and excretion -> metabolic acidosis

urine pH <5.5 normal

81
Q

Renal tubular acidosis type 2 - defect and presentation?

urine pH?

A

Defect in proximal tubule HCO3 reabsorbtion (maybe falcon’s syndrome).

leads to hypokalemia and risk of hypophatemia
-> metabolic acidosis w/out anion gap

Urine pH <5.5

82
Q

henderson haselbalch equation essentially for metabolic disorders

pH =

Normal pCO2 and HCO3

A

HCO3/pCO2

pCO2 ~ 40 (35-45mmHg)
HCO3 ~22 (22-28 mEq/L)

83
Q

what do you have when you have a normal pH and off HCO3 and pCO2

A

you have mixed metabolic presentation, you should never have complete correction of metabolic disorder w/ compensation

84
Q

What value change cues you into a metabolic acidosis?

A

HCO3 decreased below 22 mEq/L

-pCO2 may decrease as patient tries to correct by breathing faster

85
Q

What metabolic value cues you into a metabolic alkalosis

A

HCO3 greater than 22 mEq/L normal pCO2

-pCO2 may increase as the patient breathes slower to correct

86
Q

what metabolic value clues you into a respiratory alkalosis

A

pCO2 less than 40 mmHg

HCO3 may decrease if kidneys are trying to correct

87
Q

what metabolic value clues you into respiratory acidosis?

A

pCO2 greater than 40 mmHg

HCO3 may increase if kidneys are trying to correct

88
Q

focal vs diffuse renal pathology

A

whether or not 50% of the glomeruli are affected

89
Q

proliferative renal pathology

A

hypercellular glomeruli

90
Q

membranous renal pathology

A

thickening of the glomerular basement membrant

91
Q

Strictly Nephrotic syndrome renal path (5)

A 
Focal segmental glomerulosclerosis
membranous nephropathy
minimal change disease
amyloidosis
diabetic glomerulonephropathy

overlap
-diffuse proliferative glomerulonephritis - SLE loops
membranoproliferative glomrulonephritis - Hep B,C lupes, endocarditis (subacute)

92
Q

strictly nephritic syndrome renal path (4)

A

Post streptoglomerulonephritis
Rapidly progressive glomerulonephritis
Bergers IgA glomerulonephropathy
Alport syndrome

Overlap

  • diffuse proliferative glomerulonephritis - SLE loops
  • membranoproliferatve glomerulonephritis - Hep B, C, Lupes and endocardits (subacute)
93
Q

Defining nephritic syndrome

Pathology and presentation

A

inflammation of the glomeruli

-> hematuria and RBC casts in the urine (tea/brown urine)
(azotemia, oliguria, HTN (Na retention), maybe proteinuria <3.5g/day

94
Q

Acute post streptococcal glomerulonephritis

timeline

presentation on
Light microscope
EM
IF

A

nephritic
Post pharyngitis or strep pyrogens impetigo about 1-3 wks after - Type III hypersensitivity

LM see lumpy bumpy deposits sub epithelial
IF - granular appearance w/ IgG, IgM and C3 deposition in the GBM and mesangium
-> depletion of complement C3

95
Q

anti DnAse B in blood and low C3 w/ dark urine

A

Poststreptococcal glomerulonephritis

96
Q

Rapidly progressive (cresentic) glomerluonephritis

presentation?

Types (3)

A

nephritic
See proliferation of fibrin, plasma proteins and parietal cells and debris in the glomeruli

Due to

  • Goodpastures - Type II hypersen w/ linear IF (anti GBM Ig)
  • Granulomatosis w/ polyangitis (wegeners) - cANCA
  • Microscopic polyangitis - pANCA
97
Q

Diffuse proliferative glomerulonephritis

presentation

LM
EM
IF

A

Wire loopus - most common cause of death in SLE; nephritic but also nephrotic

LM shows anti DNA complexes depositing between the endothelium dBM -> thickening (wire loops)**

EM - sub endothelial and maybe intramembranous IgG based immune complex w/ 3 ( NOT as KEY)

98
Q

Bergers disease (IgA nephropathy)

associated w?

LM
EM
IF

A

nephritic
related to henoch schonlein purport (part of vasculitis w/ palpable purport on arms/legs/butt and GI changes w/ ab pain, vomitting and interstitial bleeding)

seen after URI or gastroenteritis like w/ HP above

IF - IgA based immune complexes (from the vasculitis) deposits in the mesangium

thus LM -> mesangium proliferation and EM -> mesangium deposits

99
Q

Alport syndrome nephropathy due to

See on histology?

Presentation (3)

A

nephritic
X linked mutation of Type iV collagen

-> split basement membrane

glomerulonephritis
deafness
cataracts (eye problems)

100
Q

Presentation of nephrotic syndrome (5 issues)

A

proteinuria >3.5 g/day*
hypoalbunemia* -> peripheral edema *

Also

  • decreased Anti thrombin III -> thromboembolism
  • increased risk of infection (loss of Ig)
  • hyperlipidemia (liver wants to make vascular osmolar somehow)
101
Q

Focal Segmental Glomerulonephritis

LM
EM

Associated w?

A

nephrotic
most common cause of nephrotic syndrome in the US

LM -> semental sclerosis and hyalinosis
EM - effacement of the foot process as a result

Associated w/ HIV
-Higher rate in AA and latinos

102
Q

Membranous nephropathy

LM

EM

Due to?

A

Nephrotic
Used to be #1 more common in caucasion

EM spike and dome appearance

  • w/ sub epithelial deposits (between the thick BM and podocytes)
  • BM spikes between thick deposits

->LM - diffuse capillary and GBM thickening (membranous basement membrane)

Can be SLE’s nephrotic presentation (DPGM more common)

103
Q

Minimal Change disease

LM

EM

A

nephrotic disease -> selective loss of albumin in kids ages 2-7

LM shows NORMAL glomeruli

EM shows foot process effacement

responds to corticosteriods

104
Q

Amyloidosis nephropathy

LM

A

nephrotic syndrome

LM w/ congo red stain shows apple green birefringence under polarized light -> expansion of the mesangium w/ amyloid deposits

Kidney is the most commonly affected

105
Q

Membrano-proliferative glomerulonephritis (MPGN)

LM

Associated w? (4)

A

Nephrotic syndrome or can present nephritic

Membrane proliferates -> tram track
SUBENDOthelial deposits of IgG

2 types
- type I Tram track appearance of GBM due to mesangial ingrowth

-Type II intermembranous immune complex deposits -> dense deposits

HBV; HCV; SLE; Subacute endocarditis

106
Q

Diabetic glomerulonephropathy

LM(2)

A

Nephrotic syndrome

Nonenzymatic glycosylation of basement membrane -> increase permeability

also glycosylation of efferent arterioles -> increase in GFR
mesangial expansion

See esoisinophilic nodular glomerulosclerosis - Kimmerlstiel Wilson lesions

107
Q

Kimmelseil wilson lesions

A

eosinophilic nodular glomerulosclerosis in diabetic glomerulonephropathy

108
Q

lumpy bumby deposits of IgG, IgM and C3

A

post streptococcal glomerulonephritis

109
Q

Deposits of IgA in the mesangium

A

Bergers Disesae

110
Q

Nephritis, deafness and cataracts

A

Alport

111
Q

Crescent formation in the glomeruli

A

4 types of rapidly progressive glomerulonephritis

  • goodpastures
  • Wegeners
  • Microscopic polyangitis
  • SLE
112
Q

Wire loop appearance on the LM

A

SLE loopus - diffuse proliferative glomerulonephritis

113
Q

Most common nephrotic syndrome in adults

A

Focal segmental glomerulosclerosis

114
Q

EM shows effacement of the epithelial foot processes

A

minimal change disease

115
Q

nephrotic syndrome associated w/ HBV

A

Membranoproliferative glomerulonephritis

116
Q

Nephrotic syndrome associated w/ HIV

A

Focal segmental glomerulosclerosis

117
Q

Pupura on back of arms and legs, abdominal pain and IgA nephropathy

A

Henoch schonlein

118
Q

EM shows spiking of the GBM due to dense sub epithelial deposits

A

Membranous glomerulopathy

119
Q

RBC casts indicate

A

glomerular damage - like infarction or acute glomerulonephritis

120
Q

WBC casts indicate

A

acute pyelonephritis

121
Q

Bacterial casts indicate

A

pyelonephritis

122
Q

epithelial cell cast indicates

A

Acute tubular necrosis

Toxic ingestions- ethylene glycol or mercury

123
Q

waxy casts indicate

A

chronic renal failure

124
Q

hyaline casts indicate

A

benign pathology, maybe dehydration

125
Q

fatty casts indicate

A

nephrotic syndrome - hylaine casts w/ extensive fat infiltration

126
Q

Granular casts indicate

A

chronic renal disease, ATN

muddy brown

127
Q

Causes of calcium stones(4)

A

hypercalcemia

  • CA
  • PTH
  • Vitamine C excess >2000
  • ethylene glycol
128
Q

What can you give to prevent recurrent Calcium stones?

A

thiazide diuretics

129
Q

Which bugs are associated w/ kidney stones and what kind of stones do they cause (3)

A

Urease containing bugs

  • Proteous mirabilis
  • Staphylococci
  • Klebsiella

Urea split -> Ammonia and H2O

Form ammonium magnesium phosphate stones (struvite)

130
Q

Which kidney stone is invisible on plain film?

How might you visualize the stones

A

uric acid stones

visualize on CT and US

131
Q

Hyperuricemia due to CA may lead to this type of renal pathology

A

Uric kidney stones

132
Q

See a younger kid with recurrent kidney stones suspect

Rx?

A

cystine stones

  • secondary to cystiuria

treat with alkalization

133
Q

polygonal clear cell tumor filled with lipids and carbohydrates see in the men 50 -70 who may be overweight and smoked

A

Renal cell carcinoma

134
Q

Renal cell carcinoma paraneoplastic syndromes (4)

A

ACTH
PTHrP
EPO
prolactin

135
Q

Most common renal malignancy in malignancy in kids?

Most common malignancy in adults?
- METS where?

Most common tumor?

A

Wilms

Renal cell carcinoma
- hematogenous spread to bones and lung

Transitional cell carcinoma

136
Q

inhereted renal cell carcinoma is due to ?

A

Hippel lindau syndrome

Can be sporadic deletion on chromosome 3 as well

137
Q

Presentation of Wilms tumor

A

kid that is 2-4 that has hematuria and palpable flank mass

138
Q

Deletion of tumor suppressor gene WT1 -> ?

What chromosome?

A

Wilms tumor

Chromosome 11

139
Q

Beckwith wiedmann syndrome or WAGR complex

A

Wilms tumor
Aniridia - absence of iris
Genitalurinary malformation
Retardation - mental/motor

140
Q

painless hematuria in a patient that has a history of smoking?

Other risk factors (2)

A

transitional cell carcinoma

aniline dyes
cyclophosphamide

141
Q

Cyclophosphamide renal risks (2)

A

HUS

Transitional cell carcinoma

142
Q

thyroidization of the kidney

A

chronic pylonephritis

dilated tubules look like colloid

143
Q

Acute interstitial nephritis most commonly due to?(8)

timeline?

A

Drugs taken 1-2 weeks prior

NSAIDs
PCN/cephalosporins
ciprofloxin
cimetidine
PPIs
allopurinol
indinovir
mesalamine
144
Q

Presentation of acute interstitial nephritis?(6)

A 
fever 
rash
pyuria - eosinophilia*
azotemia*
hematuria
CVA
145
Q

Diffuse cortical necrosis is?

Due to?

A

acute generalized cortical infarction of BOTH kidneys

Due to vasospasm and DIC most commonly

associated w/ obstetric catatstrophy, ARDS, multi organ failure

146
Q

Acute tubular necrosis

due to (3)

A

most common cause of intrinsic renal failure

Drugs

  • aminoglycosides
  • cephalosporins
  • polymyxins

Radiograph contrast dye
-pretreat with NaHCO3 and fluids

Rhabdomyalisis and myoglobinuria

  • crush injury
  • statin
  • seizure
  • cocaine use
147
Q

Drugs causing acute tubular necrosis(3)

A

aminoglycosides
cephalosporins
polymixins

148
Q

Key findings w/ acute tubular necrosis

A

muddy brown casts
renal failure

if due to rhadomyalisis/myoglobinuria
-renal failure
elevated CPK
4+ blood in urine w/out RBC in urine cell count

149
Q

Renal papillary necrosis is ?

Presentation? (2)

A

sloughing of the renal papillae due to ischemic triggers

gross hematuria and proteinuria

150
Q

Casuses of renal papillary necrosis (4)

A

DM
Sickle cell
acute pyelonephritis
chronic phenacetin (acetomenophen) and ASA

151
Q

prerenal azotemia is due to

BUN : Cr

A

dehydration or hypotension -> decreased GFR

Na/H2O and urea is retained by the kidney in attempt to conserve

20>1

Na is resorbed so FeNa 500)

152
Q

Intrinsic azotremia due to?

BUN:Cr

A

Intrinsic renal damage, acute tubular necrosis or ischemia or toxins

less common glomerulonephritis

Patchy necrosis -> debris obstructing the tubules so DECREASE in GFR

BUN reabsorbtion is impaired so 2% due to tubular damage

153
Q

postrenal azotremia due to?

BUN:Cr

A

outflow obstruction

  • BPH
  • Stone
  • neoplasia
  • congenital anomalies

develops only if bilateral obstruction

BUN:Cr >15:1; no problem reabsorbing but depending on the block need back pressure
FeNa > 2% due to backpressure -> tube damage

154
Q

Consequences of renal failure (6)

A

Na/H20 retention
-CHF, pulmonary edema HTN

Hyperkalemia
-not able to put out

Metabolic acidosis
-same line as K

Uremia
-high BUN/Cr

Anemia
-less EPO

Renal osteodystrophy
- Vitamin D failure

155
Q

Uremia symptoms seen in renal failure (5)

A 
Nausea vomitting
pericarditis
Asterixis (liver flap)
encephalopathy
platelet dysfunction
156
Q

Renal osteodystrophy cause and consequence

A

seen in renal failure

Vitamin D hydroxylation failure leads to decreased activated vitamin D around to reabsorb Calcium in the kidney and also in the gut

PTH is activated w/ low serum Ca

subperiosteal thinning of bones
RX- Vitamin D Supplementation

157
Q

Presentation of ADPKD

A

multiple large bilateral cysts

flank pain
hematuria
HTN
urinary infection
progressive renal failure

Due to mutation in PKD1 or PKD2

158
Q

Dialysis patients may have

A

cysts

159
Q

ARPKD presentation

A

significant renal failure in utero (can be imaged)

oligohydraminos
-> can lead to potter syndrome

160
Q

medullary cystic disease

A

inherited disease causing tubulointerstitial fibrosis and progressive renal failure

poor prognosis

USLME Kiss my ass and pray (33 decks)

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