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Renal Flashcards

1
Q

What are the three effects of Angiotensin II?

A
  1. systemic vasoconstriction
  2. constriction of efferent arteriole
  3. Increased aldosterone synthesis
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2
Q

Concentration of tubular fluid in proximal tubule

A

isotonic with plasma (300 mosm/L)

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3
Q

Concentration of tubular fluid in descending loop of henle

A

Increasing (water permeable)

400-1200mOsm/L

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4
Q

Concentration of tubular fluid in ascending loop of henle

A

Decreasing (salt permeable)

1200-200mOsm/L

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5
Q

Lowest osmolality site in nephron, assuming low ADH

A

Distal convoluted tubule. Impermeable, so fluid stays hypotonic with increased reabsorption of solutes

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6
Q

When does ARPKD present?

A

At birth. In contrast, dominant form comes years later.

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7
Q

Urea acts on which segment of the collecting duct?

A

medullary segement to increase urea and water reabsorption

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8
Q

When does the pronephros degenerate?

A

4 weeks

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9
Q

Mesonephros

A

Functions as kidney for the first trimester

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10
Q

Metanephros appears wheN?

A

5th week of gestation. It becomes the permanent kidney

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11
Q

Ureteric bud comes from

A

caudal end of mesonephros

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12
Q

Ureteric bud gives rise to:

A

ureter, pelvises, calyces, collecting ducts

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13
Q

what interaction needed to form normal kidney

A

ureteric bud pokes the metanephric tissue

–induces metanephric tissue to format glomerulus to distal tubule

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14
Q

most common site of obstruction in fetus

A

ureteropelvic junction

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15
Q

Potter’s syndrome

A

Oligohydramnios–>
limb deformities
facial deformities
pulmonary hypoplasia

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16
Q

Causes of Potter’s

A

ARPKD
posterior urethral valves
bilateral renal agenesis

IF YOU CAN”T PEE in utero, you get potters

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17
Q

Horseshoe kidney assoc’d with

A

Turner syndrome

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18
Q

Nonfunctional kidney with cysts and connective tissue in utero. What caused this?

A

abnormal interaction btw ureteric bud and metanephros

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19
Q

Describe path of blood into the kidney

A 
renal artery
segmental artery
interlobal artery
arcuate artery
interlobular artery
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20
Q

Which kidney do you harvest for donation?

A

Left kidney=it has a longer renal vein

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21
Q

ureters pass over/under the ductus deferens/uterine artery?

A

under

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22
Q

60-40-20 rule

A

60% weight is TBW
40% ICF
20% ECF

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23
Q

measure plasma volume

A

radiolabeled albumin

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24
Q

measure extracellular volume

A

inulin

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25
Q

what gives negative charge in GFR?

A

heparan sulfate

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26
Q

clearance eq:

A

C=UV/P
U=urine concenctration
V=urine flow rate
P=plasma concentration

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27
Q

how to calc GFR

A

clearance of inulin or creatinine

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28
Q

When is creatinine clearance not accurate for GFR?

A

When GFR is very low. will have higher concentration of creatinine in urine

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29
Q

Calculation for effective renal plasma flow (ERPF)

A

clearance of PAH

PAH=filtered AND secreted into the proximal tubule. all that enters the kidney is excreted

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30
Q

RBF=

A

RPF/(1-Hct)

–ERPF underestimates true RPF by 10%

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31
Q

Filtered load=

A

GFR*plasma concentration

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32
Q

NSAIDs

A

constrict afferent arteriole

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33
Q

ACE-I

A

dilate efferent arteriole

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34
Q

prostaglandins

A

dilate afferent arteriole

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35
Q

angiotensin II

A

constricts efferent arteriole

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36
Q

increased plasma protein

A

decrease GFR

decrease FF

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37
Q

constriction of ureter

A

decrease GFR

decrease FF

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38
Q

Hartnup’s disease

A

deficiency of tryptophan(neutral amino acid) transporter in proximal tubule. neutral AA excreted in urine.

results in pellagra

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39
Q

blood glucose level when glucosuria starts? max saturation?

A

160 mg/DL

350mg/DL

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40
Q

which part of nephron generates ammonia?

A

Prox tubule

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41
Q

PTH and ATII on prox tubule

A

PTH: inhibits Na/Phosphate cotransport
ATII: stimulates Na/H exchange=contraction alkalosis. Holding onto sodium at expense of alkalosis

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42
Q

What % Na absorbed at each nephron segment?

A
  1. Prox tubule=65-80%
  2. L of H=10-20
  3. DCT=5-10%
  4. 3-5%
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43
Q

Thick loop of henle

A

Na/K/2Cl resorption

  • -paracellular resorption of Mg2+ and Ca2+
  • -dilution of urine as it passes
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44
Q

What allows paracellular resorption in thick ascending limb?

A

potassium backleak.

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45
Q

DCT transporter

A

Na/Cl apical cotransporter

–urine becomes hypotonic

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46
Q

PTH effect on DCT

A

Stimulates Ca/Na Xchange on basolateral surface increasing Ca resorption

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47
Q

Thiazide mechanism

A

Blocks Na/Cl apical cotransporter

–>indirectly blocks Na/Ca2+ exchanger

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48
Q

Mechanism of amiloride/triamterene

A

Blocks ENaC channel in principal cell of CT

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49
Q

[Tubular Fluid]/[Plasma] ratio

A

If >1, solute is reabsorbed less quickly than water

If <1, solute reabsorbed more quickly than water

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50
Q

very high TF/P

A

PAH/creatinine/inulin

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51
Q

moderate TF/P

A

urea/Cl

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52
Q

TF/P=1

A

K/Na

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53
Q

TF/P <1

A

phosphorus

bicarb

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54
Q

TF/P «1

A

amino acids and glucose (virtually completely reabsorbed

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55
Q

Tx: hypovolemic hyponatremia

A

NS

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56
Q

tx: hypervolemic hyponatremia

A

Salt and fluid restriction, furosemide

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57
Q

Euvolemic hyponatremia

A

free water restriction (NOT hypertonic saline–otherwise will fluid overload them)

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58
Q

SIADH hyponatremia

A

do NOT give normal saline! will excrete sodium and retain water. Give convaptan and water restrict

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59
Q

when should you give hypertonic saline?

A

hyponatremia with NEURO deficits or seizures

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60
Q

Six effects of angiotensin II

A
  1. Vascular smooth muscle
  2. constricts efferent arteriole
  3. aldosterone
  4. ADH
  5. Increased prox tubule Na/H
  6. Stimulates hypothalamus
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61
Q

ADH regulates

A

osmolarity (except in extreme low blood volume)

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62
Q

Aldo regulates

A

blood volume

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63
Q

How do beta blockers decrease BP?

A

inhibiting B1 receptors on the JGA

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64
Q

How much K is reabsorbed along the nephron?

A

65% PCT
30% ascending L of H
5-100% at DCT

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65
Q

How does ANP work?

A

Increases Na filtration and GFR at PCT with no compensatory Na resorption distally.
–>Na and H2O loss

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66
Q

PTH effect on kidney

A

Increased Ca resorption (DCT)
Decreased PO4 resorption (PCT)
Increased activation of vitamin D

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67
Q

Causee of hyperkalemia

A 
digitalis
hyperosmolarity
insulin deficiency
cell lysis
acidosis
Beta adrenergic antagonist
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68
Q

Hyponatremia Sx

A

nausea, malaise

stupor coma

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69
Q

hypernatremia sx

A

irritability

stupor coma

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70
Q

hypokalemia sx

A

arrhythmias, muscle weakness

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71
Q

-U wave on ECG, flattened T waves

A

hypokalemia

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72
Q

hypocalcemia sx

A

tetany and seizures

–decreases threshold potential

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73
Q

Hypomagnesia

A

tetany and arrhythmias

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74
Q

hypermagnesia

A 
cardiac arrest
hypocalcemia
decreased DTRs
bradycardia
hypotension
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75
Q

hypophosphatemia

A

osteomalacia

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76
Q

Hyperphosphatemia

A

renal stones
metastatic calcifications
hypocalcemia

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77
Q

How to tell if there is a mixed disorder (acid base)?

A

pCO2 and HCO3 move in opposite directions
OR
pCO2 predicted is very different

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78
Q

predicted pCO2=

A

(1.5 HCO3 + 8) +/-2

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79
Q

Henderson-Hasselbach

A

pH=6.1+log [HCO3]/(0.03*pCO2)

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80
Q

When do you check anion gap

A

metabolic acidosis present

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81
Q

Eq for anion gap

A

Na-Cl-HCO3

–Over 12 is abnormal

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82
Q

Increase anion gap metabolic acidosis

A 
Methanol
Uremia
Diabetic ketoacidosis
Propylene glycol
Iron/INH
Lactic acidosis
Ethylene glycol
Salicylic acid
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83
Q

Causes of normal anion gap acidosis

A 
Hyperalimentation
Addison's disease
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
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84
Q

Causes of primary metabolic alkalosis

A

loop diuretics
vomiting
antacid use
hyperaldosteronism

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85
Q

Type 1 RTA

A

CT cannot excrete H+

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86
Q

Type 2 RTA

A

Cannot resorb bicarb

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87
Q

Type 4 RTA

A

lack of aldosterone effect

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88
Q

RTA: pt with urine pH > 5.5 and is hypokalemic

A

Type 1

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89
Q

RTA: Pt has a urine pH < 5.5 and is hypokalemic

A

Type 2 RTA

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90
Q

RTA: hyperkalemic patient with low urine pH and low BP

A

Type 4 RTA

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91
Q

Increased urine pH puts you at risk for

A

calcium phosphate stones

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92
Q

Type 2 RTA associated with

A

Fanconi’s syndrome

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93
Q

WBC caste:

A

tubulointerstitial inflammation
acute pyelonephritis
transplant rejection

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94
Q

fatty casts or oval fat bodies

A

nephrotic syndrome

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95
Q

granular muddy brown casts

A

acute tubular necrosis

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96
Q

Waxy casts

A

advanced renal disease

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97
Q

Hyaline casts

A

normal

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98
Q

Nephrotic syndromes

A 
Minimal change disease
Membranous nephropathy
Focal segmental glomerulosclerosis
Amyloidosis
Diabetic glomerulonephropathy
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99
Q

Nephritic syndromes

A

Acute poststreptococcal GN
Rapidly progressive GN
Berger’s IgA GN
Alport

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100
Q

Combined Nephritic and Nephrotic syndromes

A

Diffuse proliferative GN

Membranous GN

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101
Q

Sx of nephrotic syndrome

A

proteinuria
hyperlipidemia
fatty casts
edema

102
Q

Why are pts with nephrotic syndrome at risk for thromboembolism and infection?

A

AT III is lost in urine

Loss of IgG

103
Q

Most common cause of nephrotic syndrome in adults

104
Q

LM: segmental sclerosis and hylinosis
EM: effacement of foot proceses

105
Q

LM: GBM thickening
EM: spike and dome with subepithelial deposits
IF: granular

A

membranous

106
Q

causes of FSGS

A

HIV, kidney disease, heroin, obesity, interferon

107
Q

causes of membranous

A

SLE< drugs, infection

108
Q

LM: normal
EM: foot process effacement

A

minimal change

109
Q

Tx of minimal change

A

corticosteroids

110
Q

cause of minimal change

A

loss of polyanion in GBM causing ONLY albumin loss

111
Q

LM: congo red stain with apple-green birefirencence

A

amyloidosis.

assoc’d with multiple myeloma, TB, RA

112
Q

Subendothelial deposits with tram track appearance

IF: granular

A

type I MPGN

113
Q

LM: Intramembranous dense deposits

114
Q

Type I MPGN associated with

115
Q

Type II MPGN associated with

A

C3 nephritic factor

116
Q

nephritic sx:

A

azotemia
oliguria
hypertension
proteinuria <3.5 g/day

117
Q

LM: lumpy bumpy glomeruli
EM: subepithelial immune complexes
IF: granular C3, IgG, IgM

A

acute post strep GN. occurs a few weeks after infection

118
Q

LM: crescent shape made of fibrin and C3b proteins

A

rapidly progressive GN

119
Q

causes of rapidly progressive GN

A
  1. goodpasture’s syndrome
  2. Wegener’s granulomatosis
  3. Microscopic polyangiitis
120
Q

LM: wire looping of capillaries
EM: subendothelial IgG with C3
IF: granular

A

Diffuse proliferative glomerulonephritis

121
Q

LM: mesangial proliferation
EM: mesangial IC deposits
IF: IgA deposits in mesangium

A

Berger’s disease. occurs a few days after infection

122
Q

Split basement membrane with GN, deafness, and eye problems

A

Alport syndrome

123
Q

What’s mutate in alport syndrome?

A

type IV collagen.

124
Q

alport inheritance

125
Q

Which kidney stones can you NOT see on an Xray?

A

Uric acid stones

126
Q

octahedron kidney stones

A

calcium oxalate

127
Q

which stones precipitate at a high pH?

A

struvite

calcium phosphate

128
Q

Most common kidney stone presentation

A

calcium oxalate stone in a pt with hypercalciuria and normalcalcemia

129
Q

Treatment for calcium stones

A

thiazides and citrate

130
Q

Causes of oxalate stones

A

ethylene glycol and vitamin C overdose

131
Q

staghorn calculi

A

struvite stones (ammonium magnesium phosphate)

132
Q

Tx for calcium stones

A

thiazides and citrate

133
Q

Cause of struvite stones

A

urease positive bugs:

  1. proteus
  2. staph
  3. klebsiella
134
Q

hexagonal crystals

A

cysteinuria

135
Q

coffin lid stones

136
Q

rhombus red brown stones

137
Q

renal cell carcinoma histology

A

clear limid filled cells

138
Q

RCC associated with a gene deletion on

A

chromosome 3

139
Q

RCC produces

A

EPO
ACTH
PTHrP

140
Q

PPresentation of RCC

A

hematuria
flank mass
polycythemia

141
Q

Tx: RCC

A

Resection. Resistant to conventional chemo and radiation

142
Q

WWilm’s tumor (nephroblastoma) histology

A

embryonic glomerular structures. Child 2-4 has flank mass and hematuria

143
Q

Wilm’s tumor deltion

A

WT1 tumor suppressor on chromosome 11

144
Q

WAGR complex

A

wilm’s
aniridia
genitourinary malformation
mental retardation

145
Q

biopsy of kidney: papillary growth lined by transitional epithelium with mild nuclear atypia

A

transitional cell carcinoma

146
Q

Transitional cell carcinoma associated with

A 
PeeSAC
phenacetin
Smoking
aniline dyes
cyclophosphamide
147
Q

ppainless hematuria suggests

A

bladderr canceer

148
Q

Where can transitional cell carcinoma occur?

A

calyces, pelvis, ureters, bladder

149
Q

acute pyelonephritis affects which part of kidneys?

A

Cortex. glomeruli and vessels are spared

150
Q

Cause of chronic pyelonephritis

A

vesicoureteral reflux or chronic kidney stones. Normal person shouldn’t get recurrent UTIs–>chronic pyelonephritis

151
Q

WWhich parts affected in chronic pyelonephritis?

A

Corticomedullary scarring with blunted calyces. Tubules have eosinophilic casts

152
Q

HIstology of chronic pyelonephritis

A

Lymphocytic invasion with fibrosis

153
Q

presentation of drug induced interstitial nephritis

A

eosinophilic pyuria

azotemia

154
Q

How long after drug will drug TIN happenn?

A

After 1-2 weeks..

Can be months with NSAIDs

155
Q

Which drugs cause TIN (allergic reaction to drug)

A

penicillin
diuretics
sulfonamides
rifampin

156
Q

Diffuse cortical necrosis caused by

A

Vasospasm and DIC. Associated with obstetric catastrophes and septic shock

157
Q

maintenance phase of acute tubular necrosis

A

oliguric for 1-3 weeks. Risk of hyperkalemia

158
Q

Recovery phase of acute tubular necrosis

A

polyuric. Risk of hypokalemiia

159
Q

Causes of toxic ATN

A 
Aminoglycosides
heavy metals
myglobinuria
ethylene glycol-->oxalate crystals
radiocontrast dye
urate
160
Q

Renal papillary necrosis caused by

A

diabetes
acute pyelonephritis
chronic phenacetin (acetaminophen)
sickle cell

161
Q

Difference in handling of BUN vs creatinine

A

BUN is reabsorbed

Creatinine is NOT reabsorbed

162
Q

Acute renal failure: prerenal azotemia

A

BUN: Cr is increased >20

-urea retained by kidney to conserve volume

163
Q

Intrinnsic renal failure

A

BUN: Cr ratio decreased <15

  • caused by ATN/ischemia/toxins/crescentic GN
  • granular casts
  • Tubules filled with debris
  • decreased BUN reabsorption
164
Q

PPostrenal azotemia

A

BUN: Cr >15

-Caused by outflow obstruction (bilateral)

165
Q

Urine osm: >500

Urine Na < 1%

166
Q

Urine osm: 40

FeNa >2%

A

Intrinsic or post-renal. Differentiate these by looking at the BUN: Cr ratio

167
Q

Consequences of renal failure

A 
Fluid/sodium retention (CHF)
hyperkalemia
metabolic acidosis
anemia
increased triglycerides
168
Q

Side effect of increased BUN and Cr

A 
Nausea
asterixis
pericarditis
encephalopathy
platelet dysfunction
169
Q

Renal osteodystrophy

A

Failure of vitamin D hydroxylation
hypocalcemia
hyperphosphatemiia
–>2ndary hyper PTH

170
Q

WWHy does hyperphosphatemia worsen renal osteodystrophy?

A

Tissue calcifications occur within tissues–>calcium phosphate instead of being excreted

171
Q

Why do pts with ADPKD get hypertension?

A

Increased renin production

172
Q

ADPKD associated with

A

berry aneurysms
mitral valve prolapse
benign hepatic cysts

173
Q

AARPKD

A

presents in infant, often as potter’s syndrome

174
Q

AARPKD associated with

A

congenital hepatic fibrosis. After birth, will have HTN, portal HTN, progressive renal insufficiency

175
Q

Medullary cystic disease

A

tubulointerstitial fibrosis and renal insufficiency–>cannot concentrate urine.

Inherited with shrunken kidneys seen on ultrasound

176
Q

where does mannitol affect the nephron?

A

The thin descending limb

177
Q

where does acetazolamide work its effect?

A

Proximal tubule

178
Q

mmannitol indications

A

Drug overdose

elevated ICP

179
Q

Mannitol toxicity

A

pulmonary edema

180
Q

when is mannitol contraindicated

A

CHF and anuria

181
Q

iindications acetazolamide

A

urinary alkalization
altitude sickness
glaucoma
metabolic alkalosis

182
Q

acetazolamide toxicity

A

metabolic acidosis
NH3 tox
sulfa allergy

183
Q

calcium wasting diuretic

A

loop diuretics

184
Q

furosemide indications

A

CHF, cirrhosis, nephrotic syndrome, pulmonary edema (too much fluid)

hypertension, hypercalcemia

185
Q

Toxicity of loops

A 
ototoxicity
hypokalemia
dehydration
allergy (sulfa)
nephritis
Gout
186
Q

Ethacrynic acid

A

Non sulfonamide loop diuretic. Virtually the same, can also cause gout

187
Q

indications for hCTZ

A

HTN CHF
hypercalciuria
nephrogenic diabetes insipidus

188
Q

Name the K sparing diuretics

A

Spironolactone
Triamterene
Amiloride

189
Q

Mehcanism: spironolactone and eplerenone

A

Competitive aldosterone antagonists.

190
Q

mmechanism triamterene and amiloride

A

Block ENaC at cortical collecting duct

191
Q

IIndications for spironolactone

A

hyperaldosteronism
K depletion
CHF

192
Q

side effects of spironolactone

A

Hyperkalemia

Antiandrogenic effects–man boobs

193
Q

WWhich diuretics cause acidemia?

A

carbonic anhydrase inhibitors–decrease HCO3 reabsorption

aldosterone–blocks K/H secretion. Also, hyperkalemia increases H leak from cells

194
Q

Which diuretics cause alkalemia?

A

loop and thiazide diuretics

  • -Contractiion alkalosis
  • -hypokalemia worsens alkalosis
195
Q

Urine calcium increases with

196
Q

Why are ARBs better than ACE-Is?

A

they don’t increase bradykinin

–>no cough or angioedema. ACE is still able to break down bradykinin

197
Q

What do ACEI do to GFR?

A

Decrease GFR, b/c efferent arterioles are opened

198
Q

Why is ACE good for CHF?

A

prevents remodeling

199
Q

ACE-I toxicity

A 
Cough
angioedema
Teratogen
decrease GFR
Hyperkalemia
hypotension
200
Q

When are ACE inhibitors contraindicated?

A

bilateral renal artery stenosis

201
Q

dysplastic kidney–how is it inherited?

A

Not inherited. COngenital malformation of renal parenchyma characterized by cysts and abnormal tissue, especially CARTILAGE. NOT BILATERAL LIKE ADPKD

202
Q

baby with portal htn

203
Q

berry aneurysm

A

ADPKD. cysts in the liver, kidney, and brain.

204
Q

mitral valve prolapse

A

ADPKD association

205
Q

how is medullary cystic kidney disease inherited?

A

autosomal dominant with SHRUNKEN kidneys

206
Q

IF Fena is <1% this tells you

A

tubular function is intact=can resorb sodium. this happens in prerenal ATN

207
Q

why is BUN:cr <15 in intrarenal renal failure

A

epithelial cells are not working, cannot resorb BUN, so it is excreted through the kidneys

208
Q

Why is BUN:Cr>20 in pre-renal failure?

A

Kidneys reabsorb as much fluid as possible and BUN follows

209
Q

Why is BUN:Cr>15 in post-renal failure?

A

High pressure in ureters “pushes” BUN and fluid back into the body from tubular fluid

210
Q

If pre-renal failure doesn’t resolve…

A

becomes ischemic acute tubular necrosis. Prox tubule and medullary thick ascending limb are susceptible

211
Q

What are consequences of ATN?

A

hyperkalemia with metabolic acidosis. Can’t excrete potassium or organic anions (lactic acid)

212
Q

hyperlipidemia seen in

A

nephrotic syndrome

213
Q

minimal change associated with

A

hodgkin’s lymphoma

214
Q

most common cause of nephrotic syndrome in hispanics and A-As

215
Q

FSGS associated with

A

HIV
heroin
SCD

216
Q

Minimal change and FSGS immunofluorexcence

A

None. Also poor response to tx/steroids. will progress to renal failure

217
Q

Pt with lupus gets nephrotic syndrome

A

membranous nephropathy

218
Q

Membranous nephropathy also associated with

219
Q

nephritic syndrome in lupus pt

A

DIffuse proliferative GN

220
Q

granular immunofluorescence

A

immune complex deposition

  • membranous
  • membranoproliferative
221
Q

type I membranoproliferative

A

subendothelial
HBV/HCV
more likely to have tram track

222
Q

what determines if GAS can cause nephritic syndrome?

A

presence of M proteins

223
Q

In adults with post-strep GN

A

more likely to present to crescent rapidly progressive GN

224
Q

lupus patient with rapidly progressive glomerulonephritis

A

diffuse proliferative GN

225
Q

Negative IF rapidly progressive nephritis

A

wegener, churg-strauss,

226
Q

pt with rapidly progressive GN, hemoptysis, hematuria, and sinus infections

A

Perform cANCA–could be wegeners not goodpasteur’s (classic)

227
Q

most common cause of nephritis world wide

A

Berger’s igA. Usually after mucosal infection, episodic.

228
Q

churg strauss features not present in microscopic polyangiitis

A

Asthma
granulomatous inflammation
eosinophilia

229
Q

tests for UTI

A

leukocyte esterase and nitrites
>10 WBC/hpf
culture: >100K CFU

230
Q

sterile pyuria

A

chlamydia and n. gonorrhea

231
Q

Most common pathogens for pyelonephritis

A

E. Coli
Klebsiella
Enterococcus

232
Q

“thyroidization” of kidney

A

Chronic pyelonephritis

233
Q

problem with staghorn calculi

A

can serve as a nidus for additional UTIs

234
Q

what produces EPO

A

renal peritubular interstitial cells

235
Q

why are crohn’s pts more likely to make calcium oxalate stones?

A

Not able to absorb calcium necessary to bind oxalate

236
Q

shrunken kidneys with cysts

A

Dialysis patients. Pts at increased risk for RCC

237
Q

Triad of RCC

A

hematuria
palapable mass
flank pain

238
Q

Cause of RCC

A

loss of VHL

  • increased IGF-1
  • Increased HIF=VEGF PDGF
239
Q

wilms tumor cell

240
Q

beckwith-Wiedemann

A

wilms tumor
neonatal hypoglycemia
muscular hemihypertrophy
organomegaly (tongue)

241
Q

Serum lab levels of calcium, phoshorus, and PTH in chronic kidney disease

A
  1. Phosphate retention
  2. Low calcium from low vitamin D
  3. Increased PTH
242
Q

loop diuretics act on

A

thick ascending loop of henle. Decrease medullary concentration gradient

243
Q

osmotic diuretics act on

A

thin descending loop

244
Q

when do you see states of hypercalcemia and hypercalciuria?

A

Hyper PTH and sarcoidosis

245
Q

Situations with hyperoxaluria

A

excesive intake

low calcium diets (less calcium in gut to bind oxalate for excretion)

246
Q

VHL deletion

A

chromosome 3P

247
Q

Upper part of ureter is supplied by

A

The renal artery

248
Q

Explain what happens with hypoaldosteronism to Na, K, HCO3 and Cl

A

Low Na
High K
acidosis=Low bicarb (H+ATP pump)
High chloride to balance out HCO3-

249
Q

Thiazide tox

A

Hyperuricemia
Hypercalcemia
Hyperglycemia
Hyperlipidemia

Hypokalemia and hypotension

250
Q

how to treat post GN glomerulonephritis

A

loop diuretics and vasodilators.

–Kids recover well. Adults do not

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