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1
Q

what is the most common tumor stage for prostate cancer? why?

A
  • 1c, it’s not palpable but patients come in because of elevated psa
2
Q

what is dilution anemia

what condition can you see it with?

A
  • increased rbcs, but there is so much increased blood volume that it seems like you have anemia
  • pregnancy
3
Q

what is the different between hypersthenuria, hyposthenuria, and isosthenuria?

A

hyper- urine has specific gravity >1.010

hypo- urine has specific gravity <1.010

iso- urine has specific gravity=1

4
Q

for type 1 (distal) renal tubular acidosis:

what can cause it?

at steady state, what is the urine pH, serum K level?

if you administer HCO3, what happens to urine pH and serum K level

A
  • decreased secretion of H into urine at distal tubule –> defect H-ATPase, defective CL-HCO3 exchanger
  • urine pH >5.5, K value can be anything
  • urine pH >5.5, k value can be anything

URINE PH ALWAYS >5.5

5
Q

what electrolyte imbalances/lab values can be observed in rhabdomyolysis?

A
  • hypocalcemia
  • SUPER HIGH CPK >20000
  • hyperphosphatemia
  • hyperkalemia
  • high creatinine
  • high uric acid

CCCUPP

6
Q

if a patient has hypovolemic hyponatremia, when should you give normal saline vs hypertonic saline

A
  • normal saline usually

- hypertonic saline if patient is symptomatic or has Na<120

7
Q

what is the normal concentration of HCO3 in plasma? what is the pK of HCO3; what is normal PCO2 of blood? What is the normal concentration of H2CO3?

A
  • 24 mM
  • 6.1
  • 40 mmHg
  • [H2CO3]= [CO2] = 40*.03= 1.2
8
Q

what enzyme converts testosterone to dht?

what drug can block this?

A

Type II 5 alpha reductase

finasteride

9
Q

what type of retinopathy finding in hypertension is optic disc bulging due increased intracranial pressure

is it a hypertensive emergency

A

papilledema

YES

10
Q

what demographic is usually affected in renal carcinoma?

A
  • elderly men who smoke
11
Q

what kind of acid base disorder is chronic renal failure?

A

metabolic acidosis (loss of nephron means less H excreted)

12
Q

name causes of hypomagnesemia

how does it present?

how do you treat?

A
  • cisplatinum,aminoglycosides,ppi, diuretics, starvation, etoh, refeeding syndrome, laxatives, malabsorption, hypercalcemia, barter’s syndrome
  • like hypokalemia and hypocalcemia (tetany, muscle spasms, hyperreflexia), prolonged qt interval, arrhythmias, ataxia, vertigo, anorexia, nausea, paralytic ileus
  • oral and iv repletion, stop medication
13
Q

what is the formula for net reabsorption or secretion?

A

filtered load- excretion rate

if f>e, means net reabsorption
if f

14
Q

what type of receptor is abundant in the bladder neck and prostate? what specific subtype is dominant in the prostate

A

alpha adrenergic

alpha 1a

15
Q

how does grapefruit juice affect drug levels

A
  • inhibits cyp3a4 which is responsible for drug metabolism in the liver and absorption in the gi tract
  • this can cause decreased absorption in the gi tract, and increased levels of drug in blood
16
Q

which zone of the prostate does bph affect?

what about prostate cancer?

A
  • transitional zone (also called adenoma)

- peripheral zone (also called capsule) (can also affect transitional and central)

17
Q

what condition do alpha blockers treat?

alpha blockers mnemonic

A
  • bph
A TaD underSTAFFed
Alfusozin
Terazosin
Doxazosin
Tamsulosin
silodosin

AFF= alpha blocker

18
Q

what are two effects of the sympathetic nervous system in response to decrease Na content, decrease EABV, and decrease Pa

what hpappens what there is increased na content, eabv, and Pa

A
  • constriction of afferent arterioles and increase of Na reabsorption in the proximal tubules
  • reverse happens, sympathetics is inhibited
19
Q

what is an example of hyposmotic volume expansion?

what is gained?

A
  • increased water intake or SIADH

H20

20
Q

how does increased urine flow rate affect K secretion?

what medication can cause this?

A
  • increased flow rate dilutes K in the tubule –> increased driving force for secretion
  • loop and thiazide diuretics
21
Q

what are two scenarios in which you shouldn’t use alpha blockers?

A

congestive heart failure and PDE5 inhibitor use

22
Q

if you have asymptomatic bacteruria during pregnancy, what should you treat it with and for how long?

A
  • sulfonamides, nitrofurantoin, or fosfomycin for 3 days
23
Q

what is the difference between osmolarity and osmolality

A
  • both measure total solute concentration
osmolarity = mOsmoles/L
osmolality= mOsmoles/kg of H2O
24
Q

what condition is associated with a tram tracks appearance

A

membranoproliferative glomerulonephritis

25
Q

what is a side effect of nonselective alpha blockers?

name three examples of nonselective alpha blockers

A
  • orthostatic hypotension, so dizziness, fatigue

terazosin, doxazosin, alfuzosin

26
Q

if a patient is significantly hyponatremic and you need to give hypertonic saline, what rate should you administer it at?

A

rate of sodium rise should be no more than 1 mEq/L/hr

27
Q

what stimulates angiotension II secretion

what inhibits it?

A
  • increased renin

- ace inhibitors

28
Q

when does autosomal dominant polycystic kidney disease present vs autosomal recessive?

A
  • adulthood vs. present at birth
29
Q

where is the only place in the nephron that phosphate is reabsorbed?
What can prevent its reabsorption?

how much is left in the urine?

A
  • proximal tubule (early 70% and late 15%)
  • PTH
  • 15%
30
Q

describe the three places where K secretion/reabsorption happens in the nephron; state whether it is secreted or reabsorbed.

A
  • proximal convoluted tubule- reabsorbed (follows Na+)
  • thick ascending limb of loop of henle- reabsorption via Na-K-2Cl pump (a little K leaks back)
  • distal convoluted tubule/collecting duct- intercalated cells reabsorb sometimes) and principal cells (variable secretion)
31
Q

what are the three criteria for orthostatic hypotension

A

decrease in systolic by 15 OR

decrease in diastolic by 10
OR

increased in Hr by 15

32
Q

strong acids have ____ (high or low) equilibrium constants and _____ pK

A
  • high equilibrium constant, low pK
33
Q

for wilms tumor:

what gene is most commonly affected

describe the pathophysiology

what demographic is commonly affected

what three conditions is it associated with?

A
  • WT1 on chromosome 11
  • Wt1 is a tumor supressor gene, that is necessary for renal development, mutation causes abnormal primitive neprhogenic rests to form
  • children
  • WAGR syndrome (wilms, aniridia, genital abnormalities, mental retardation), denys- drash (gonadal dysgenesis, wilms, progressive renal disease, beckwith widemann syndrome (organomegaly, hemi hypertorphy, macroglossia, wilms tumor)
34
Q

body ____ content is the major determinant of ECF volume.

body ____ content is the major determinant of body fluid oxmolarity

A
  • Na+

- water

35
Q

if a urinalysis has a positive dipstick for blood, but no rbcs are present, what condition is most likely present?

what is causing the positive dipstick?

what is a classic presentation?

how do you treat?

A
  • rhabdomyolysis
  • myoglobin
  • someone on statins or someone that hella exercised
  • hydrate until euvolemic
36
Q

what are the front line anti-hypertensive drugs? (mnemonic)

A
CAATs are HYPER
Calcium channel blockers
ACE inhibitors
ARBs
Thiazide diuretics
37
Q

for type 2 (proximal) renal tubular acidosis:

what can cause it?

at steady state, what is the urine pH, serum K level?

if you administer HCO3, what happens to urine pH and serum K level

A
  • defect in reabsorption of HCO3 in proximal tubule –> acetozolomide, topiramate, hereditary defect in carbonic anhydrase, fanconi syndrome
  • steady stage: urine ph <5.5, hypokalemic
  • urine ph>5.5, hypokalemia worsens
38
Q

in responsee to _____, ANP is released by the ____ and BNP is released by the _____

A
  • stretch (atrial pressure)/increased blood (ECF) volume
  • atria
  • ventricles
39
Q

what does a sieving coefficient of 1 mean?

what has a sieving coefficient of 1?

A
  • it is freely filtered across the glomerular capillary border

inulin

40
Q

what is a unique side effect spironolactone that is different than other k sparing diuretics and other diuretics

how does spironolactone differ from other k sparing diuretics?

A

gynecomastia

  • spironolactone blocks mineralocorticoid receptor, whereas k sparing diuretics block Na channel in principal cells
41
Q

which would have elevated renin levels: primary hyperaldosteronism or renal artery stenosis?

A

renal artery stenosis

42
Q

in the steady state, Na+ input is matched by

A

Na+ excretion by the kidneys + extrarenal sources (GI, sweat, usually negligible)

43
Q

how do you treat hyperphosphatemia

A
  • phosphate binders
  • saline
    decrease intake
    dialysis if renal failure
44
Q

where is fgf23 made? by what?

what is its main functions? how does it accomplish them

A
  • made in bone by osteocytes
  • prevent supersaturation of phos and Ca in the blood and prevent loss of Ca and phos from bone

increase phosphaturia
inhibit 1 alpha hydroxylase –> decrease calcitriol
inhibit pth synthesis –> decrease pth

45
Q

what causes type b lactic acidosis?

A
  • ethanol, diabetes, lymphoma/malignancy, salicylates
46
Q

myelomas and uric acid can accumulate where in the kidney?

A

tubules! (can form casts)

47
Q

does prostate size increase or decrease with age?

does incidence of bph increase or decrease with age?

A

both increase with age

48
Q

what stage does prostate cancer become palpable?

A

T2

49
Q

the RAA system detects changes in blood volume on the ____ (arterial/venous) side

stretch receptors detects changes in blood volume on the ____ (arterial/venous) side

A
  • arterial

- venous

50
Q

what are intradialytic complications (name at least 5)? which one is most common?

name side effects of dialysis?

A
  • HYPOTENSION (MOST COMMON)
  • hypertension
  • bleeding
  • air embolism
  • electrolyte imbalances
  • muscle cramps
  • anaphylactoid reactions
  • dialysis dysequilibrium (brain makes osmoles during uremia, if you remove solute from plasma will cause fluid to rush into the cells –> swelling)
  • insomnia, fatigue
  • anorexia
  • restless leg syndrome
  • cramps
51
Q

prerenal azotemia, if undetected, can progress to _____

A

acute tubular necrosis

52
Q

why can you get itching in chronic kidney disease?

A
  • due to hyperparathyroidism of chronic kidney disease, calcium phosphate complexes deposit in the skin and cause itching
53
Q

what is the risk for end stage renal disease for kidney donors?

who is at highest risk?

what other side effects can you get

A

less than 1%

black men (still less than 1%)

  • urinary protein, increase in bp, gestational htn or pre-eclampsia
54
Q

which two acid base disorder types would have increased HCO3 and increased CO2?

A
  • metabolic alkalosis

- respiratory acidosis

55
Q

can you get edema with acute kidney injury?

A

ABSOLUTELY (fluid retention because your kidney isn’t working)

56
Q

Is the fractional excretion of Na increased or decreased in prerenal azotemia?

what about renal disease?

A
  • very decreased (<1%)

- increased (>2%)

57
Q

are wbc casts diagnostic of acute pyelonephritis?

A

yes

58
Q

name 5 functions of calcitriol

A
increase CA absorption in GI
increase Ca reabsorption in the kidney
increase phosphate absorption in GI
downregulate PTH
increase bone mineralization
59
Q

for incipient diabetic nephropathy, what are the main pathologic features?

what would a glomerulus look like on h and e stain?

A
  • microalbuminuria (30-300 mg), htn, normal gfr
  • thickened glomerular and tubular basement membrane, mesangial proliferation, thickened mesangium, arteriolar hyalinosis
60
Q

what are the four edema states that can lead to signs of volume overload?

A
  • CHF, cirrhosis and nephrotic syndrome

renal failure

61
Q

name at least 5 scenarios of complicated urinary tract infection

A
  • kidney transplant
  • recurrent infections
  • resistant infections
  • anatomical defect
  • kidney stones
  • hospital acquired infection
  • diabetes
  • pregnancy
  • immunocompromised
  • fungal infection
62
Q

criteria for nephritic syndrome

A
Hematuria (RBC casts are diagnostic)
Proteinuria (<3.5 gm/day)
   -Salt &amp; water retention
-----Hypertension
------Weight gain
Edema (late finding)
Decreased GFR (frequent finding)
63
Q

what chromosome mutation is involved in invasive urothelial carcinoma

A

17p

64
Q

what new pathologic condition can thiazide diuretics cause as a side effect?

A
  • increased glucose –> diabetes
65
Q

what is the hormonal influence of the prostate?

what are other minor hormonal influences

A

dihydrotestosterone (DHT)

Androstendione
Prolactin
Estrogens

66
Q

what is the general cause of post renal obstruction?

what specific things can cause it?

what symptoms will they usually present with?

A
  • urinary tract obstruction (can be anywhere along it)
  • bph, tumors, kidney stones, endometriosis

severe oliguria, anuria, dribble, subrapubic tenderness

67
Q

name at least 3 risk factors that increase your chance of getting diabetic nephropathy (6 total)

A
  • type 1 dm (get diagnosed at a younger age)
  • smoking
  • oral contraceptives
  • poor blood pressure control
  • poor blood sugar control
  • low birth weight (activates catch up genes that promote weight gain –> obesity –> predisposed to diabetes)
68
Q

what are two urine values that are distorted in an edema state (excluding renal failure)

explain why each value is distorted

A
  • urine Na is low- due to decreased renal perfusion prssure –> increased renin –> increased angiotension II –> aldosterone –> increase na reabsorption –> decreased urine na
  • increased urine osmolality- due to either increased na reabsorption or decreased bp –> adh stimulation –> increased water reabsorption –> increased urine osmolality
69
Q

What percent (range and average) of of weight is total body water?

what two demographics tend to have the highest total body water

A

50- 70 (60)

males and infants (75%)

70
Q

define isolated systolic hypertension

are you at greater risk for cvd?

A

htn >140/<90

hell yeah!

71
Q

what is the formula for volume of a marker substance?

A
  • volume= amount given- amount lost (excretion)/ concentration
72
Q

thiazide diuretics _____ (increase/decrease) Na excretion and ______ (increase/decrease) Ca excretion

A
  • increase Na excretion (block reabsorption)

- decrease Ca excretion (increase reabsorption)

73
Q

what is the formula for the henderson hasselbach equation

A

pH= pK’ + log ( [A-]/[HA])

AHA! (a is on top of ha)

74
Q

if someone has chronic hypernatremia and is hypotensive, at what rate would you want administer normal saline?

why?

A
  • .5mEq/L/hour

in chronic hypernatremia, the brain shrinks and creates its own osmoles that take a while to clear, if you give saline too quickly, brain will swell and herniate

75
Q

define oliguria; what is the common etiology

define polyuria; what are the common etiologies?

A

<400 mL excreted/day –> renail failure

> 2000 mL excreted/day –> glycosuria, diabetes insidipidus, brain tumor, aneurysm, granuloma, psychogenic polydipsia

76
Q

Where is prorenin converted to renin?

what does renin do?

A

juxtoglomerular cells

converts angiotensinogen to angiotensin I

77
Q

when calculating the anion gap for a metabolic disorder, if your HCO3 is higher than expected, then what type of acid base disorder do you have in addition to a metabolic acidosis?

what about if your HCO3 is lower than expected?

A
  • metabolic alkalosis

- additional normal anion gap metabolic acidosis

78
Q

if a patient has frequent daytime urination, what do they have?

if a patient has excessive nighttime urination, what do they have?

A

pollakiuria

nocturia

79
Q

when there is no activated ADH, papillary and medullary interstitium osmolarity is significantly decreased. Give two reasons

A
  • decreased adh –> decreased Urea recycled into interstitium –> decreased osmolarity
  • decreased adh –> decreased reabsorption at Na-K-2Cl pump in the thick ascending limb –> decreased osmolarity (counter current multiplication is decreased)
80
Q

what type of hypertension is normal when in the doctor’s office but high when at home?

A

masked hypertension

81
Q

name 3 causes of hypokalemia and 5 causes of hyperkalemia

what is a pump present in all cells that plays a role in hypo and hyperkalemia?

A
  • hypokalemia: insulin, beta agonist, alkalosis
  • hyperkalemia: lack of insulin, beta antagonist, acidosis, exercise, cell lysis

H- K pump

82
Q

what part of the nephron is affected in toxic acute tubular necrosis?

what about ischemic acute tubular necrosis?

A
  • proximal tubule

- patchy, segmental areas along the tubules

83
Q

in familial hypocalcuric hypercalcemia, what is defective? what happens as a result

A
  • calcium sensing receptor

as a result, the body thinks it is hypocalcemic, and does not inhibit the Na-K-2Cl receptor

84
Q

does renal artery stenosis cause prerenal or intrarenal azotemia?

why?

A
  • prerenal azotemia

- kidney perceives decreased perfusion due to narrowed lumen

85
Q

is diabetic nephropathy a macrovascular or microvascular complication of diabetes?

what progressive urine finding is common? can it be detected on a urine dipstick?

which demographics are at increased risk?

A

microvascular

micro or macro albuminuria
micro cannot, but macro can

african americans, hispanics, and native americans

86
Q

what are some advantages to using creatinine as a marker of gfr?

what are some disadvantages?

A
  • cheap, endogenous, increases as gfr decreases
  • only increases after significant gfr decrease (can’t detect mild impairment), increased with use of cimetidine and trimethoprim, decreased in liver disease
87
Q

decreased levels of citrate in the urine increase risk for what?

A

calcium stones

88
Q

what is an example of hyperosmotic volume expansion?

what is gained?

A
  • increased NaCl intake

- NaCl

89
Q

if a patient has hypertension and edema, what condition should you think of?

A
  • hyperaldosteronism
90
Q

phenobarbital and aspirin are ____ (bases or acids), addition of bicarb would ____ (increase or decrease) renal clearance

A

acids

increase

91
Q

give two example of weak bases and weak acids in urine?

A
  • weak base: morphine and quinine

weak acid- PAh and salicyclic acid

92
Q

what is a staghorn stone?

A

a kidney stone that involves the renal pelvis and at least two caluces

93
Q

does lupus more commonly cause nephritic or nephrotic syndrome?

A

nephritic (rapidly progressive glomerulonephritis)

94
Q

what is free water clearance (CH20)

what is the formula?

A
  • the amount of free water that must be added to or substracted from urine to make urine isoosmotic with plasma
  • V- Cosm
V= urine flow rate
Cosm= UosmV/Posm
95
Q

name an example of an mtor inhibitor; what does it do?

side effects?

A
  • sirolimus: inhibits mtor, which is important for the cell cycle
  • nephrotoxicity (atn, proteinuria, tubulotoxicity)
  • impaired wound healing, dyslipidemia
  • pneumonitis
  • anemias and cytopenias
96
Q

where is a common place/direction that renal cell carcinoma likes to spread to?

A

renal vein/ivc

97
Q

describe the two main effects of ANP and BNP

A
  • dilation of afferent arterioles and constriction of efferent arterioles –> increased GFR –> increased Na excretion
  • inhibition of Na reabsorption at distal tubules and collecting ducts –> increased Na excretion –> decreased ECF volume and BP
98
Q

what drug is in 80% of transplant protocols?

how does it function?

A
  • corticosteroids!

- suppresses cytokines (esp IL2), inhibits dendritic cells, inhibits translocation to nucleus of nk-kfb

99
Q

what is a scenario in which you can have physiologic hydronephrosis?

explain why

which kidney is more dilated? why?

A
  • pregnancy
  • progesterone, prostacycline, and relaxin dilating smooth muscle of ureters

right kidney because uterus is dextrorotated

100
Q

what type of acid base disorder is diarrhea?

A

metabolic acidosis

101
Q

what is tertiary hyperparathyroidism in the context of chronic kidney disease

what is the treatment

what serious complication can occur as a result of treating this?how can you fix it

A
  • parathyroids are so stimulates that hyperplasia increases so much that autonomous adenoma occurs
  • parathyroidectomy
  • hungry bone syndrome: after pth stimulus is removed, ca and phos flood back into the bone, which can cause profound hypocalcemia and hypophosphatemia
  • give vit d and calcium
102
Q

what are the two main things that cause adh release?

what are three other causes

what can inhibit adh?

A

1% increase in plasma osmolarity, 10% decrease in blood volume (stronger effect)

  • pain, nausea, adh
  • alcohol
103
Q

what risk factors could cause papillary ischemic necrosis?

A

nsaids, sickle cell disease, diabetes, pyelonephritis

104
Q

where does prostate cancer metastasize to?

who should get ct screening for mets?

A
  • bone and obturator and para-aortic lymph nodes

- people with psa >20
- gleason score 8-10
- tumore stage T2C (palpable and bilateral
think 20/10=2)

105
Q

what are signs/symptoms of uremia?

A
  • uremic frost
  • asterixis (tremoring of hand while wrist is extended)
  • nausea
  • vomiting
  • small mental status changes
  • loss of appetite
106
Q

name at least 5 causes of respiratory alkalosis.

describe whether each of the following should be increased or decrease: pH, CO2, HCO3

describe the acute and chronic compensation

what is the treatment

A
  • anxiety
  • sepsis
  • fever
  • liver disease
  • pregnancy
  • pulmonary edema
  • heart failure
  • mitral valve disease
  • interstitial lung disease
  • mild pneumonia
  • mechanical ventilation
  • aspirin toxicity
  • altitude

pH= increased, CO2= decreased, HCO3= decreased

  • acute: mass action –> for every 1 decrease in PCO2, .2 decrease in HCO3
  • chronic: kidneys decrease reabsorption –> for every 1 decrease in PCO2, .4 decrease in HCO3
  • breathe into a paper bag, treat the underlying disorder
107
Q

what are the mutations for autosomal dominant and autosomal recessive polycystic kidney disease?

which chromosomes are affected

A

autosomal dominent- polycystin 1 (chromosome 16) and 2 (ca channel complex) (chromosome 4)

autosomal recessive- fibrocystin (function unknown) (chromosome 6)

108
Q

what can cause pseudohyerkalemia?

A

issues with drawing blood

  • ischemic blood draw
  • too many platelets or wbc’s in sample
  • cell lysis
109
Q

what are three places in the glomerulus where immune complexes can be deposited?

A
  • subepithelial (between podocytes or under them)
  • mesangial
  • subendothelial (under the basement membrane)
110
Q

invasive urothelial carcinoma is associated with what (name 3 things)

A

smoking

arylamines (dyes)

SCHISTOSOMA

111
Q

what happens to ECF volume and arterial pressure in volume contraction? what about volume expansion?

what extra symptom can you get in volume expansion

A
  • decrease ECF volume, decrease Pa

- increase ECF volume, increase OR decrease Pa, edema!

112
Q

what is the formula for renal plasma flow (true and effective)

A

true rpf= V * [U] pah/ ([RA]pah - [RV]pah)

effective rpf = V* [U]pah/Ppah

RA= renal artery
RV= renal vein
113
Q

dsecribe Tm and threshold in terms of glucose reabsorption

A

Tm is the point in which reabsorption is saturated and the rate stays constant

threshold is the point at which glucose first appears in the urine

114
Q

what is the preferred imaging for kidney stones?

A

spiral CT

115
Q

usually, effective arterial blood volume determines _____ and parallels _____

What is one situation in which it doesn’t parallel?

A
  • tissue perfusion
  • ECF volume
  • heart failure, ECF is increased, but EABV is not because the increase ECF volume is in the interstitium not the circulation (which leads to increases Na+ retention and edema)
116
Q

what can plasma osmolarity be approximated by

A

2 * [Na+]

117
Q

name 2 scenarios where Fractional excretion of Na (FeNa) is not reliable

A

chronic renal failure and diuretics

both are high

118
Q

Name two things renin is stimulated by?

name one thing renin is inhibited by?

A
  • increased sympathetic stimulation and decreased perfusion pressure
  • ANP
119
Q

for cystinuria:

what is the genetic inheritance?

what is the defect

what population can this commonly be seen in

what shaped crystals would you see? are they correlated with stones?

does it precipitate in alkaline or acidic urine?

A
  • autosomal recessive
  • defect in amino acid transport in renal tubule of cysteine, ornithine, lysine, arginine (COLA)
  • children
  • hexagonal, yes
  • acidic
120
Q

what does aliskiren do?

A

block renin

121
Q

what is the mechanism of action for minoxidil

what is something very important you must do when you prescribe minoxidil

A
  • binds to vascular smooth K channels –> decreased bp
  • minoxidil causes activation of sympathetic nervous system and RAAS so you MUST prescribe diuretic and beta blocker with it
122
Q

in what part of the nephron does Ca2+ and Mg2+ both get reabsorbed and what can prevent this?

where is another location where ca is reabsorbed? what can stimulate it?

A
  • thicc ascending limb of loop of henle

loop diuretics

early distal tubule, thiazide diuretics and pth

123
Q

what is an angiomyolipoma made of?

is it benign or malignant?

  • what demographic is it associated with
  • what condition is it associated with
A
  • blood vessels, smooth muscle, fat
  • benign (can be life threatening if it hemorrhages)
  • female
  • tuberus sclerosis
124
Q

where is ADH stored

A

posterior pituitary

125
Q

name the four stages of diabetic nephropathy

A
  • pre/latent –> incipient –> overt –> renal failure
126
Q

name 3 alpha antagonists

what is the mechanism of action

what are side effects?

A
  • doxazosin, serzosin, etc (can treat bph)
  • phenoxybenzamine (can treat pheochromocytoma)
  • phentolamine (nonselective)
  • decreases vasoconstriction
  • postural hypotension, reflex tachycardia
127
Q

what are two things that make a good buffer?

A
  • need to have a large concentration of it

- should have a pK that is + or - 1 of pH

128
Q

what are the two major determinants of whether a substance can cross the glomerular capillary border

A

molecular weight (anything under 5500 daltons can cross)

  • charge (barrier lined with negative charges, negatively charged molecules can’t get through)
129
Q

Androgen receptors with ____ (longer or shorter) repeats of _____ codon have increased androgen sensitivity

which demographic have shorter codons?

which demographic have longer codons?

A
  • shorter repeats
  • CAG (glutamine) codon
  • black
  • asian
130
Q

if a patient has edema, 99% of the time it is due to what/

A
  • increased na (whether ingestion or retention)
131
Q

what kind of acid base disorder does diabetic ketoacidosis cause?

A
  • metabolic acidosis (due to overproduction of fixed keto acids)
132
Q

do loop diuretics increase or decrease Ca excretion? explain why?

what is another ion that operates exactly like Ca in response to loop diuretics?

A

increased excretion
- loop diuretics block the Na-K-2Cl pump in the TALH, which decreases the positive luminal difference necessary for Ca to be reabsorption, so it is excreted

  • magnesium!!
133
Q

what is the most common genetic kidney disease ?

A

autosomal dominant polycystic kidney disease

134
Q

mnemonic for chromosome abnormalities in clear cell and papillary renal carcinoma

A

C3P- fo

  • c= clear
    3- chromosome 3
    p= papillary
    fo= four chromosomes (1,trisomy 7,16,17)
135
Q

when doing a crossmatch for kidney transplant, what is used?

A
  • recipient serum and donor’s lymphocytes + complement

- if preformed antibodies are present in the serum and bind to lymphocytes and cause >20% cell lysis, not a match

136
Q

where does titration of H+ by HPO42- happen in the nephron

A

late distal tubule/collecting ducts in the alpha intercalated cells

137
Q

what prostaglandins does cox 1/2 make? what are they responsible for ? what happens to them if you take nsaids

A
  • PGE2: decreases reabsorption of Na at TALH (nsaid would allow for increased reabsorption and less diuretic efficacy)
  • PGI2: vasodilator and releases renin (nsaids can cause hyporenin hypoaldosteronism aka type 4 renal tubular acidosis)
138
Q

what is a normal BUN:Cr ratio

name two scenarios where you can have an increased ratio

A

10-15:1

pre renal azotemia and high catabolic states (gi hemorrhage, infection)

139
Q

describe the driving force behind glomerulotublar balance?

what 2 scenarios can override it?

A
  • increase in oncotic pressure in peritubular capillary from water being filtered out of afferent arteriole drives water and Na into capillary, keeps Na reabsorption in proximal tubule at 67%
  • ecf volume expansion, more water in peritubular capillary, less oncotic pressure, less water and na reabsorbed –> more water and na reabsorbed
  • ecg volume contraction, less water in peritubular capillary, higher oncotic pressure, more water and na reabsorbed –> less water and na excreted
140
Q

Does aldosterone cause an increase or decrease in K secretion?

Give two reasons why?

A
  • increase
  • it increase ENaC, which increases the driving force for the Na-K pump to bring more K in –> increased intracellular K –> increased driving force for K secretion
  • it also increases the number of K channels for secretion
141
Q

what cystic kidney disease is commonly associated with nephrolithiasis?

A

medullary sponge kidney

142
Q

the _____ (lower/higher) the urine pH, the more H+ is secreted as NH4+

why?

A
  • lower
  • acidic pH provides an even larger gradient for NH3 to diffuse from the interstitium to the lumen of the tubule (use henderson hasselbach formula)
143
Q

what is a side effect that all antihypertensive drugs cause

A

impotence

144
Q

parathyroid hormone blocks reabsorption of what in which part of the nephron?

A
  • phosphate in the early proximal tubule
145
Q

when determining what the source of hypokalemia is, what measurement can be used?

A
  • urine K/g creatinine

if greater than 22, due to renal loss

146
Q

what are the four main effects of adh

A
  • acts on V2 receptor on principle cells in the collecting duct –> increased Gs and cAMP –> increased aquaporin 2 channels –> increased water reabsorption
  • acts on V1 receptor on blood vessels to increase tpr and Pa
  • works on Na K 2 Cl channel in thick ascending limb
  • increases urea reabsorbing in the inner medullary collecting ducts
147
Q

what is the threshold for starting drug therapy for hypertension? what are the two exceptions?

what is the goal bp?

A

> 130/80, UNLESS primary stroke (cvd risk <10%) or cvd risk <10%, then >140/90

<130/80

148
Q

if a patient has afib and hypertension what would be a good drug to consider to treat both?

A

ARBs

149
Q

mnemonic for causes of toxic acute tubular necrosis

A

CRAMming is so TOXIC for ME

Cisplatinum
Radiographic contrast
Aminoglycosides
Mannitol

Myoglobin (from rhabdomyolysis)
Ethylene glycol

150
Q

What condition is the gleason grading system used to describe?

describe the grading system

A
  • prostate carcinoma
  • you characterize the dominant histologic pattern 0-5 (0 well diff 5 poorly diff) and then do the same thing for the second dominant pattern and add them together, the higher the score the worse the prognosis (6 is decent, 10 v bad)
151
Q

for multicystic dysplastic kidney:

what is the cause?

what does the kidney look like grossly?

what is the prognosis?

A
  • error in embryonic differentiation (no genetic mutation)
  • shrunken, doesn’t resemble kidney shape, doesn’t have kidney structures
  • if unilateral, great prognosis because other kidney can compensate
152
Q

what specific part of a protein provides the most buffer capacity?

A

imidazole group of histidine (pK 6 but argued to be 6.4-7)

153
Q

rbc casts in urine is 100% specific for what??

what color is hematuria?

A
  • glomerulonephritis

- cola/tea colored (mickey mouse ears microscopically)

154
Q

what are the two types of invasive urothelial carcinoma precursors?

  • do they tend to be low grade or high grade
  • are they malignant?
  • what chromosome is affected
A
  • non invasive papilary carcinoma [in situ] (has papillary)
  • non invasive flat urothelial carcinoma [in situ] (hard to detect cuz flat)
  • can be either
  • no, but can become malignant if breaks through basement membrane (low grade less likely to become malignant)
  • chromosome 9
155
Q

what arteriole in the kidney can nsaids affect in prerenal azotemia?

A

afferent arteriole (inhibit prostaglandins, which inhibits arteriole’s ability to vasodilate)

156
Q

what is adynamic bone disease?

in what group of people is this common?

A
  • aggressive treatment of hyperparathyroidism with calcium and vitamin d can lead to normalization of pth values and hypercalcemia –> bone turnover decreases –> increases fractures, calciphylaxis, ca complex deposition in soft tissue and skin
  • dialysis patients
157
Q

for rapidly progressive glomerulonephritis:

what is the clinical presentation?

what would you see on histology?

what are the three types

what is the treatment?

A
  • RENAL FAILURE (elevated Cr), oliguria, hematuria, proteinuria
  • CRESCENTS (proliferation of partietal layer of bowman’s capsule)
  • anti gbm (goodpastures), immune-complex mediated, and pauci-immune (vasculitis!)
  • aggressive immunosuppression (cyclophosphamide) and steroids
158
Q

what buffer is responsible for excreting 60% of H+ in the urine

A

NH3/NH4+

159
Q

what is desmopressin used for in chronic kidney disease?

A
  • if a patient has uremia, that can cause platelet dysfunction; desmopressin increases von willebrand factor release from endothelial cells and improves platelet aggregation
160
Q

name physiologic pulmonary changes during pregnancy

A
  • increased tidal volume
  • increased minute ventilation
  • respiratory alkalosis
  • diaphragm pushed upward
161
Q

what is the main volatile acid in the body?

Name at least 3 non-volatile/fixed

A
  • CO2

sulfuric acid (methionine, cysteine)
phosphoric acid (phospholipids)
salicylic acid (aspirin)
beta hydroxybutyric acid and acetoacetic acid (ketoacids)
lactic acid
formic acid (methanol)
glycolic and oxalic acid (ethylene glycol)

162
Q

what causes av knicking

A
  • artierolar thickening which compresses on the vein, making it look paler
163
Q

match the following urine casts with the most representative condition:

  • muddy brown casts, wbc casts, rbc casts, fatty casts
  • acute interstitial nephritis, nephrotic syndrome, acute tubular necrosis, nephritic syndrome
A

acute tubular necrosis- muddy brown casts

acute interstitial nephritis- wbc casts

nephrotic syndrome- fatty casts

nephritic syndrome- rbc casts

164
Q

what is the cockroft gault formula for gfr/creatinine clearance?

A

Ccr= (140-age) X (Lean Weight in Kg)/(Scr X 72) [ *.85 if female]

165
Q

for goodpasture syndrome, what other organ can be involved besides the kidney? What happens?

what would immunofluorescence reveal
what would you see on EM?

A
  • lung
  • pulmonary hemorrhage (igg on basement membrane of alveolar capillary)
  • linear fluorescence of capillary loops
  • no deposits
166
Q

what is the urine anion gap charge for type 1 and type 4 RTA?

what is urine anion gap charge for type 2 RTA?

A
  • less negative than usual

- negative

167
Q

what is the formula for renal blood flow

A

renal blood flow= renal plasma flow/ (1-Hct)

hct= hematocrit (fraction of blood volume occupied by rbcs)

168
Q

if the measured serum osmolality and calculated serum osmolality do not = each other, what could be the cause

A
  • toxin ingestion of methanol or ethylene glycol –> increasing measured osmolarity
169
Q

What separates a simple cyst from a complex cyst?

A

complex cysts tend to have septations, calcifications, thickened walls, soft tissue components, enhanced contrast on ct, etc and a higher risk for malignancy

170
Q

which part of the nephron do loop diuretics work on?

which channel?

give an example

A
  • thick ascending limb of loop of henle
  • Na K 2 Cl
  • furosemide
171
Q

in what scenario can you get a kidney transplant?

do you need to have done dialysis to quality for transplant?

what are some contraindications?

name 3 conditions that are no longer contraindicated?

A
  • chronic kidney disease with gfr <20
  • nope!
  • liver cirrhosis, heart failure, dementia, drug use, etoh use
  • HIV, Hep C, Hep B
172
Q

kussmaul respirations are associated with what acid base disorder?

A

metabolic acidosis

slow, deep gasping breaths

173
Q

minimal change disease mnemonic

A

He SAID he would CHANGE his AWFUL T SHIRT after injecting STEROIDS into his FOOT

Said= nsaids
Change- minimal change disease
Awful- nephrOtic
Tshirt- t cell damage
Steroids- steroids treatment
Foot- reversible podocyte injury
174
Q

mnemonic for renal carcinoma paraneoplastic syndromes

A

HHHH

hyper calcuria (pthrp)
hypertension (renin)
high rbcs (polycythemia from epo)
hepatic dysfunciton (stauffer's syndrome)
175
Q

acute onset of flank pain, dysuria, fever, and opaque urine could be a sign of what?

A

acute pyelonephritis

176
Q

what is the formula for fraction of filtered water that is reabsorbed

A

1- 1/ (TF/P)inulin

TF= tubular fluid concentration of inulin
P= plasma concentration of inulin
177
Q

for overt diabetic nephropathy, what are the main pathologic features?

what would a glomerulus look like on h and e stain?

A
  • decreased gfr (cr might start to increase), macroalbuminuria/proteinuria, edema
  • kimmelstiel wilson nodules, glomerular/tubular sclerosis, interstitial fibrosis, hyalinized vessels (arteriosclerosis)
178
Q

name 2 antihypertensive drugs that block adrenergic neurons

how do they do it

what are the side effects for each

A
  • guanethedine: prevents NE release from adrenergic neurons (guane= gone, adrenergic neurons are GONE)
  • reserpine: prevents NE uptake into storage vesicles (reser= reserves, destroying NE reserves)
  • guanethedine: diarrhea, fluid retention
  • reserpine- sedation, depression, gastric acid secretion
179
Q

how does spironolactone affect K secretion?

A
  • it’s an aldosterone receptor antagonist, so it decreases K secretion
180
Q

when is your blood pressure usually the lowest?

A

at night (nocturnal dip)

181
Q

for autosomal recessive polycystic kidney disease

where are the cysts located? are they large or small?

how does it present?

A
  • located at a 90 degree angle to the cortical surface, v
    small (kidney has spongelike appearance)
  • usually presents at birth with serious complications; improper renal function in utero can lead to oligohydramnios–> potter sequence (flattened face, low set ears, pulmonary hypoplasia; can also have hepatic fibrosis and cysts and biliary proliferation
182
Q

name causes of hypermagnesemia

what are symptoms

how would you treat it?

A

iatrogenic- laxatives, enema, maalox, milk of magnesia, infusion for preeclampsia cerebral edema or severe asthma,

  • decreased reflexes, heart block , respiratory depression, paralysis, coma, hypocalcemia, hypotension bradycardia
  • calcium gluconate to stabilize membranes, saline to encourage excretion, ,dialysis if severe
183
Q

the kidneys recognize changes in Na+ by deteching changes in what?

A

ECF volume (Na determines it)

184
Q

what is the steady state body fluid osmolarity

A

290 mOsm/L

185
Q

for contrast induced nephropathy:

what causes it?

what happens as a result?

what should you avoid when treating?

A
  • contrast from ct imaging usually (mri contrasts are safe)
  • renal vasoconstriction –> medullary ischemia –> acute tubular injury
  • nsaids, volume depletion, and repeat studies (don’t repeat them to the same contrast!)
186
Q

where in the nephron do k sparing diuretics work?

name 3 k sparing diuretics

how does it work?

what is it indicated for?

side effects?

A
  • late distal convoluted tubule and collecting ducts (both principal and alpha intercalated cells)
  • spironolactone, triamterene, amiloride (the k STAys)
  • triamterene and amiloride inhibit na channels in principal cells, spironolactone competitively binds to aldosterone receptor and prevents translocation to nucleus
  • used with loop or thiazide diuretics to prevent K wasting, refractory edema
  • hyperkalemia, type IV RTA (metabolic acidosis), gynecomastia (spironolactone)
187
Q

which layer of a blood vessel does Ca lay down and calcify after being resorbed in chronic kidney disease

A

media

188
Q

what is an example of isoosmotic volume contraction?

what is lost?

A

diarrhea

NaCl and water

189
Q

if you have a catheter related or post- instrumentation bacteruria, what medication should you give and for how long?

A
  • fluoroquinolones for 7-10 days
190
Q

for type 4 renal tubular acidosis:

what can cause it?

at steady state, what is the urine pH, serum K level?

A
  • hyporenin- hypoaldosteronism –> decreases ammonia production
  • urine ph always <5.5, always hyperkalemic
191
Q

what are surgical complications during kidney transplant (specifically in regards to attaching the kidney)

A
  • artery thrombosis and stenosis
  • veinous thrombosis and stenosis
  • ureter leak and stenosis
  • lymphocele
192
Q

what are three things that affect effective arterial blood volume?

A
  • cardiac output, tpr, and intravascular volume (if any of these decrease, eabv decreases)
193
Q

what are the two soluble receptors released in preeclampsia and which factor do they correspond with

A
  • sFlt –> antagonist for VEGF

- sEng- soluble coreceptor for tgfb

194
Q

what is the lowest ph that can be tolerated in the urine?

A

4.4

195
Q

name causes of hypophosphatemia

A
  • decreased intake (starvation, etoh, malabsorption, vit d deficiency, phosphate binders)
  • redistribution (hungry bone syndrome, refeeding, uptake during blood sample)
  • renal wasting (fanconi syndrome, tenofovir, aminoglycosides, amphotericin b, cyclosporine, cisplatinum, diuretics, hypophosphatemic rickets)
  • Gi wasting aka DIARRHEA
196
Q

for membranous glomerulonephropathy:

what is the histology?

what can cause it?

what demographic is it common in

what is the treatment?

A
  • thick basement membrane with spikes between subepithelial immune complex deposition
  • granular deposits on immunofluorescence
  • primary: PLA2R antigen on podocytes
    secondary: SLE, RA, solid tumor, HEpatitis b, syphillis, penacillamine
  • white people!
  • steroids AND immunosuppressants
197
Q

weak acid diuretics are inhibited by what

give an example of these diuretics (3)

A
  • probenecid

- acetazolamide, loop diuretics, thiazide diuretics

198
Q

mnemonic for causes of Allergic/Acute Interstitial Nephritis

A
  • allergic interstitial nephritis = AINs
A= antibiotics/amoxicillin
I= infection
N= nsaids
s= sjogrens/SLE
199
Q

what is the normal pH of blood?

what range is it tightly regulated within?

what range is compatible with life

A
  • 7.4
  • 7.35-7.40
  • 6.8-8
200
Q

what is an example of hyperosmotic volume contraction?

what is lost?

A

diabetes insipidus or water deprivation (FEVER)

just water

201
Q

what are causes of hypokalemia

what is the treatment?

what other ion imbalance must you consider before treating?

A
  • vomit, diarrhea, alcohol, hyperaldosteronism, drug toxicity, hypokalemic periodic paralysis, diuretics, excess catecholamines,

10 mEq/hr for ever .1 decrease

  • must check for hypomagnesemia, can cause hypokalemia
202
Q

what are the 5 most likely bacterial causes of urinary tract infection, and are they gram + or -

A

KEEPS

  • klebsiella (-)
  • Enterococcus (+)
  • E. Coli (-)
  • Proteus mirabilis (-)
  • staph saprophyticus (+)
203
Q

what is a good medication to use if you have bph and erectile dysfunction

A

pde 5 inhibitor

204
Q

what genetic mutation significantly increases your risk for prostate cancer

A
  • BRCA 2
205
Q

symptoms of hypokalemia

A

muscle weakness/rhabdomyolysis

nausea vomitingg

respiratory failure (weak diaphragm)

  • increased NH3/4 in urine and increased HCO3 in blood
206
Q

what is the formula plasma osmolarity

A

2 [Na+] + glucose/18 + BUN/2.8

207
Q

name at least 6 causes of metabolic alkalosis (saline responsive and saline resistant.

what is the underlying problem with all types of metabolic alkalosis?

describe whether each of the following should be increased or decrease: pH, CO2, HCO3

describe the compensation

what is the treatment

A
  • saline responsive: vomit, Cl diarrhea, ng tube, villous adenoma, diuretics
  • saline resistant: primary hyperaldosteronism, adrenal adenoma, bilateral adrenal hyperplasia, cushings, licorice, post hypercapnic, renal artery stenosis
  • aldosterone secretion
  • pH= increased, CO2= increased, HCO3= increased
  • for every 1 increase in HCO3, CO2 increases by .6
  • saline if volume depleted, acetozolomide, aldosterone inhibition
208
Q

what are treatments for prostate cancer?

A
  • radiation therapy
  • cryoablation
  • da vinci prostatectomy
  • hormonal therapy
  • surgical castration (orchiectomy), medical castration (leuprolide, degarelix), antiandrogens (bicalutamide)
209
Q

name the 4 steps towards diagnosing primary hyperaldosteronism. describe the purpose of each step.

what is the treatment?

A

1) aldosterone: renin ratio- screening test (20-30 is positive)
2) salt loading- biochemical diagnostic test
3) abdominal ct- to check for adrenal carcinoma
4) adrenal venous sampling- to distinguish between adrenal adenoma and bilateral adrenal hyperplasia

  • surgical resection of adenoma if possible, mineralocorticoid receptor antagonist
210
Q

for dialysis associated cystic disease:

what is the cause

where are the cysts?

what serious complication can occur?

A
  • kidneys are not being used due to dialysis, eventually form cysts and calcify and fibrose also
  • medullary and cortical cysts
  • some of these cysts can come renal cell carcinoma
211
Q

does drowning cause hypernatremia or hyponatremia?

is it euvolemic, hypervolemic, or hypovolemic?

how would you treat it

A
  • hypervolemic hypernatremia

D5W and diuretics

212
Q

increase in what two things in diet can increase calcium excretion

A
  • sodium and animal protein
213
Q

name at least 5 risk factors for acute kidney injury

A
  • age >75
  • chronic kidney disease
  • diabetes
  • myeloma
  • proteinuria
  • heart failure
  • cirrhosis
  • peripheral vascular disease
  • volume depletion
214
Q

for post-infectious glomerulonephritis:

what is the histology?

what is the pathophysiology

what is the classic presentation

what would urinalysis reveal?

any high serum titers?

what is the treatment?

A
  • granular lumpy bumpy pattern along capillary loops, can resemble lobar simplification like in mpgn (cauliflower), very cellular due to exudate and mesangial+endothelial proliferation
  • antigen from infection (most likely strep) has similarity to basement membrane and deposits subepithelial( VLARGE DEPOSIT); complement activation
  • hematuria (cola urine), proteinuria, edema, azotemia (increased cr) oliguria 1-4 weeks after strep A infection (also staph, pneumococcal, measles, chickenpox, hep b)
  • rbc and wbc cast
  • high aso titers
  • supportive treatment, antihypertensives, diuretics
215
Q

name four scenarios in which you should suspect primary hyperaldosteronism?

A
  • htn and an adrenal adenoma
  • htn resistant to three medications
  • htn and hypokalemia
  • early onset htn, esp with stroke
216
Q

what should the hepcidin, hemoglobin, TIBC (transferrin), serum iron level, % saturation, and ferritin values be in anemia of chronic kidney

A
hepcidin- high (increased production and decreased clerance)
hgb- low
TIBC- low
Serum iron- low
%saturation- low
ferritin- high
217
Q

where does the prostate arise from embryologically?

at which week gestation?

A

urogenital sinus

10 weeks

218
Q

high K diet results in ______ (increased or decreased) K secretion in the principal cells?

low K diet results in ______ (increased or decreased) K secretion in the principal cells?

A
  • increased

- decreased

219
Q

where in the nephron do loop diuretics work?

name 3 loop diuretics

how does it work?

what is it indicated for?

contraindications?

side effects?

A
  • thicc ascending loop of henle
  • furosemide, bumetanide, ethacrynic acid
  • anion form competitively binds to Cl site and prevents reabsorption (most powerful diuretic) of Na, K, Cl, Mg, and Ca, also increases uric acid reabsorption in PCT by causing ECF contraction
  • edema and severe hypercalcemia
  • sulfonamide allergy (bumetanide and furosemide)
  • hypokalemia, hypomagnesemia, ototoxicity, hyperuricemia, metabolic (contraction) alkalosis, hypernatremia, hyponatremia (OHH DAANG)
220
Q

what type of acid base disorder does acetazolamide cause

what about loop diuretics?

thiazide diuretics?

K sparing diuretics?

A
  • Type II renal tubular acidosis (metabolic acidosis)
  • metabolic (contraction) alkalosis
  • metabolic (contraction) alkalosis
  • type IV renal tubular acidosis (metabolic acidosis)
221
Q

a widened mediastinum is indicative of what

A

aortic dissection

222
Q

if a medication is easily cleared renally, should you give the medication before or after dialysis?

can ace inhibitors be removed by dialysis?

A

after!

YES

223
Q

would increasing calcium intake make kidney stones worse or better?

A

better! calcium will bind oxalate in the gut and prevent absorption

224
Q

do loop diuretics cause hypernatremia or hyponatremia?

is it euvolemic, hypervolemic, or hypovolemic?

how would you treat it?

A

hypovolemic hypernatremia

normal saline if hypotensive
oral water to replace volume loss

225
Q

name a scenario in which renal compensation for metabolic alkalosis will NOT happen?

A
  • if you have metabolic alkalosis due to ECF volume contraction (have to treat volume contraction first before treating alkalosis)
226
Q

in what cells of the prostate is 5alpha reductase located mostly?

is bph more due to cells living longer or more cells forming

A

stromal cells

cells living longer

227
Q

does decreased renin cause hypo or hyperkalemia?

name three things that can decrease renin and subsequently affected potassium levels?

A

hyperkalemia

  • cyclosporine, nsaids, and diabetic nephropathy
228
Q

name treatment methods of secondary parathyroidism in chronic kidney disease

A
  • phosphate binders (calcium carbonate, sevelemer)
  • vitamind d analogs
  • cinacalcet (binds to calcium sensing receptor)
229
Q

what gfr values correspond to the 5 stages of kidney disease?

A

1: >90
2: 60-89
3: 30-59
4: 15-29
5: <15

230
Q

what is a kidney stone that involves the renal pelvis and at least two caluces

A

staghorn stone

231
Q

what ions/molecuels are reabsorbed in the kidney

which ones are secreted?

A

I NAGginly HAC the CPU
- Na, glucose, HCO3, amino acids, ca2+, Cl, phosphate, urea

  • PAHK My Hair
  • pah, K+, Morphine, H+
232
Q

what two glomerular diseases would have negative immunofluorescence?

A

minimal change disease and focal segmental glomerulosclerosis (no immune complex deposition)

233
Q

where does NH4+ that is used to buffer H+ originally come from?

A

via glutamine in the proximal tubule

glutamine gets converted to NH4 via glutaminase

234
Q

for squamous cell carcinoma of the penis

what two situations is it associated with?

where does it metastasize to?

A
  • uncircumsized people and hpv 16 and 18

regional lymph nodes

235
Q

what does positive Ch20 (positive free water clearance) mean

what does negative Ch20 mean?

A
  • urine osmolarity is less than plasma, meaning more water was excreted, water diuresis
  • urine osmolarity is more than plasma osmolarity, meaning less water was excreted (more water reabsorbed), water antidiuresis
236
Q

which part of the nephron do thiazide diuretics work on?

which channel?

give an example

A
  • early distal tubule

Na Cl channel

hydrochlorothiazide, chlorothiazide

237
Q

what are common causes of secondary hypertension

A
- DRROP
drugs or alcohol
renal parenchymal disease
renovascular disease
obstructive sleep apnea
primary aldosteronism
238
Q

which cystic kidney disease can you get berry aneurysms, mitral valve prolapse or liver cysts?

A

autosomal dominant polycystic kidney diseasee

239
Q

Where in the body does angiotensin converting enzyme work?

What does it convert?

A
  • lungs

- angiotensin I to angiotensin II

240
Q

what can cause normal anion gap metabolic acidosis?

A
  • diarrhea, all types of renal tubular acidosis
241
Q

name the places in which urea is impermeable in the nephron

name the places in which water is impermeable

A
  • from thick ascending limb to outer medullary collecting duct
  • from thick ascending limb to early distal tubule
242
Q

what is used to estimate renal plasma flow/renal blood flow

why

A

para aminohippuric acid (PAH, an organic acid)

  • it has high clearance, aka is filtered and secrete
243
Q

what is the most common bacterial cause of pyelonephritis? where does it originate from?

what are two uncommon causes and where do they originate from?

A
  • ecoli, ascending from perinum and vesicouteral reflux
  • staph aureus, hematogenous spread
  • mycobacterium tuberculosis, from lung
244
Q

demeclocycline is used to treat what?

what is a side effect

A

SIADH

nephrogenic diabetes

245
Q

What fraction of TBW is ECF? ICF?

what separates ECF and ICF

A

ECF –> 1/3
ICF –>2/3

cell membrane

246
Q

what is the formula for filtered load?

A

GFR * [P]x (*% of x unbound in plasma)

GFR= clearance of inulin or creatinine
Px= plasma concentration of x
247
Q

what cardiac changes occur during pregnancy

A
  • decreased svr due to progesterone, prostacyclin and relaxin relaxing the muscle
  • increased cardiac output
  • dilution anemia
  • increased blood volume from RAAs and adh but also desensitive AII
248
Q

all diuretics are filtered AND secreted in the ________ tubule

A

late proximal

249
Q

name 6 changes in renal physiology during pregnancy

A
  • increased gfr and rbf
  • increased adh
  • increased RAAS
  • hyponatremia and edema
  • increased Na retention
  • glycosuria
250
Q

hypophosphatemic rickets is due an activating mutation in ____ or ____

A

fgf23 or vitamind d receptor

251
Q

what acid base disorder is primary hyperaldosteronism associated with?

if a person with primary hyperaldosteronism has muscle cramps, what could be the reason?

A

metabolic alkalosis

hypokalemia

252
Q

how much does the glomerulus filter initially vs how much urine is the final product after reabsorption and secretion

A

180L/day vs 1-1.5 L/day

253
Q

for chronic glomerulonephritis:

what causes it?

what does histology look like

what would the kidney grossly look like?

what is the treatment?

A
  • essentially any nephrotic or nephritic syndrome besides minimal change can cause it (esp rapidly progressive glomerulonephritis), BUT it is so far progressed that you can’t find the original etiology
  • global glomerular sclerosis and interstitial fibrosis
  • it would be smol! (<9.5 cm)
  • dialysis and kidney transplant
254
Q

name and describe the three components of the juxtaglomerular apparatus

what arre the two main functions of the juxtaglomerular apparatus

A

mesangial cells (line afferent, efferent arterioles and glomerulus)

juxtaglomerular cells (surround afferent arterioles and release renin)

macula densa (part of early distal convoluted tubule and comes very close to its own glomerulus)

  • secrete renin and tubuloglomerular feedback
255
Q

what signs of a kidney stone suggest urgent intervention is necessary?

A

fever
high wbc
uncontrolled pain
renal failure

256
Q

for IgA nephropathy:

what is the histology?

what is the pathophysiology?

what is the classic presentation?

what is a vasculitis that is associated with it?

A
  • mesanial hyperplasia matrix expansion in response to IgA complex deposition; “prune bush” pattern on IF
  • abnormally increased IgA possibly due to upper respiratory or mucosal infection that deposits in the mesangium; complement activation subsequently
  • hematuria coinciding with upper respiratory infection ( can also have proteinuria, htn, edema etc)
  • henoch- schoenlein purpura (purpura, arthralgias and flank pain triad)
257
Q

if a medication has a high volume of distribution, then it is _____ (easy, hard) to clear it renally/via dialysis

give an example

A

hard

digoxin!

258
Q

for hypergycemic, hyperosmotic non-ketotic diabetic coma:

what demographic is most often affected?

what is the cause

what often precipitates it?

what is the blood sodium concentration

what is the treatment?

A
  • elderly with type 2 diabetes
  • hyperglycemia –> glycosuria –> loss of water with glucose in urine
  • stress, infection, steroids
  • can be high, low or normal
  • .9% saline to replace volume loss, almost always insulin, and water
259
Q

what is the classic triad seen with renal cell carcinoma? which is most common?

A

hematuria (most common), palpable mass, flank pain

260
Q

what three vitamins can increase the absorption of Ca

A

C A D

261
Q

what ekg abnormalities can be present due to hyperkalemia?

A

peaked t waves

262
Q

do invasive urothelial carcinomas recur if removed?

A

yes, esp if high grade

263
Q

mnemonic for medications that can cause htn

A

The DON’TS of hypertension

D- decongestants
O- oral contraceptives
N- NSAIDS
T- Tricyclic Antidepressants
S- steroids
264
Q

what are complications of using a tunnel catheter for dialysis?

A
  • endocarditis
  • bacteremia to the spine
  • thrombus
  • infection
  • extruded cuff
265
Q

what gender, age group, and ethnicity/race is more likely to get hypertension?

A
  • older african american men
266
Q

when is urine sodium >20 and urine osmolality high in volume depleted states?

A

RENAL LOSSES OF FLUID

  • diuretics
  • glycosuria
267
Q

what three hormones relax smooth muscle during pregnancy

A

relaxin, progesterone, prostacyclin

268
Q

what are normal values for gfr for young and elderly men and women

A

Males: Age 20-30 approximately 110ml/min
Age 70-80 approximately 65 ml/min

Females:Age 20- 30 approximately 100 ml/min
Age 70-80 approximately 50 ml/min

269
Q

does diabetes insipidus cause hypernatremia or hyponatremia?

is it euvolemic, hypervolemic, or hypovolemic?

how would you treat it

A
  • euvolemic hypernatremia

D5w

270
Q

for (Type II) Immne complex mediated rapidly progressive glomerulonephritis, what is the cause?

what is the fluorescence pattern?

what is the treatment?

A
  • any cause of immune complex glomerulonephritis
    ex: SLE, iga nephropathy, postinfectious GN

granular deposits

treat the underlying cause!

271
Q

for (type III) pauci-immune rapidly progressive glomerulonephritis:

what causes it (3 things)

what does IF show?
what does H & E stain show

what titers will be elevated

A
  • vasculitides: wegners, microscopic polyangitis, churg strauss syndrome
  • doesn’t show anything! no antibodies or immune complexes
  • crescent (proliferation of partial layer of bowman’s capsule)
  • C-ANCA for wegners, P-ANCA for microscopic polyangitis and churg strauss
272
Q

what is diffusion trapping?

A
  • the concept that once NH3 diffuses from the interstitium of the medulla to the lumen and combines with H+ to form NH4+, it is now charges and cannot diffuse back to the interstitium and gets excreted
273
Q

can you get hyperkalemia from high K food intake?

A

NAH, only can happen if you have end stage renal disease

274
Q

what two demographics of renal cell carcinoma are hereditary?

A
  • hereditary papillary carcinoma (multiple bilateral nodules, mutation in met oncogene)
  • Von Hippel Landau Syndrome (autosomal dominant, inactivating mutation of VHL tumor suppressor gene)
275
Q

how should prerenal azotemia be treated?

A
  • if true volume depletion, normal saline

- treat underlying cause

276
Q

what is the most common genetic cause of end stage renal disease in people less than 30 years old?

what is it characterized by?

A
  • medullary cystic disease

hella cysts in the cortico-medullary junction

277
Q

what are the two antimetabolite drugs used for kidney transplant/how do they work?

side effects?

A
  • azathioprine- incorporated into rna and stops cell cycle
  • mycophenylate- inhibits inosine monophosphate dehydrogenase–> inhibits cell cycle
  • azathioprine- bone marrow suppression, hepatitis, don’t use with allopurinol
  • mycophenylate- nausea vomiting diarrhea
278
Q

for autosomal dominant polycystic kidney disease:

what is the pathogenesis?

what are the symptoms?

what are three major systemic manifestations?

what is the treatment?

A
  • have dominant mutation that will cause asymptomatic cysts or no cysts until a second hit causes rapid proliferation of cysts, causes significant cystic dilation of nephrons
  • hematuria, proteinuria, polyuria, hypertension, back pain
  • polycystic liver disease, berry aneurysm, mitral valve prolapse
  • transplant (curative), dialysis, caffeine avoidance, tolvaptan, anti-hypertensives
279
Q

what are the two major processes responsible for establishing the corticopapillary gradient?

A
  • countercurrent multiplication

- urea recycling

280
Q

speed of flow through the vasa recta MUST be ____ (slow or fast). explain why

A

slow other wise vasa recta will wash away solute and dissipate corticopapillary gradient

281
Q

what is the pK of Hb-O2? what about Hb

A

HbO2 6.7

Hb 7.9

282
Q

what are treatment options for renal cell carcinoma

A
  • IL2, only curative option, but toxic af and not always effective
  • tyrosin kinase inhibitor, temsirolimus
  • radical nephrectomy
  • partial nephrectomy
  • checkpoint inhibitors (nivolumab and ipilimummab)
283
Q

what is specific gravity

what specific gravity value indicates that there is intact kidney function?

A
  • ratio of weight of urine to equal volume of distilled water (helps you figure out if kidneys are capable of concentrating urine
  • > 1.018
284
Q

what is the difference between essential hypertension and secondary hypertension

A
  • essential has an unknown cause but secondary this is a definite/known cause
285
Q

which condition does rule of thirds refer to?

what is the rule of thirds?

A

membranous glomerulonephropathy

  • third will go into remission
    third will have partial remission and slow progression
    third will get esrd
286
Q

for membranoproliferative glomerulonephritis:

what is the histology?

what is the cause?

who is affected?

is it a nephrotic or nephritic syndrome?

A
  • subendothelial immune complexes +complement lead to second basement membrane (tram tracks); igg and complement granular fluorescence; lobular simplification (cauliflower), mesangial interposition

primary idiopathic
secondary: SLE, hep c, endocarditis, lymphoma

primary: young adults and children
secondary: adults

  • mix of both nephrotic and nephritic syndrome
287
Q

what are the four effects of angiotensin II in response to decrease Pa

A
  • increases thirst –> increased H20 intake
  • increases aldosterone synthesis –> increased aldosterone –> increase Na channels in distal tubules and collecting ducts –> increase Na reabsorption
  • increases TPR
  • stimulates Na+ H exchange in proximal tubule, increasing Na reabsorption
288
Q

for pheochromocytoma:

what is it?

what are symptoms

how do you diagnose it

how do you treat it

A
  • catecholamine secreting tumor (can be in adrenals or elsewhere= paragangliomas)
  • htn, pallor, palpitations, headaches, diaphoresis, orthostatic hypotension (due to intravascular volume loss)
  • screen by checking metanephrine levels in serum or 24 hr urine, then abdominal ct
  • alpha blocker then surgery, DON’T USE BETA BLOCKERS
289
Q

what is the 60-40-20 rule?

A

60% of weight is total body water
40% of weight is ICF
20% of weight is ECF

290
Q

what is the definition of proteinuria?

what is a common tell tale visible sign of proteinuria?

A

> 150 mg protein in 24 hr urine specimen
or
150 mg/g creatinine in random sample

foamy urine

291
Q

How can you differentiate prostate intraepithelial neoplasia and prostate carcinoma?

A

stain the basement membrane

  • prostate carcinoma invades the basement membrane whereas pin does not
292
Q

describe three reasons why you can get glucosuria

A
  • diabetes, increased plasma glucose concentration –> increased filtered load (fl= GFR * Px)
  • pregnancy, increased gfr –> increased filtered load (fl= GFR* Px)
  • renal glucosuria, decreased affinity or amount of na-glucose transporters –> decreased Tm –> increased excretion
293
Q

in saline resistant metabolic alkalosis, what would the urine chloride be and why?

what about saline sensitive metabolic alkalosis?
Will the urine sodium match urine chloride in the urine?

A
  • would be higher >15, not in volume depleted state, don’t need to reabsorb as much Na Cl
  • would be low because body is trying to retain as much Na Cl as possible in volume depleted state
  • nope, because after Cl is reabsorbed, remaining Na is obligated to pass through urine with HCO3
294
Q

mnemonic for marker substances

A
  • I HAD MARC jacobs’ pRIMER

MARC= MARKERS

H TO
A ntipyrene
D 2O

R adioactive sulfate
I nulin
M annitol

E van’s blue dye
R adioiodinated serum albumin

295
Q

what antihypertensive drugs are safe for pregnancy?

which ones are not safe?

A
  • methyldopa, labetalol, hydralazine, calcium channel blockers
  • ace inhibitors, arb’s spironolactone
296
Q

what are poor predictors of membranous glomerulonephropathy ?

A
tubulointerstitial fibrosis
 elevated creatinine at diagnosis
 male sex
 hypertension
 older age
 heavy proteinuria
297
Q

what condition do lower urinary tract symptoms refer to?

name some

A
  • benign prostate hyperplasia

- nocturia, urgency, frequency, hesitancy, post void dribble, slow stream

298
Q

what is urodilatin?

where does it act?

A
  • similar in structure to ANP, causes local prevention of Na reabsorption–> increased Na excretion
  • distal nephron
299
Q

does alkalemia result in increased or decreased K secretion?

what about acidemia?

what channel facilitates this?

A
  • increased secretion
  • decreased secretion
  • H- K pump
300
Q

name four common ways you lose K?

A
  • the four D’s
  • diarrhea
  • diuretics
  • drinking water
  • alDosterone
301
Q

what type of acid-base disorder does aspirin overdose cause?

A
  • TRICK QUESTION IT CAUSES TWO TYPES (mixed disorder)
metabolic acidosis (ingestion of Fixed H)
respiratory alkalosis (has direct effect on medulla
302
Q

does acute cystitis present with fever?

does acute pyelonephritis present with fever?

A
  • no (not systemic infection)

- yes

303
Q

what increases aldosterone secretion?

what decreases aldosterone secretion?

A
  • increase angiotensin II, hyperkalemia (& decreased pressure)
  • decreased angiotensin II, hypokalemia (increased pressure)
304
Q

how can you treat aspirin poisoning by excreting more aspiring?

A
  • by alkalinizing the urine –> favor A- form of aspirin over HA –> A- is water soluble and can’t diffuse back into blood -> more aspirin is excreted
305
Q

all diuretics are filtered AND ____ in the late proximal tubule

A

secreted

306
Q

name 5 target-organ damage due to hypertension?

A
  • retinopathy
  • stroke, hemorrhage, dementia
  • peripheral vascular disease
  • renal failure
  • LVH, HF, CHD
307
Q

antihistamines and amphertamines are ____ (bases or acids), addition of bicarb would ____ (increase or decrease) renal clearance

A

bases

decrease

308
Q

what causes of metabolic acidosis can cause a normal anion gap

A

diarrhea and all types of renal tubular acidosis

309
Q

name 5 functions of PTH

name three things that regulate the parathyroid glands

A
increase Ca reabsorption in the kidney
increase Ca resorption in bone
increase calcitriol production
increase bone turnover
decrease phosphate reabsorption
  • vitamin d (via vitamin d receptor)
  • calcium (via calcium sending receptor)
  • phosphate
310
Q

what are the three criteria of benign prostatic hyperplasia?

A
  • prostatic volume (enlarged prostate)
  • histology- hyperplasia of epithelial and smooth muscle cells
  • lower urinary tract symptoms- nocturia, urgency, frequency, hesitancy, post void dribble, slow stream
311
Q

for Liddle syndrome:

what is the cause

what are the aldosterone and renin levels

A
  • autosomal dominant disorder in which na channels on principal cells are over activated
  • low aldosterone, low renin
312
Q

what type of retinopathy finding in hypertension is due to swollen/damaged axons?

A

cotton wool spots

313
Q

when you should consider doing ct or sonogram for a patient with acute pyelo nephritis?

A
  • if symptoms don’t decrease after 3 days
  • has more than 2 episodes of pyelonephritis in a year
  • complicated nephritis
  • urine culture reveals yeast
  • symptoms returns less than 2 weeks after treatment
314
Q

name three erythropoiesis stimulating agents

what do they do

name side effects

what should you give with esa’s

A
  • erythropoietin, darbepoietin, mircera
  • stimulate erythropoiesis
  • iron deficiency, worsening htn
315
Q

what are treatment options for bladder cancer (5)

A
  • radical cystoprostatectomy
  • partial cystectomy (difficult because usually multifocal)
  • neoadjuvant chemo + cystectomy
  • turbt
  • bladder preservation protocol
316
Q

what are the two hereditary causes of nephrogenic diabetes insipidus? what is their inheritance?

what are two non-inheritable causes of nephrogenic diabetes?

A
  • V2 receptor mutation- x linked recessive
  • aquaporin defect- autosomal recessive
  • lithium (used to treat bipolar) and demeclocycline (treats siadh)
317
Q

does hypoaldosteronism cause hyper or hypokalemia?

A
  • hyperkalemia
318
Q

give an example of positive Na+ balance

describe how the body compensates

A
  • increased ingestion of Na+ (and water)
  • Na and subsequently water will fill the ECF, both values increase, and body weight increases, then a few days later the kidneys sense the increase in ECF volume, which causes them to excrete more Na+ than what is being ingested, bringing the ECF and Na content back to normal
319
Q

which two acid base disorder types would have decreased HCO3 and decreased CO2?

A
  • metabolic acidosis

- respiratory alkalosis

320
Q

for glucocorticoid remediable aldosteronism:

what is the cause

what are the aldosterone and renin levels

what is the treatment?

A
  • autosomal dominant inherited chrimer gene that causes acth, not raas, to be the main stimulator of aldosterone synthase
  • high aldosterone, low renin
  • steroids!
321
Q

what is an example of hyposmotic volume contraction?

what is lost?

A
  • adrenal insufficiency

- NaCl

322
Q

name three scenarios in which you would have no ADH turned on

A
  • drink hella water
  • central diabetes insipidus
  • nephrogenic diabetes insipidus
323
Q

what is the difference between chronic hypertension, gestational hypertension, and preeclampsia during pregnancy?

A
  • chronic- hypertension before 20 weeks
  • gestational - htn after 20 weeks
  • preeclampsia- htn after 20 weeks WITH at least one severe feature (ex: 160/110, proteinuria, HELLP syndrome, visual disturbances, seizures, thrombocytopenia, acute kidney injury, pulmonary edema)
324
Q

what dietary intake should you increase if you have hypertension

A

potassium

325
Q

for apparent mineralocrticoid excess:

what is the cause

what are the aldosterone and renin levels

A
  • either too much cortisol (cushing) that 11 B hydroxysteroid dehydrogenase is overwhelmed OR glycyrrhizinic acid (licorice, tobacco) inhibits 11BHSD –> cortisol is not all converted to coritsone and can activate mineralocorticoid receptor
  • low aldosterone, low renin
326
Q

what is the treatment for low and high grade superficial bladder cancer (and carcinoma in situ)?

A
  • transurethral resection of bladder tumor (TURBT) + intravesicle mitomycin
  • intravesicle BCG for 6 weeks
327
Q

what can cause tumor lysis syndrome?

what causes it?

how should you treat it?

A
  • initiation of chemo for hematologic cancer
  • increased tumor cell turnover –> increased uric acid
  • hydration with isotonic fluid and allopurinol
328
Q

what stain is used to differentiate diabetic nephropathy from amyloidosis? what would you see on the stain?

A

congo red stain

apple green birefringence to light

329
Q

Concentration of what urinary molecule would reflect PTH action?

A

urinary cyclic AMP! (from when PTH binds to cells in the proximal convoluted tubule to inhibit phosphate reabsorption)

330
Q

what are three different type of uric acid nephropathies that can occur

A
  • uric acid stone
  • acute urate nephropathy: when you start treating malignancy, increased cell turnover leads to increased uric acid in the tubules, –> acute tubular necrosis
  • chronic urate nephropathy: in people with gout, you can get depositions of uric acid (similarly to how it deposits in joints)
331
Q

the half half point of a weak acid/weak base is when?

A

pH= pK

half is A- and half is HA

332
Q

what are the first two signs of recovery in acute tubular necrosis?

should you give saline?

A
  • first urine output increases
  • second cr decreases
  • ONLY IF HYPOVOLEMIC, if they’re not making urine, it doesn’t mean you should give saline
333
Q

name in increasing order which populations are affected by prostate cancer

black asian white

A

asians, white, black

334
Q

what is an example of isoosmotic volume expansion?

what is gained?

A
  • isoosmotic saline infusion

- water and NaCl

335
Q

what is the treatment for acute pyelonephritis? for how long?

what if you need parental abx?

A

trimethoprim/sulfamethoxazole for 14 days
(can also use fluoroquinolones)

  • ceftriaxone with aminoglycoside, if enteroccous, ampicillin and aminoglycoside
336
Q

for medullary sponge kidney:

what is the cause?

what is the presentation?

what are they at more increased risk of getting?

what is the treatment?

A
  • some developmental abnormality causes dilation of the medullary collecting ducts, which can pinch off and form cysts
  • can be asymptomatic, can also have flank pain, hematuria, kidney stones, UTIs, nephrocalcinosis
  • kidney stones (nephrolithiasis)
  • none! benign
337
Q

what are three ways to increase blood pressure?

A
BP= CO* TPR
CO= SV*HR

increase the rate (HR)
increase the amount the heart pumps (SV)
increase the resistance (TPR)

338
Q

what two things can increase calcium reabsorption in the distal tubule?

A

pth and thiazide diuretics

339
Q

mnemonic for indications for dialysis

A
AEIOU
A- acidosis
E- electrolytes (severe hyperkalemia)
I- ingestions/intoxications
O- (volume) overload
U- Uremia (pericarditis, encephalopathy)
340
Q

what is the pc1-pc2 complex?

what is it important for?

what do mutations in this cause?

A
  • Ca2+ channel complex in the primary cilia, lets the cell know when it’s bent
  • it releases the centrosome during mitosis which provides the cell with correct polarity and makes sure it divides in the correct direction/orientation
  • mutations in this (or in the centrosome) result in loss of polarity and direction of mitosis (loss of architecture) and formation of cysts (in addition to increase in ion and h20 channels)
341
Q

which part of the nephron does aldosterone work on?

which channels?

A
  • late distal tubule and collecting ducts
  • Na reabsorption channel and K secreting channel of principle cells and H ATPase secretion channel of intercalated cells
342
Q

what is the formula for excretion rate

A

V* [U]x

Ux= urinary concentration of x
V= urinary flow rate
343
Q

reabsorption of HCO3- in the proximal tubule involves the net secretion of how many H+?

A
  • ZERO! (H is recycled)
344
Q

what is more of a medical emergency, hyperkalemia or hypokalemia?

what should you do to treat it?

A

HYPERKALEMIA V BIG EMERGENCY

  • buy time initially by giving calcium gluconate to stabilize membrane and b agonist (inhaled abuterol) and insulin
  • then you MUST remove the K from the body by either diuresis, dialysis, polystyrene resin
345
Q

which condition can cause hypocalcemia, hypogammaglobulinemia, and hypercoagulability? why?

A
  • nephrotic syndrome, due to loss of proteins (vit d binding protein, protein c and s, globulins)
346
Q

name three clinical presentations of acute tubular necrosis?

A

OAF!
Oliguria
azotemia
FeNa>2% (means tubules are damaged and can’t reabsorb Na)

347
Q

name at least 5 medications medications/substances that are nephrotoxic?

A
cyclosporine
amphotericin
radiocontrast
tacrolimus
heavy metals 
aminoglycosides
acyclovir 
sulfathiazole
348
Q

for latent diabetic nephropathy, what is the main pathologic feature?

what would a glomerulus look like on h and e stain?

A
  • increased GFR

- nothing really, MAYBE slight increased in size

349
Q

name the intracellular and extracellular buffer proteins and which ones are most important

A

mnemonic: ahh! it’s a bop!
ecf: albumin, HCO3/H2CO3/CO2 (most important), HPO4/H2PO4
icf: “bone”, organic phosphates (adp, atp, etc), proteins (Hemoglobin, most important)

350
Q

what is splay?

name two reasons why it occurs?

A
  • when the Tm for reabsorption of a substance is reached after the threshold for excretion
  • nephron heterogeneity (individual nephrons have different Tm
  • low affinity high capacity Na- Glucose transporter in the early proximal tubule
351
Q

mnemonic for focal segmental glomerulosclerosis

A

The SMALL AFRICAN HISSING COCKROACH FOCUSED on HER FOOD-hunting SKILL from her HIVE.

Small= small kidney for size (low birth weight, morbid obesity)
African- aa most affected
Hissing- Hispanic

Cockroach- cmv
Focused- focal segmental glomerulosclerosis
HER- heroin
FOOD- FOOT process
Skill- sclerosis
Hive= hiv
352
Q

if ct urogram is negative for renal or bladder cancer what is the next step? why?

A

cytoscopy, carcinoma in situ or very small tumors won’t show up on ct

353
Q

what condition can look like a cystic kidney disease but actually is not?

A

hydronephrosis

354
Q

what is the formula for anion gap?

what is a normal range?

what is it used to distinguish?

A

[Na] - ( [Cl]+ [HCO3])

8- 16 mEq/L

different types of metabolic acidosis; if it’s due to overproduction or ingestion, the anion gap will be larger than normal; if it’s due to diarrhea/RTAs, it will be normal because Cl will increase

355
Q

which part of the nephron do K+ sparing diuretics work on?

which channel?

give an example

A
  • late distal tubule and collecting ducts
  • Na channel
  • spironolactone, amiloride
356
Q

what is the standard work up imaging done for suspected kidney stones/urolithiasis

what are treatment options?

A
  • renal colic CT

- let it pass on own, pain meds, hydration, alpha receptor antagonist, uteroscopy + LASER lithotripsy, SMASH IT, stent

357
Q

what medication is retrograde ejaculation a side effect for?

A

alpha blockers

358
Q

what are the 2 criteria for nephrotic syndrome?

what are 3 symptoms

A

proteinuria >3.5/day
hypoalbuminemia <3.5 g/dl

edema (due to intense sodium retention or decreased oncotic pressure), hyperlipidemia, and lipiduria (liver is inhibited from making albumin, so it makes lipoproteins instead)

359
Q

where in the nephron do thiazide diuretics work?

name 3 thiazide diuretics

how does it work?

what is it indicated for?

side effects?

A
  • early distal convoluted tubule
  • hydrochlorothiazide, chlorithalidone, metolazone
  • blocks Na Cl transporter, increases Ca reabsorption, decreases GFR
  • htn, edema, hypercalculria, nephrogenic DI (increases salt excretion and increases h2o reabsorption)
  • hypokalemia, metabolic alkalosis, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia (hyperGLUC)
360
Q

what is calciphylaxis in the context of chronic kidney disease

A
  • significant calcifications in micro blood vessels of skin and adipose tissue that cause ischemic painful lesions
361
Q

what are the symptoms/ pathologies of chronic kidney disease (mnemonic)

A

MAD HUNGER
Metabolic
Acidosis
Dyslipidemia
Hyperkalemia
Uremia (encephalopathy, pericarditis, asterixis, platelet dysfunction, anorexia, nausea)
Na/H2O retention (HTN, CHF, pulm edema)
Growth retardation and developmental delay
Erythropoietin failure (anemia of chronic disease)
Renal osteodystrophy

362
Q

what is diagnostic of acute pyelonephritis?

A

wbc casts

363
Q

what is considered the gold standard treatment for UTI

how many days should you take it

which medications are not effective, why?

A
  • trimethoprim/sulfamethoxazole (nitrofurantoin good for ecoli, fluoroquinolones good but expensive, should be used if resistant to bactrim)
  • 3 days
  • ampicillin and sulfonamides, 50% of ecoli is resistant
364
Q

where in the nephron does mannitol work?

how does it work?

what is it indicated for?

what is it contraindicated for?

A
  • proximal tubule
  • increases osmolarity of proximal tubule lumen; in order to maintain isoosmolarity, Na gets reabsorbed and then goes back down it’s concentration gradient into the lumen –> increases Na and H2O excretion
  • increased intracranial or intraocular pressure
  • edema (will make it worse)
365
Q

what causes type A lactic acidosis?

A
  • overall due to ischemia

- hypotension, cardiac failure, hypoperfusion, seizures, sepsis

366
Q

a specific gravity of 1.010 tells you what?

A

a person’s kidney are not capable of concentrating urine (it’s <1.018) and they probably have some degree of kidney injury

367
Q

what drug class are tacrolimus and cyclosporine?

what do they do?

what are they used for?

are there drug drug interactions?

side effects?

A
  • calcineurin inhibitors
  • block calcineurin –> prevent NFAT from activating t cell response
  • yee calcium channel blocks and azoles (increase serum level), anticonvulsants (decrease serum level)
  • htn, tremors, hirsutism, neurotox
368
Q

is respiratory alkalosis or respiratory acidosis common in pregnancy? why

A

respiratory alkalosis because you are breathing more heavily and blowing off CO2 due to increased CO2 sensitivity

369
Q

lesions on ct that increase by 15-20 houndsfield units are considered suspicious for ____________

A
  • renal cancer
370
Q

name 6 causes of hyperphosphatemia

A
  • increases intake (junk food, milk)
  • vitamin d therapoy
  • rhabdomyolysis
  • tumor lysis syndrome
  • hypoparathyroidism
  • renal failure
  • familiak tumoral calcinosis
371
Q

what is chlorpropamide?

what is the mechanism of action

what are side effects?

A
  • hypoglycemic agent used to increase water reabsorption and enhance adh
  • increase Na reabsorption in TALH and increase permeability of H2O in collecting ducts
  • hypoglycemia (give thiazide) and hyponatremia
372
Q

What is ECF further divided into?

How much of ECF is each part and what separates them?

A
  • plasma (1/4) and interstitial fluid (3/4)

capillary wall

373
Q

which of the following are weak acids and which are weak bases:

thiazide diuretics, amiloride, loop diuretics, triamterene, acetazolamide

A
  • weak acids: acetazolamide, loop diuretics, thiazide diuretics
  • weak bases: amiloride, triamterene
374
Q

what part of the kidney does clear cell carcinoma usually arise?

what about papillary carcinoma?

chromophobe renal cell carcinoma?

collectin duct carcinoma?

A
  • proximal convoluted tubule
  • distal convoluted tubule
  • collecting duct
  • medullary collecting duct
375
Q

what are some advantages to using BUN as a marker of gfr?

what are some disadvantages?

A
  • cheap and widely accepted
  • has variable tubular reabsorption and it’s production is variable (can change with diet, infection, GI hemorrhage, protein catabolism)
376
Q

In an alkalemic state, albumin minds more ____ (Ca or H) than _____ (Ca or H).

what happens as a result?

A

Ca than H

  • decreased ionized Ca –> tetany, tingling, numbness, cramping
377
Q

what is a medication class that can cause acute kidney injury but also treat kidney disease longterm?

A
  • ace inhibitors/ arbs
378
Q

for renal artery stenosis:

name two causes?

what lab/physical findings point towards renal artery stenosis

what are the screening tests

what is the gold standard diagnostic test

treatment?

A
  • fibromuscular dysplasia (yong women and atherosclerosis (people >50)
  • elevated renin (differentiates from primary hyperaldo) , abdominal bruit, metabolic alkalosis, hypokalemia
  • MRA, CT, duplex ultrasound
  • intraarterial arteriography
  • angioplasty, stent
379
Q

vomiting is what kind of acid base disorder?

A
  • metabolic alkalosis
380
Q

what cause familial tumoral calcinosis

A
  • deficiency or resistance to fgf 23 –> hyperphosphatemia –> ca and phos deposition in tissues
381
Q

If a patient presents with a rash, eosinophiluria, fever pyuria, and wbc casts, what condition do they most likely have

A

allergic/acute interstitial nephritis

eosinophiluria + rash are v unique features to remember

382
Q

aside from acting on the distal convoluted tubule, name two other actions of thiazide diuretics?

A
  • increases reabsorption of na in proximal tubule

- increases thirst

383
Q

what is pre-renal azotemia?

what causes pre-renal azotemia?

what is one lab value that would signify this?

A
  • increased in nitrogenous substances in the blood
  • due to decreased renal perfusion (regardless of etiology, think chf, cirrhosis, nenphrotic syndrome) –> increased reabsorption of Na, H20 and urea in the process
  • increased BUN: Cr ratio
384
Q

name at least 5 causes of respiratory acidosis.

describe whether each of the following should be increased or decrease: pH, CO2, HCO3

describe the acute and chronic compensation

what is the treatment

A
  • COPD, apnea, etoh, benzos, narcotics, brain stem injury, severe pneumonia or pulmonary embolism, guillan barre, myasthena gravis, polio, diaphragmatic paralysis, severe hypokalemia, severe hypophosphatemia,
  • ph- decreases, CO2- increased, HCO3, increased
  • acute: mass action= for every 1 increase in PCO2, HCO3 increases by .1
  • chronic: kidney increase HCO3 reabsorption= for every 1 increase in PCO2, HCO3 increases by .3
  • mechanical ventilation if not able to breathe on their own, treat underlying condition
385
Q

is polyuria indicative of bph? why or why not?

what about nocturnal polyuria?

A
  • no, peeing greater than 3 L means that you are drinking too much
  • no, if 1/3 of peeing is at night it’s usually do to a non urologic cause
386
Q

what is the most common cause of chronic kidney transplant failure

A

accumulation of comorbidities esp cardiovascular disease

387
Q

what are the two ways in which the kidney autoregulates blood pressure

A
  • myogenic (Q=P/R, vessel contracts to increases resistance when pressure is high and vice versa)
  • tubuloglomerular feedback (macula densa senses transient increase in Na and Cl, releases adenosine and causes contraction of afferent arteriole)
388
Q

where in the nephron does acetazolamide work?

how does it work?

what is it indicated for?

what is it contraindicated for?

side effects?

A
  • early proximal tubule
  • inhibits luminal carbonic anhydrase
  • glaucoma (aqueous humor cells have hella HCO3 and carbonic anhydrase), alkalinizing urine (cystine and uric acid stones, acid overdoses), altitude sickness
  • hepatic cirrhosis
  • metabolic acidosis (ACETazolamide causes ACIDosis), hypokalemia (increased flow rate)
389
Q

what stones precipitate more in alkaline ph

what stones precipiate more in acidic ph

A
  • calcium phosphate and ammonium magnesium phosphate (struvite)
  • uric acid and cystine
390
Q

the higher the urinary flow rate, the ____ (less or more) urea is excreted. explain why

A
  • more
  • the higher the flow rate, the less water that is reabsorbed, which means the less urea concentration gradient that is made , which leads to less reabsorption
391
Q

define resistance hypertension?

A
  • htn >130/80 on 3 meds OR bp <130/80 on 4 meds
392
Q

what can cause respiratory alkalosis

A

hysteria
brain stem tumor
aspirin poisoning
hypoxemia

393
Q

mnemonic for elevated anion gap metabolic acidosis?

A

MUDPILES

M- methanol
U- uremia
D- DKA (acetoacid acid and bhydroxybutyric acid)
P- Propylene Glycol (in icu sedtives)
I- Isoniazid
L- lactic acidosis
E- ethylene glycol/ETOH
S- salicylates
394
Q

what happens in hepatorenal syndrome?

what liver conditions is it associated with

can you treat it?

A

renal vasoconstriction and systemic vasodilation in response to increase volume and bp (unknown mechanism)

  • associated with cirrhosis and ascites

vasopressin analogues, octreotide (splanchnic vasoconstrictor), midodrine, transplant

395
Q

what are three things that can cause hypertonic hyponatremia

A
  • glucose, glycerol, mannitol

would have high plasma osmolality but low plasma sodium concentration

396
Q

give an example of negative Na+ balance

describe how the body compensates

A

diarrhea (loss of Na+ and fluid)

  • Na and subsequently fluid leaves the ECF, after a few days kidney senses the decrease of ECF volume and decreases excretion of Na, making Na ingestion greater than excretion until Na and ECF volume return to normal
397
Q

what is the net ultrafiltration pressure

A

the sum of hydrostatic pressure of the glomerular capillaries, hydrostatic pressure of bowman’s space, and the oncotic pressure of the glomerular capillaries

398
Q

in hyponatremia, how low does the sodium value need to decrease before you experience symptoms

below what sodium value would you experience seizures and coma?

A
  • under 125 mEq/L

- under 115 mEq/L

399
Q

what ions/molecules make up the ECF (3) vs. the ICF (4)

A
  • ECF: Na+, Cl-, HCO3-

- ICF: organophosphates (ADP, ATP, 23DPG), K+, Mg2+, proteins

400
Q

is your chance of death higher if you have high systolic blood pressure or high diastolic blood pressure?

A

systolic

401
Q

what is BCG used to treat?

What is its mechanism of action

A
  • high grade superfical bladder cancer and carcinoma in situ (drug of choice for CIS)
  • helps increase TH1 response and il2 and ifn g
402
Q

what histologic renal changes occur in preeclampsia

A

swelling of endothelial cells (endothelial dysfunction) which can lead to closing of some capillary loops

403
Q

what is the nephrotic range for proteinuria

what is the subnephrotic range?

A

> 3.5 g/day

<3.5 g/day

404
Q

what is the single most factor that limits progression of diabetic nephropathy to chronic kidney disease/renal failure?

what is the #1 thing you would use to achieve this?

A

BLOOD PRESSURE CONTROL!!

ACE inhibitors and ARBs

405
Q

what is the space between foot processes called?

what two things is it made of?

A

filtration slit

podocin and nephrin proteins

406
Q

what is the formula for renal clearance rate for a substance x

A

Cx= [Ux] * V/[Px]

Cx= clearance of substance x (volume of plasma removed of substance x per unit time

[Ux] = urine concentration of x
V= urinary flow rate
[Px]= plasma concentration of x
407
Q

describe how systolic and diastolic blood pressure change as your age?

A
  • systolic continues to increase as you age

- diastolic increases to a point and then decreases

408
Q

if the kidney doesn’t recover from acute tubuler necrosis, what secondary acute condition can result?

A

acute cortical necrosis

409
Q

when should you give Na HCO3 in a person with metabolic acidosis?

what should you be careful of?

A

if the pH is less than 7.2

make sure not to give too much, can cause metabolic alkalosis

410
Q

when on a loop diuretic, do you lose the ability to concentrate urine or dilute urine?

what about thiazide diuretics?

A

both! (lose diluting segment and lose cp gradient)

dilute urine(can’t still concentrate because cp gradient is maintained)

411
Q

substances with high clearance rates are filtered and _____

substances with low clearance rates are filtered and ______

A
  • secreted

- reabsorbed

412
Q

name 2 alpha 2 agonists that can be used for hypertension

what is the mechanism of action

what is one special scenario in which one of these drugs may be used

side effects

A
  • methyldopa and clonidine
  • enter brain and bind to presynaptic a2 receptors which causes negative feedback and prevents NE from being released –> CNS mediated decrease in sympathetic tone
  • methyldopa is v safe to use in pregnancy
  • drowsiness, dry mouth, rebound hypertension
413
Q

what is a risk factor for renal and bladder cancer?

A

smoking

414
Q

what ekg abnormalities can be present due to hypokalemia

A

u waves, torsades de pointes

415
Q

describe the process of how diabetic nephropathy affects the kidney

A
  • increased glucose in the glomerulus –> increased advanced glycation end products –> release of TGF b, IGF-1, renin-angiotensin –> afferent arteriole dilation and increased gfr –> efferent arteriole constriction (increased glomerular capillary pressure)
416
Q

what happens grossly to the kidney as a result of chronic pyelonephritis?

what kind of stone can occur due to chronic pyelonephritis?

A
  • dimpling of the kidney due to scarring, shrinking of the overall kidney

struvite (magnesium ammonium phosphate) staghorn stone

417
Q

what is the formula for filtration fraction

A

GFR/RPF (aka clearance of inulin/clearance of PAH)

418
Q

what drug can be synergistically added with alpha blockers to improve symptoms and address the cause of bph?

A

5 alpha reductase inhibitor aka finasteride

419
Q

is prostate specific antigen (PSA) organ specific? what about cancer specific?

A

organ specific but not cancer specific (can be elevated in benign conditions like bph)