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renal Flashcards

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1
Q

list which diuretics work at the different points of the renal tubules

what transporters are affected

A

mannitol: inhibit aquaporin in PT
acetazolamide: inhibit carbonic anhydrase (HCO3/Na) in PT

Furosemide, ethcrynic acids, numetanide, torsemide= Na-K-2Cl transporter

hydrochlorothiazide, chlorthalidone, metolazone= xNaCl in DT

spirinolactone, eplerenone,= ALD-R antagonist in CD

triamterene, amiloride= inhibit Na channels [resorb] (and the paired K/H channel [excrete K]) in CD

MAFTSA

Make -mannitol (P)

America= acetatzolamide (P)

For = Furosemide (LoH)

T= thiazides (DT)

S= spironolactone (CD)

Again= amiloride (CD)

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2
Q

fanconi syndrome

  • where in the tubule is the defect and what is it
  • what are the causes, be specific
  • what are the main electrolyte effects
  • presents similar to what? trx?

A
  1. PT- generalized reabsorption defect in PCT –> excretion of all substances
  2. hereditary (wilson ds, glycogen storage ds), ischemia, multiple myeloma, nephrotoxins=isofamide, cislatin, lead, expired tetracycines
  3. metabolic acidosis, hypophosphatemia, osteopenia
  4. IS RTA type II
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3
Q

bartter syndrome

  • where in the tubule is the defect and what is it
  • what are the causes, be specific
  • what are the main electrolyte effects
  • presents similar to what? trx?

A
  1. resorptive defet in TAL = xNa/K/2Cl

***bartter for as many electrolytes as possible, so hit the channel w 3 ions**

  1. AR inherit
  2. met alk, hypoK, hypercalciuria
  3. present siilar to chronic loop diuretic use
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4
Q

Gitelman syndrome

  • where in the tubule is the defect and what is it
  • what are the causes, be specific
  • what are the main electrolyte effects
  • presents similar to what? trx?

A
  • xNaCl in DT= no resorb Na
    2. AR inherit
    3. met alk, hypoMg, hypoK, hypocalciuria
  • AR inherit
  • present ~ lifelong thiazide use
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5
Q

Liddle syndrome

  • where in the tubule is the defect and what is it
  • what are the causes, be specific
  • what are the main electrolyte effects
  • presents similar to what? trx?

A

-GoF in CT –> inc Na resorp

**gain a liddle**

  • AD inherit
  • met alk, hypoK, HTN, dec ALD
  • v similar to hyperALD BUT the ALD is not detectable
  • trx w amiloride (ALD inhibitor)
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6
Q

SAME: syndrome of apparent mineralcorticoid excess

  • where in the tubule is the defect and what is it
  • what are the causes, be specific
  • what are the main electrolyte effects
  • presents similar to what? trx?

A
  • inc ALD receptor acitivty in CD: deficiency in 11β hydroxysteroid dehydrogenase –> excess corticol –> inc mineralcorticoid receptor activity
  • AR inh OR acquired from glycerrhetinic (licorice)
  • trx w K-sparing diuretics, or corticosteroids (to stop endogenous creation)
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7
Q

how do low and high serum concentrations of Na present

A

low: nausea and malaise, stupor, coma, seizures
high: irritability, stupor, coma

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8
Q

what are the causes of inc Na serum levels

be specific

A

water loss: inc ADH or inc Uosm

diabetes Insipidus (can be caused by lithium or amphotericin) = ~~relative~~”inc” levels

  • central= dec ADH activity
  • nephorgenic= dec renal response to

*amphotericin can cause RTA T11= x NaCl = inc Uosm

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9
Q

how do low and high serum concentrations of K present

A

low: U waves and flat T waves on ECG : arrhythmias : M cramps : spasms: wkness

**low key= flat tones w “yoU” **

high: wide QRS and peaked T waves : arrhythmias : M wknss

*high K= “up to here” (at the peak), w a “big Qs” (wide QRS) ****

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10
Q

how do low and high serum concentrations of Ca present

A

low Ca= tetany seizures, QT prolonged, Chvostek’s sign (twitching) and Troussau sign (BBP spasm)

**low Care =prolong the TasQ**

high: stones, bones (pain), groans (abd pain), thrones (inc urinary requency), psychiatric overtones (anxiety, AMS)

**high on California–> LA devotee vibes**

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11
Q

how do low and high serum concentrations of Mg present

A

low: tetany, Torsades des pointes, hypoK+hypoCa

**low status w Magneto –> causes the TdP when he pulls the iron in your blood**, he don’t care if he kill you

high: dec DTRs, lethargy, bradycardia, hypotension, cardiac arrest, hypoCa

**up high w Magneto –> bad guy, gotta diminish that deep reflex to care for people: stop your heart from Caring; ignoring ethics for your self gain is the lazy thing to do”

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12
Q

how do low and high serum concentrations of PO4 present

A

low: bone loss –> osteomalacia (adult), rickets (kids)
high: serum hypoCa, renal stones, metastatic calcification

**once bones are saturated?? just depo the Ca everywhere else??**

***to meet your (phos)FATE, you need strong bones****

**phosphate–> Ca depo into bones**

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13
Q

outline the causes of hypoNa + ↑ serum osmolality

A

-hypoglycemia

mannitol use

(both are powerful osmoles themselves)

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14
Q

outline the causes of hypoNa w n osmolality

A

= hyperlipidemia,

=hyperproteinemia (i.e multiple myeloma)

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15
Q

outline causes of hypoNa w ↓osmolality

A

= ADH does NOT bring in Na, it translocates aquaporins to the membrane (vs ALD)

1) HF and cirrhosis = states of hyervolemia that the body perceives as hypoV so is constantly trying to retain H20 –> non-osmotic release of ADH
- 2° to low C.O in HF, low vasc resistance in cirrhosis
2) kidney ineffective
- advance renale failure= even w low ADH, the min Uosm will rise bc the urine can’t dilute
- diuretics : thiazides >> diuretics
3) inc ADH

= 2° to vomiting, diarrhea, adrenal insuficiencty (x corticol inhibition of ADH)

=1° –> dec ADL, inc ADH

= SIADH:

  • 2° small cell LC, strokes, brain bleed/tumor, pulm ds
  • drug induced: carbamezapine, cyclophosphamide)
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16
Q

causes of respiratory acidosis?

explain the physiology if applicable

A

(CO2> 44= less exhales per min)= hypoventilation

  • airway obstruction, acute lung ds, chronic lung ds
  • opioids, sedatives,
  • weakening of respiratory Ms (i.e. MG, ALS, Guillan Barre, M dystrophy)
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17
Q

causes of metabolic acidosis?

A

(HCO3<24)

NAGMA

  • H= hyperalimentation (i.e. IV nutrients)
  • A=acetozolamide
  • R= RTA
  • D= diarrhea (so much poop, butt b hard)
  • A= Addison’s Ds
  • S= spironolactone
  • S= saline infusion

HAGMA

  • M= methanol
  • U= uremia
  • D= DKA
  • P= proponyl glycene
  • I= INH(isoniazid)/ iron
  • L= lactic acidosis
  • E= ethylene glycol
  • S= salicylates(late) (hardass would not be late)
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18
Q

causes of respiratory alkalosis

how can it be treated?

A

CO2<36= most exhales/min= hyperventilate

  • panic attack
  • hypoxemia (high altitude) **MAX height= MAX brthe= MAX amount CO2 blown out**
  • salicylates(early)
  • tumor
  • pulmonary embolism ***like coughing it out, but breathing it out????***

-trx w acetazolamide (augment the compensatory NAGMA)

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19
Q

how does an ASA affect the pH balance of the body

A

acute: medullary stimulation –> resp alk (hyperventilate)

hrs later: HAGMA via x(citric acid cycle)

= a mixed disease, w CO2 dec more than expected for just a compensation mechanism, and HCO3 dec over time

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20
Q

causes of metabolic alkalosis

A

=HCO3>28 / H+ loss

  • loop diuretics and thiazides : volume contraction and inc H+ lost in urine
  • vomiting (lose acid)
  • antacid use
  • hyperALD
  • hypoK (K into cells, H out of cells–>alk)

contraction alkalosis –> inc RAAS –> H loss in PT(ATII) and CD(ALD), inc HCO3 resop in PT

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21
Q

hyperaldosteronism

  • causes?
  • presentation?
A

-inc adrenal production

=adrenal hyperplasia

=Conn’s Syndrome (adrenal adenoma)

-present w inc K/H+ secretion

:suspicious triad: hypoK + resistant HTN!!

  • often no edema via ALD escape (inc ALD but then ANP will cause the excretion of Na/H2oO)
  • inc urinary Cl- (dilute the medulla–> dec LoH action–> less K excrete (^^ lost later in CD) + less Cl- resrob)
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22
Q

renal tubular acidosis is a __anion gap MA, w __ Cl- serum levels

23
Q

RTA Type 1

–where is it

–what is the defect

–urine pH

– serum K levels

–causes

–associations

Study These Flashcards
A

RTA ~ D.P.A

  1. distal tubule (HCO3 oftn <10)
  2. inability of α-intercalated cells to acidify urine: xsecrete H+ –> met acid
  3. UpH> 5.5 (no able to acidify)
  4. dec K: secrete K to maintain charge balance
  5. caused by AMPHOTERICIN B TOXICITY, analgesic nephropathy, obstruction of urinary tract, autoimmune (Sjogren &RA>SLE)

6- inc, oft bilat, Ca-PO4 nephrolithiasis (inc urine pH+inc bone turnover) : rickets +growth failure in children

24
Q

RTA Type 2

–where is it

–what is the defect

–urine pH

– serum K levels

–causes

–associations

–trx

Study These Flashcards
A

RTA ~ D.P.A

  1. defect in PT (HCO3~ 12-20)
  2. xHCO3 reabsorp = inc excreted in urine, overwhelm the DT/CD ability to acidify the urine
  3. pH < 5.5 (still able to acidify)
  4. hypoK:
  5. causes: Fanconi syndrome (lost everything in urine), multiple myeloma, carbonic anhydrase inhibitors
  6. inc risk hypoPhosphatemia = bone wasting
  7. trx= sodium bicarb
25
RTA Type 4 --where is it --what is the defect --urine pH -- serum K levels --causes --classic presentation --trx
RTA ~ D.P.A (A for ALD) 1. problem @ the DT and cortex part of CD 2. hypoALD or ALD resistance --\> hyperK --\> in pH in PT--\> dec NH3 synthesis in PT --\> dec ammonium excretion **(NH4 =major H+ vessel)**--\> acidosis 3. UpH\<5.5 4. hyperK (non excreted) 5. causes: - dec ALD production: diabetic hyporenin, ACE-I/ARBs, NSAIDs, heparin, cyclosporine, adrenal insuff - ALD resistance: K+ sparing diuretics, nephropathy 2° to obstruction, TMP-SMX 6. classic: diabetic w renal insuff, and unexplained hyperK 7. fludrocortisone
26
where in the renal tubule does urine acidification take place?
DT
27
how do the diff diuretic classes affect serum pH? name the drugs in each class, just for funsies
MAFTSA: make america for the smart again cause MET ALK - LOOP: furosemide, Bumetanide, Torsemide, ethcrynic acids \*\***fur**ious _loops_ **tore** **B-nide** (behind) **cry-**babies\*\* - Thiazides: hydrochlorthiazide, chlorthalidone, metolazone (\*\***me to**o! en **la**"*thia***zone**") cause MET ACID - Acetazolamide = NAGMA - Spironolactone= NAGMA
28
SLE is associated with which glomerular pathologies?
Type 5 Lupus Nephritis = membranous nephropathy in the setting of SLE diffuse capillary and GBM thick, granular IC deo, spike and dome Type 4 Lupus Nephritis= diffuse proliferative glomerulonephritis (\>50 glomeruli involved) -"wire lupus" w wiring capillaries, subendothelial IC+C3 depo, granular RPGN T2: DPGN in SLE can progress to RPGN
29
henoch shonloein what is it how does it present which glomerular disease is it associated with
=mc comon childhood systemic vasculitis =palpable purpura on butt + legs, abd pain/melena, joint pain, =diffuse igA depo across body, including mesangium of glomerulus IgA nephropathy
30
which glomerular diseases will present with decreased complement levels
PSGN (post strep GN), DPGN, MPGN
31
compare and contrast membranous nephropathy and MPGN (membrano-proliferative GM)
causes: both can be associated a HBV/HCV * MN: 1°~ anti-phospholipase A2-R Abs, or 2° ~ NSAIDs, penicillamine, gold, syphilis, SLE.. * MPGN: type 1 ∝ hepatitis, type 2 associated w C3 nephritic factor ( cause persistant complement activation till run out) LM * MN= diffuse capillary + GBM thick * MPGN: tram-track GBM split by mesangial overgrowth IF , both =granular * MN= IC, subepithelial (under feet) * MPGN: type 1= IC, subendothelial, type 2= intramambranous **_dense deposit (ds)_** EM: * MN= spike and dome OTHER: * MPGN= PAS+
32
subepithelial humps (of IC deposits) is pathognomonic for which glomerular ds?
acute post-strep glomerulonephritis seen on EM
33
which glomerular diseases are TIII hypersensitivity (which means?)? which are TII?
TIII hypersensitivity= immune complex deposition (IC activate complement) =PSGN, RPGN type 2 TII= direct AB =RPGN Type 1 = anti-type 4 collagen Ab
34
describe the infection after which PSGN wll develop
post group A strep (pyogenes) = pharyngitis or impetigo (skin)
35
describe the immunflourescent findings in RPGN
Type 1= linear IF (Goodpasture) Type 2= granular IF (PSGN/sle progressed DPGN) Type 3= pauci-immune = ANCA+ PR3/cANCA= wegeners MPO/p-ANCA= microscopic polyangiitis
36
kidney stones: Ca oxalate - crystal type - causes - trx
Ca oxalate: - envelope/dumbbell shaped - caused by hypocitratura, ∝ ↓urine pH - ethylene glycol, Vit C abuse, malabsorption (Crohn's) - trx= thiazides, citrate, low Na diet
37
Ca phosphate kidney stones - crystal type - causes - trx
wedge-shaped come out w high pH trx= low-Na diet, thiazides
38
ammonium-magnesium-phosphate kidney stones - crystal type - causes - trx
aka struvite coffin lid crystal: staghorn calculi causes: infection with **urease (+) bugs** = proteus miribalis, Staph saprophyticus, Klebsiella trx- eradication of underlying infection, surgical removal of stone
39
uric acid kidney stone - crystal type - causes - trx
=rhomboid or rossette crystals = risk w dec urine volume, arid climates, acidic pH =strong association w gout (hyperuricemia), high cell turnover (leukemia, chemo) trx- alkalize the urine, allopurinol for gout
40
cystine kidney stones - crystal type - causes - trx
=hexagonal crystals =AR xcystine resorb in PT (∝ low lysine, arginine, and ornithine too): begin in childhood and can form staghorn calculi ∝ (+) sodium cyanide nitroprusside test trx= low Na diet, alkalize urine, chelating agents
41
what is the most common CA of the kidney - pathophys - histo - clin present - trx
renal cell carcinoma --=originate from PCT--\> invade renal V - R renal V --\> IVC--\> met to lung and bone - L renal V --\> varicocele --histo= most common is clear cell carcinoma (clear bc full of poor-staining lipids and carbs, golden yellow cells) --clin: 50-70 yo obese M smoker classic triad (\<10% have al 3) = hematuria, palpable abd pain, flank pain +fever, weight loss, polycythemia 2° to inc EPO production RCC paraneoplastic syndromes: r**cc**= **P.E.A.R** P= inc PTHrP = hyperCa E= inc EPO = 2° polycythemia A= inc ACTH= Cushing R= inc renin= HTN trx= rarely curative, trx w IL-2 recomb (induce fever like syndrome)
42
renal angiomyolipomas are associated with what syndrome
tuberous sclerosis = AD =cortical subepindymal hamartomas, renal angiomyolipomas (benign, kids), cardiac rhabdomyomas, ash-leaf patches
43
nephroblastoma - cin presentation - path - associated syndromes
aka Wilms Tumor =most common renal malginancy of early childhood = 2-4yo w large palpable unilateral flank mass, hematuria, HTN -path= LOG WT1 or WT2 on ch 11 syndromes: WAGR (xWT1) = Wilms, Aniridia, Genitourinary malform (cryptochordism, ambiguous genitals), Retardation intellectural Denys Drash Syndrome (xWT2)= Wilms, Diffuse mesangial sclerosis (early onset nephrotic syndrome), Dysgenesis of gonads Bekwith-Weidemann Syndrome (xWT2) \*\*pediatric overgrowth syndrome\*\* = wilms, macroglossia, organomegaly, \>95% height/weight, hemihyperplasia (one extremity bigger than other)
44
what is the most common tumor of the bladder pathophys? clin? causes? trx?
transitional cell carcinoma aka urothelial carcinoma = tumor of the urothelium which is the layer of cells that lines the entire urine collecting system and bladder, so it *\*can\* be in the renal calyces, pelvis, ureter, and bladde*r causes: **P**ee **SAC** **P**henacetin, **S**moking, **A**niline dyes (hair), **C**yclophosphamide clin: old WM, smoker w **painless** hematura and no casts in the urine trx= platinum based chemo= cisplatin and caboplatin
45
what are the risk factors for squamous cell carcinoma of the bladder
chronic cystitis smoking chronic nephrolithiasis schistosoma haematobium infection (in the middle east= fresh water larvae penetrate skin--\> liver--\> bladder will proliferate and infect--\> hematuria --*can*--\> SqCC \*\*the men in Egypt menstruate\*\*
46
what are the sx of uremia
anorexia n/v platelet dysfunction --\> bleed uremic pericarditis asterixis encephalitis (confusion
47
what drugs will lead to decreased renal function
loop diuretics + thiazides + K+ saring drugs via x conentration ability ACE-I = vasodilate efferent arterioles = dec GFR NSAIDS= x prostoglandins = dec GFR
48
pathphys of renal osteodystrophy
chronic renal failure --\> 2° hyperPTH --\> bone pain+path frx+osteitis fibrocystica = renal osteodystrophy \*\*osteitis fibrocystica = bone cysts, brown tymors
49
how does acute interstitial nephritis present path? causes? trx?
"sterile pyuria" (wbc casts w/o pyelonephritis) can be asx, or fever, rash, hematura, CVA tend =allergic inglammation after drug administation ∝ of TMP-SMX (classic)diuretcs, penicillin, PPI, sulfonamides, rifampin, NSAIDs ∝ less common = Mycoplasma, sjogren, SLE, sarcoidosis
50
acute tubular necrosis causes stages labs clin
causes: ischemia to PT/TAL toxicity to PT (uric acid from tumor lysis syndrome, rhabdomyolysis myoglobin) stages: - clinically silent inciting event - maintenance phase = oliguria, risk of hyperK - recovery phase= polyuria, risk hypoK labs= granular, muddy brown casts, inc BUN/Cr (reverse in stage 3) clin: most common cause of AKI in hospitalized patients many will spontaneously resolve, can be fatal during oliguric phase
51
when does diffuse cortical necrosis of the kidney take place
w acute generalized infarction of both kidneys, oten due to vasospasm and DIC ∝ w obstetric catastrophies or septic shock
52
renal papillary necrosis pathophys associations clin?
= sloughing of necrotic renal papillae --\> gross hematuria and proteinuria -may be triggered by recent infection/immune system ∝w sickle cell, acute pyelonephritis, NSAIDs, DM clin: first the trigger --\> gross PAINLESS hematuria
53
what renal pathologies can be caused by NSAID overuse/OD
chronic insterstitial nephritis (i.e. chronic pain) ATN (ischemia) membranous GN papillaru necrosis
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