Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

First Aid, UWorld sets > renal > Flashcards

renal Flashcards

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how do low and high serum concentrations of Na present

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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) ****

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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**

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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**

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

outline the causes of hypoNa + ↑ serum osmolality

A

-hypoglycemia

mannitol use

(both are powerful osmoles themselves)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

outline the causes of hypoNa w n osmolality

A

= hyperlipidemia,

=hyperproteinemia (i.e multiple myeloma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

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

A

NAGMA

inc Cl-

23
Q

RTA Type 1

–where is it

–what is the defect

–urine pH

– serum K levels

–causes

–associations

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

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
Q

RTA Type 4

–where is it

–what is the defect

–urine pH

– serum K levels

–causes

–classic presentation

–trx

A

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
Q

where in the renal tubule does urine acidification take place?

A

DT

27
Q

how do the diff diuretic classes affect serum pH?

name the drugs in each class, just for funsies

A

MAFTSA: make america for the smart again

cause MET ALK

  • LOOP: furosemide, Bumetanide, Torsemide, ethcrynic acids **furious loops tore B-nide (behind) cry-babies**
  • Thiazides: hydrochlorthiazide, chlorthalidone, metolazone (**me too! en la“thiazone”)

cause MET ACID

  • Acetazolamide = NAGMA
  • Spironolactone= NAGMA
28
Q

SLE is associated with which glomerular pathologies?

A

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
Q

henoch shonloein

what is it

how does it present

which glomerular disease is it associated with

A

=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
Q

which glomerular diseases will present with decreased complement levels

A

PSGN (post strep GN), DPGN, MPGN

31
Q

compare and contrast membranous nephropathy and MPGN (membrano-proliferative GM)

A

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
Q

subepithelial humps (of IC deposits) is pathognomonic for which glomerular ds?

A

acute post-strep glomerulonephritis

seen on EM

33
Q

which glomerular diseases are TIII hypersensitivity (which means?)?

which are TII?

A

TIII hypersensitivity= immune complex deposition (IC activate complement)

=PSGN, RPGN type 2

TII= direct AB

=RPGN Type 1 = anti-type 4 collagen Ab

34
Q

describe the infection after which PSGN wll develop

A

post group A strep (pyogenes) = pharyngitis or impetigo (skin)

35
Q

describe the immunflourescent findings in RPGN

A

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
Q

kidney stones: Ca oxalate

  • crystal type
  • causes
  • trx
A

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
Q

Ca phosphate kidney stones

  • crystal type
  • causes
  • trx
A

wedge-shaped

come out w high pH

trx= low-Na diet, thiazides

38
Q

ammonium-magnesium-phosphate kidney stones

  • crystal type
  • causes
  • trx
A

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
Q

uric acid kidney stone

  • crystal type
  • causes
  • trx
A

=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
Q

cystine kidney stones

  • crystal type
  • causes
  • trx
A

=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
Q

what is the most common CA of the kidney

  • pathophys
  • histo
  • clin present
  • trx
A

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: rcc= 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
Q

renal angiomyolipomas are associated with what syndrome

A

tuberous sclerosis

= AD

=cortical subepindymal hamartomas, renal angiomyolipomas (benign, kids), cardiac rhabdomyomas, ash-leaf patches

43
Q

nephroblastoma

  • cin presentation
  • path
  • associated syndromes
A

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
Q

what is the most common tumor of the bladder

pathophys?

clin?

causes?

trx?

A

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 bladder

causes: Pee SAC

Phenacetin, Smoking, Aniline dyes (hair), Cyclophosphamide

clin: old WM, smoker w painless hematura and no casts in the urine

trx= platinum based chemo= cisplatin and caboplatin

45
Q

what are the risk factors for squamous cell carcinoma of the bladder

A

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
Q

what are the sx of uremia

A

anorexia

n/v

platelet dysfunction –> bleed

uremic pericarditis

asterixis

encephalitis (confusion

47
Q

what drugs will lead to decreased renal function

A

loop diuretics + thiazides + K+ saring drugs

via x conentration ability

ACE-I = vasodilate efferent arterioles = dec GFR

NSAIDS= x prostoglandins = dec GFR

48
Q

pathphys of renal osteodystrophy

A

chronic renal failure –> 2° hyperPTH –>

bone pain+path frx+osteitis fibrocystica = renal osteodystrophy

**osteitis fibrocystica = bone cysts, brown tymors

49
Q

how does acute interstitial nephritis present

path?

causes?

trx?

A

“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
Q

acute tubular necrosis

causes

stages

labs

clin

A

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
Q

when does diffuse cortical necrosis of the kidney take place

A

w acute generalized infarction of both kidneys, oten due to vasospasm and DIC

∝ w obstetric catastrophies or septic shock

52
Q

renal papillary necrosis

pathophys

associations

clin?

A

= 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
Q

what renal pathologies can be caused by NSAID overuse/OD

A

chronic insterstitial nephritis (i.e. chronic pain)

ATN (ischemia)

membranous GN

papillaru necrosis

First Aid, UWorld sets (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions