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Jenna's Shit List > Shit - Renal > Flashcards

Shit - Renal Flashcards

1
Q

Kidney development

A

Pronephros –> mesonephros (vas def) –> gives off ureteric bud (CD-ureter) –> interacts with metanephric messenchyme/blasthema –>(glomerulus-DCT)

*abn interaction –> Multicystic dysplastic kidney (unilat, congenital)*

*if man is missing one vas def, he may be missing that kidney*

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2
Q

MC site of hydronephrosis in fetus

A

uretero-pelvic junction (last to canalize)

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3
Q

COD potters

A

Lung hypoplasia

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4
Q

Horseshoe kidney:

  • point it get stuck
  • associations
A

IMA.

Assoc: uretero-pelvic obstuction (hydronephrosis), renal stones, infections, chromosomal aneuploidy (13, 18, 21, XO), rarely renal cancer

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5
Q

JG cell location

A

between afferent arteriole and macula dense (DCT)

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6
Q

%s of body weight:

  • TBWater
  • ECF - plasma
  • ICF - RBC vol
A

TBW = 60%

ECF = 20% (inulin); 75% interstitial fluid, 25% plasma (albumin)

ICF = 40%; 10% is RBCs

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7
Q

size barrier

A

fenestrated endothelium

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8
Q

charge barrier

A

GBM - lost in nephOTIC syndromes

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9
Q

Estimating GFR;

normal value

A

**Filtered, but NOT resorbed or secreted**

Estimate = creatinine (slight overestimate)

Better = inulin

GFR = 120ml/min

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10
Q

Estimating eRPF

Using eRPF to find RBF

A

PAH clearance because filtered AND SECRETED so all of it excreted

RPF = RBF * plasma%

RPF = RBF * (1-hct%)

RBF = RPF/(1-hct%)

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11
Q

FF

A

FF = GFR/RPF

FF = 20%

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12
Q

Filtered load

A

FL = GFR * plasma []

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13
Q

Excretion =

A

excretion = filtered + secreted - resorbed

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14
Q

Pregnancy and kidneys

A

Normal pregnancy can decrease PCT resorption of glucose and amino acids –> out in urine

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15
Q

glucose and kidney: threshold and Tm

A

Threshold = 200mg/dL

Tm = 375mg/dL

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16
Q

Hartnup’s =

A

NEUTRAL amino acid transporter problem.

In GIT and PCT

s/s = pellagra (no Tryp for B3) Rx = B3 supplements and high protein diet

DDX = fanconi anemia, which is ALL AA (i.e. proline)

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17
Q

contraction alkalosis

A

When volume low (contracted), ATII stimulates Na//H+, leading to volume restoration with Na+ but loss of H+ leading to alkalosis

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18
Q

Major role of PCT

A
  • Resorb glucose/AA/PO4 (blocked by PTH)
  • exchange with H+ (stim by AT-II)
  • excrete bases i.e. NH3 (for Cl-)
  • ISOtonic absorption
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19
Q

tAL

A

NKCC-T

MG and Ca

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20
Q

DCT

A

NaCl-T Ca//Na @ BL to resorb Ca (stim by PTH)

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21
Q

PTH locations and actions in kidney

A

Inhibits:

  • PCT = Na/PO4

Activates:

  • DCT = Na//Ca (@BL)
  • PCT = 1-aOHase activity
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22
Q

CD

A

Principal:

  • ADH @ AQP
  • Aldosterone @ Na, K, Na//K

A-intercalated:

  • H+ ATPase
  • HCO3//Cl- @ BL
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23
Q

Fanconi syndrome: Where Lost S/s Causes

A

Where: PCT

Lost: all AA, glucose, HCO3-, PO4

S/s: prox. renal tubular metabolic ACIDosis

Causes: wilsons, tyrosinemia, glycogen storage diseases, expired tetracyclins, tenofovir, multiple myelomas, ischemia, lead poisoning

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24
Q

Bartters

A

Loop NKCC

Hypokalemia –> resorbed in CD –> exchange for H+ –> metabolic alkalosis Hypercalciuria

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25
Q

Gitelman

A

DCT hypokalemia –> metabolic alkalosis

Hypo Mg

Hypocalciuria (Ca absorbed)

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26
Q

Liddle

A

GAIN OF FUNCTION, AD

HTN, met. alk., hypo K, low aldosterone and renin

Rx = amiloride (to block ENaC)

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27
Q

Syndrome of apparent mineralocorticoid excess

A

Really just lacking 11-beta-HSD, so can’t turn cortisol to cortisone, so cortisol acts on mineralocorticoid receptors (aldosterone-like so like liddle’s)

Can be acquired from liquorice (glycyrrhetic acid)

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28
Q

ADH triggers and role

A

trigger = increased osmolarity and low BV

role = osmolarity (via AQP)

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29
Q

Aldosterone triggers and role

A

Trigger = low BV (via ATII) and high K+

roles = ECF volume and Na+ content (via ENaC, K+, K+//H+, H+ ATPase

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30
Q

Macula densa pathway (increase osm)

A

high NaCl to macula densa (DCT) –> cells swell –> release adenosine –>

1) A1-R: afferent VC
2) A2-R: efferent VD
3) decreased JG release of renin

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31
Q

Renin release signalled by:

A

1) beta1 activation (SNS)
2) decreased RAP
3) decreased NaCl to macula densa

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32
Q

AT-II mechanism

A

VC efferent –> decrease RPF and increase GFR –> increase FF (of Na+) –> so more Na+ must be resorbed later on –> resorbed with water –> increase BV/BP

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33
Q

ANP: - released by/why - mechanism

A

Release from atria via increased blood volume

Aff: cGMP –> smooth muscle relaxation –> increased GFR and RPF together, so NO increase in FF

DCT: blocks Na/Cl transporter -> lose Na+ so overall loss of Na+ and H2O

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34
Q

Causes of Hyperkalemia

A

Digoxin: block Na/K ATPase

Hyperosmolarity: K+ is high outside

Cell lysis (crush, rhabdo, cancer): leaks from cells

Acidosis

Beta-blockers: prevent insulin release

High blood sugar: low insulin

*insulin causes K+ to go into cells via Na/K ATPase activation*

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35
Q

Causes of hypokalemia

A

hypoosmolarity: less K+ outside

alkalosis

beta agonists (no decreasing insulin so insulin high)

High insulin (increases Na/K ATPase –> K+ into cells)

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36
Q

Hypertension with HYPOkalemia causes:

A

1’ hyperaldosteronism: high aldost, low renin

2’ hyperaldosteronism: high renin causing high aldosterone. Via RAStenosis, renin tumour, diuretic abuse

low renin and aldosterone: other things acting as mineralocorticoids i.e. CAH, deoxycorticosterone tumour, cushings, exogenous mineralocorticoids

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37
Q

Electrolyte Disturbances

A
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38
Q

Winter’s Formula

A

PCO2 = 1.5 [HCO3] + 8

if real PCO2 is within +/- 2 of the predicted CO2, then you have a pure metabolic acidosis

if it is outside +/-2, then it is a mixed acid/base disorder

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39
Q

Normal anion gap (8−12 mEq/L)

A

HARD-ASS:
Hyperalimentation
Addison disease

Renal tubular acidosis

Diarrhea

Acetazolamide

Spironolactone

Saline infusion

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40
Q

high anion gap (>12)

A

MUDPILES:
Methanol (formic acid)

Uremia
Diabetic ketoacidosis

Propylene glycol
Iron tablets or Isoniazid

Lactic acidosis
Ethylene glycol (oxalic acid)

Salicylates (late)

41
Q

increased pH favours what stones?

A

Anyhting with phosphate:

  • CaPO4
  • ammonium magnesium phosptate (struvite)
42
Q

Amphotericin B major toxicity

A

Hypo Mg and K

Causes type I (distal) renal tubular acidosis

(also can make EPO, arrythmyas, normocytic anemia)

43
Q

Type I renal tubular acidosis (distal)

A

CD

Alpha-intercalated cant secrete H+ → retention of H+

→ no K//H exchange → K+ lost in urine

→ acidosis causes bone resorption

→ urine is basic >5.5

→ 5.5 + Ca and PO4 –> CaP stones

Causes:

amphoteraxcin B, analgesic nephropathy, urinary tract obstructions

pH > 5.5

44
Q

Proximal/Type 2 renal tubular acidosis

A

Defective PCT HCO3- absorption @BL –> cant resorb Na with it (Na/HCO3 cotransport) –> Na gets resorbed at CD, so K+ lost

Metabolic acidosis from HCO3- loss

Hypokalemia from Na CD resorption

K+ tried to get resorbed in exchange for H+ @ alpha-intercalated (K//H) –> acidifies urine

Causes: Fanconi syndrome, CAH inhibitors (acetazolamide)

pH < 5.5

45
Q

Hyperkalemic (type 4) renal tubular acidosis

A

Hypoaldosteronism –> no Na resorption in CD in exchange for K+ –> hyperkalemia –> high K+ to less K+//H+ activity –> cant secrete acid –> acidemia

  • K+ also decreases PCT NH3 synthesis and thus decreases urine NH4+ levels –> acidic urine

Causes:

  • hypoaldosteronism (ACE-I, ARB, NSAIDS, DM hyporeninism, adrnal insufficiency, heparin, cyclospirin)
  • Aldosterone resistance (K+ sparing diuretics, obstructoin nephropathy, TMP/SMX)

pH

46
Q

Lumpy bumpy:

  • disease; deposits; where; EM
A

PSGN

IgG, IgM, C3

GBM and messangium

EM = sub-epithelial

47
Q

Crescents on LM:

Name; content; types; diseases

A

Crescentic/RPGN

Fibrin, parietal cell layer, monocytes, macrophages, plasma proteins (C3b)

I = linear

II = granular

III = pauci

Type I: Goodpastures (II)

Type III: Wegners (granulomatosis with polyangiitis) - c-ANCA

Type III: microscopic polyangiitis or churg strauss - p-ANCA

48
Q

Nephotic syndrome post illness:

  • few days =
  • few eeks =
A
  • days = IgA nephropathy [mucosal infection i.e. GIT or throat]
  • weeks = PSGN [impitigo or pharyngitis]
49
Q

IgA nephropathy:

  • deposits (what and where)
  • timeline
A

Messangial proliferation becasue of IgA deposits

Episodic; few days post mucosal infection

50
Q

Subepithelial:

GBM:

Subendothelial:

A

Subepithelial: PSGN

GBM: Type II MPGN (C3 nephirtic factor)

Subendothelial: Type I MPGN (tram tracks; Hep B or C))

51
Q

Wire-looping capilaries: disease

A

DPGN, via SLE or MPGN

52
Q

Blood changes in nephrotic syndrome

A
  • Hypercoagulable ( via AT-III loss in urine)
  • Hyperlipidemia (liver makes Apolipoproteins to refill blod proteins)
  • infections (loss of Igs)
53
Q

FSGS:

  • deposits
  • Causes
A

IgM, C3, C1 deposits with podocyte effacement

Causs: HIV, sickle, heroin, obesity, INF, CKD

54
Q

minimal change disease causes

A

Idiopathic, infection, atopic disorders,immunizatoins, immune stimulus (bee sting), rarely lymphoma

55
Q

MCC of nephrotic syndrome: kids, adults (by race)

A

Kids = MCD

Black/Hispanic = FSGS

White = Membranous nephropathy

56
Q

Spike and dome:

disease; histo; causes

A

Membranous glomerulonephropathy

capillary and GBM thickening

Nephotic SLE, anti-PLA2, NSAIDs, penicillamine, HBV, HCV, solid tumours

57
Q

Eosinophilic casts

A

Multiple myelomas, nephrotic amyloidosis

(tamm-horsefall protein)

58
Q

MC kidney stone presentation and type

Rx

A

Hypercaciuria with normocalcemia

Ca-oxalate

Rx = thiazides, hydration, B6 (decreases oxalate production), cirtate (binds Ca)

59
Q

Stone shapes:

Dumbbell/envelope

Coffin

Rhomboid

Hexagon

A

Dumbbell/envelope - Ca-oxalate

Coffin - struvite

Rhomboid - uric acid

Hexagon - cystein

60
Q

Urease +ve organisms

A

(Smelly Puke CHUNKS)

Staph saprophiticus

Proteus

Cryptococcus

H. pylori

Ureaplasma

Nocardia

Klebsiella

Staph epidemidis

61
Q

Radioluscent stone

A

Uric acid

62
Q

Kids with stones: MCC, test

A

Cystine (PCT doesnt resorb via dibasica AA transporter problem; AA COLA not absorbed

*could also be leukemia rx or malabsorption Ca-ox)

Test = sodium cyanid nitroprusside (turns red/purple)

63
Q

When does serum creatinine increase with hydronephrosis

A

Bilateral or unilateral with only one kidney

64
Q

RF RCC

A

Smoking, obesity, male, 50-70, VHL

65
Q

RCC paraneoplastics

A

EPO, ACTH, PTHrp

66
Q

RCC mets and complications

Rx

A

MEts = lung and bone

Compl = block left renal vein = left varicocele

Rx = IMMUNOtherapy (resistant to chemo and radiation)

67
Q

Origins:

RCC

Oncocytoma

Difference in histo:

A

Rcc = PCT

Oncocytoma = CD

Histo:

  • RCC = pale polygonal
  • Onco = eosinophilic, lots of mitochondria
68
Q

Beckwith Widemann

A

Wilms tumour

Organomegally

macroglossia

hypoglycemia

hemi-hypertrophy

hepatoblastoma

69
Q

WAGR

A

Wilms

Aniridia

Genitourinary malformation

Retardation

70
Q

angiomyolipoma

A

Tuberour sclerosis

HAMARTOMAS: Hamartomas in CNS and skin; Angiofibromas; Mitral regurgitation; Ash-leaf spots ; cardiac Rhabdomyoma; (Tuberous sclerosis); autosomal dOminant; Mental retardation (intellectual disability); renal Angiomyolipoma; Seizures, Shagreen patches.􏰂incidence of subependymal astrocytomas and ungual fibromas.

71
Q

bladder cancer: glands on histo

A

Adeno-CA

From malformations i.e. urachal remnants, bladder exstrophy

72
Q

RF for urothelial (transitional) CA

A

Phenacetin, Smoking, Analine dyes, cyclophosphamide, rubber textiles, leather

73
Q

smoking and uriniary cancers:

A

RCC

Urothelial CA

Squamous cell CA bladder

74
Q

Striated cortical parencymal enhancements

A

Acute pyelonephritis

75
Q

Acute pyeloneohritis: cell infiltrate; location affected; location spared

A

Neutrophils

Affected = cortex (interstitium and tubular lumen)

Spares = glomerulus and vessels

76
Q

thyroidizatoin of kidneys: cause

A

Chronic pyelonephritis; actually eosinophilic casts

77
Q

Drug-induced nephritis/TIN

  • inflammatory cell type
  • timeline with causes
  • S/s
  • complication
A
  • Eosinophils
  • 1-2 weeks = penicillins, diuretics, PPI, sulfonamides, rifampin
  • few months = NSAIDs
  • S/s = fever, maculopapular rash, hematuria, CVA
  • complication is PCT cell damage leading to: 1) proteinuria for LC, AA, B2-micoglobulin, retinol-BP; 2) PCT cells into interstitium –> foreign body granuloma
78
Q

Shock or abrupto placentae: renal concequence; mechanism

A

Diffuse cortical necrosis of both kidneys

Via vasospasm and DIC

79
Q

Ischemic ATN:

Area affected

A

Area = PCT and Thick AL

80
Q

Nephrotoxic ATN:

Areas affected:

Causes:

A

Areas = PCT

Causes: aminoglycosides, radiocontrast, lead, cisplatin, crush injury, hemoglobinuria

81
Q

Renal papillary recrosis causes

A

ALL via ISCHEMIA:

sickle or trait

analgesics (NSAIDS)

Acute pyelonephritis

DM

*also recent infection or immune stimulus*

82
Q

Acute renal failure: causes and chart

A

Prerenal: decreased RBF

Renal: ATN, ischemia/toxins (AIN), RPGN - tubule obstruction

Post-renal: bilateral outflow obstruction

83
Q

Uremia s/s

A

Urea crystal skin deposits

encephalopathy

asterixis

nausea and anorexia

functional hypothyroidism

pericarditis/tamponade

platelet dysfunction (bleeding)

84
Q

Associatoins with ADPKD

A

Berry aneurism

hepatic cysts

MVP

pancreatic cysts

85
Q

ADPKD genes

A

85% = PDK1 = chrom 16

15% = PKD 2 = Chrom 4

86
Q

ARPDK associations

A

congenital hepatic fibrosis –> portal hypertension

systemic HTN

renal insufficiency

87
Q

ADPKD and ARPKD at birth

A

AD = microscopic cysts (but still there)

AR = >1cm

88
Q

Diuretic for altitude sickness with mechanism

A

Acetazolamide (carbonic anhydrase inhibitor)

Decrease oxygen → hyperventilation → decreased CO2 → respiratory alkalosis.

Prevent with drug to induce metabolic acidosis

89
Q

NSAID + specific diuretic

A

Loops; inhibit their PDE stimulation effects

(so lost their afferent dilation effects)

90
Q

Diuretic for quick (days) relief of HF

A

Loops

91
Q

Loop drug interactions:

A

Ototoxicity: increases with aminoglycosides

Lithium toxicity: resorb with Na in PCT, increased when you’re losing Na+ elsewhere in the tubules

Digoxin toxicity: via kypokalemia from Na//K later on in CD

92
Q

Loop AE:

A

Ototoxicity

Nephrotoxicity (AIN)

Sulfa (use ethacrynic acid as substitute loop)

Gout

93
Q

Thiazdize AE

A

Hyper GLUC + sulfa

(glycemia, lipidemia, uricemia, calcemia)

94
Q

—| ENaC

A

Triamterene

Amiloride

95
Q

Paradoxical aciduria: explanation and causes

A

Patient is alkalotic, but also has low K+, so in CD when Na+ comes in H+ is secreted for exchange (instead of K+)

So there is acid secretion when you should be saving it

Causes: loops and thiazides –> hypo Na and K

96
Q

ACE-I contraindications

A

Pregnancy - renal malformations

Hereditary angioedema (prevent bradykinin breakdown)

Bilateral renal artery stenosis (need ANG-II to maintain GRF)

97
Q

aliskiren MOA

A

renin inhibitor

98
Q

Diuretics with sulfa

A

Acetazolamide

Loops: furosemide, turosemide, bumetanide

Thiazides

Jenna's Shit List (23 decks)

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