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Flashcards in Shit - Renal Deck (98):
1

Kidney development

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*

2

MC site of hydronephrosis in fetus

uretero-pelvic junction (last to canalize)

3

COD potters

Lung hypoplasia

4

Horseshoe kidney:

- point it get stuck

- associations

IMA.

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

5

JG cell location

between afferent arteriole and macula dense (DCT)

6

%s of body weight:

- TBWater

- ECF - plasma

- ICF - RBC vol

TBW = 60%

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

ICF = 40%; 10% is RBCs

7

size barrier

fenestrated endothelium

8

charge barrier

GBM - lost in nephOTIC syndromes

9

Estimating GFR;

normal value

**Filtered, but NOT resorbed or secreted**

Estimate = creatinine (slight overestimate)

Better = inulin

GFR = 120ml/min

10

Estimating eRPF

Using eRPF to find RBF

PAH clearance because filtered AND SECRETED so all of it excreted

 

RPF = RBF * plasma%

RPF = RBF * (1-hct%)

RBF = RPF/(1-hct%)

11

FF

FF = GFR/RPF

FF = 20%

12

Filtered load

FL = GFR * plasma [ ]

13

Excretion =

excretion = filtered + secreted - resorbed

14

Pregnancy and kidneys

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

15

glucose and kidney: threshold and Tm

Threshold = 200mg/dL

Tm = 375mg/dL

16

Hartnup's =

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)

 

17

contraction alkalosis

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

18

Major role of PCT

- Resorb glucose/AA/PO4 (blocked by PTH)

- exchange with H+ (stim by AT-II)

- excrete bases i.e. NH3 (for Cl-)

- ISOtonic absorption

19

tAL

NKCC-T

MG and Ca

20

DCT

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

21

PTH locations and actions in kidney

Inhibits:

- PCT = Na/PO4

 

Activates:

- DCT = Na//Ca (@BL)

- PCT = 1-aOHase activity

22

CD

Principal:

- ADH @ AQP

- Aldosterone @ Na, K, Na//K

 

A-intercalated:

- H+ ATPase

- HCO3//Cl- @ BL

23

Fanconi syndrome: Where Lost S/s Causes

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

24

Bartters

Loop NKCC

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

25

Gitelman

DCT hypokalemia --> metabolic alkalosis

Hypo Mg

Hypocalciuria (Ca absorbed)

26

Liddle

GAIN OF FUNCTION, AD

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

Rx = amiloride (to block ENaC)

27

Syndrome of apparent mineralocorticoid excess

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)

28

ADH triggers and role

trigger = increased osmolarity and low BV

role = osmolarity (via AQP)

29

Aldosterone triggers and role

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

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

30

Macula densa pathway (increase osm)

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

31

Renin release signalled by:

1) beta1 activation (SNS)

2) decreased RAP

3) decreased NaCl to macula densa

32

AT-II mechanism

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

33

ANP: - released by/why - mechanism

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

34

Causes of Hyperkalemia

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*

35

Causes of hypokalemia

hypoosmolarity: less K+ outside

alkalosis

beta agonists (no decreasing insulin so insulin high)

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

36

Hypertension with HYPOkalemia causes:

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

 

37

Electrolyte Disturbances

38

Winter's Formula

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

39

Normal anion gap (8−12 mEq/L)

 HARD-ASS:
Hyperalimentation
Addison disease

Renal tubular acidosis

Diarrhea

Acetazolamide

Spironolactone

Saline infusion 

40

high anion gap (>12)

MUDPILES:
Methanol (formic acid)

Uremia
Diabetic ketoacidosis

Propylene glycol
Iron tablets or Isoniazid

Lactic acidosis
Ethylene glycol (oxalic acid)

Salicylates (late) 

41

increased pH favours what stones?

Anyhting with phosphate:

- CaPO4

- ammonium magnesium phosptate (struvite)

42

Amphotericin B major toxicity

Hypo Mg and K

Causes type I (distal) renal tubular acidosis

 

(also can make EPO, arrythmyas, normocytic anemia)

43

Type I renal tubular acidosis (distal)

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

Proximal/Type 2 renal tubular acidosis

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

Hyperkalemic (type 4) renal tubular acidosis

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

Lumpy bumpy:

- disease; deposits; where; EM

PSGN

IgG, IgM, C3

GBM and messangium

EM = sub-epithelial

47

Crescents on LM:

Name; content; types; diseases

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

Nephotic syndrome post illness:

- few days = 

- few eeks = 

- days = IgA nephropathy [mucosal infection i.e. GIT or throat]

 

- weeks = PSGN [impitigo or pharyngitis]

49

IgA nephropathy:

- deposits (what and where)

- timeline

Messangial proliferation becasue of IgA deposits

 

Episodic; few days post mucosal infection

50

Subepithelial:

GBM:

Subendothelial:

Subepithelial: PSGN

GBM: Type II MPGN (C3 nephirtic factor)

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

51

Wire-looping capilaries: disease

DPGN, via SLE or MPGN

52

Blood changes in nephrotic syndrome

- Hypercoagulable ( via AT-III loss in urine)

- Hyperlipidemia (liver makes Apolipoproteins to refill blod proteins)

- infections  (loss of Igs)

53

FSGS:

- deposits

- Causes

IgM, C3, C1 deposits with podocyte effacement

 

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

54

minimal change disease causes

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

55

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

Kids = MCD

Black/Hispanic = FSGS

White = Membranous nephropathy

56

Spike and dome:

disease; histo; causes

Membranous glomerulonephropathy

 

capillary and GBM thickening

 

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

57

Eosinophilic casts

Multiple myelomas, nephrotic amyloidosis

(tamm-horsefall protein)

58

MC kidney stone presentation and type

Rx

Hypercaciuria with normocalcemia

Ca-oxalate

 

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

59

Stone shapes:

Dumbbell/envelope

Coffin

Rhomboid

Hexagon

Dumbbell/envelope - Ca-oxalate

Coffin - struvite

Rhomboid - uric acid

Hexagon - cystein

60

Urease +ve organisms

(Smelly Puke CHUNKS)

Staph saprophiticus

Proteus

Cryptococcus

H. pylori

Ureaplasma

Nocardia

Klebsiella

Staph epidemidis 

61

Radioluscent stone

Uric acid

62

Kids with stones: MCC, test

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

When does serum creatinine increase with hydronephrosis

Bilateral or unilateral with only one kidney

64

RF RCC

Smoking, obesity, male, 50-70, VHL

65

RCC paraneoplastics

EPO, ACTH, PTHrp

66

RCC mets and complications

Rx

MEts = lung and bone

Compl = block left renal vein = left varicocele 

Rx = IMMUNOtherapy (resistant to chemo and radiation)

67

Origins:

RCC

Oncocytoma

 

Difference in histo:

Rcc = PCT

Oncocytoma = CD

 

Histo: 

- RCC = pale polygonal

- Onco = eosinophilic, lots of mitochondria

68

Beckwith Widemann

Wilms tumour

Organomegally

macroglossia

hypoglycemia

hemi-hypertrophy

hepatoblastoma

69

WAGR

Wilms

Aniridia

Genitourinary malformation

Retardation

70

angiomyolipoma

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

bladder cancer: glands on histo

Adeno-CA

From malformations i.e. urachal remnants, bladder exstrophy

72

RF for urothelial (transitional) CA

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

73

smoking and uriniary cancers:

RCC

Urothelial CA

Squamous cell CA bladder

74

Striated cortical parencymal enhancements

Acute pyelonephritis

75

Acute pyeloneohritis: cell infiltrate; location affected; location spared

Neutrophils

Affected = cortex (interstitium and tubular lumen)

Spares = glomerulus and vessels

76

thyroidizatoin of kidneys: cause

Chronic pyelonephritis; actually eosinophilic casts

77

Drug-induced nephritis/TIN

- inflammatory cell type

- timeline with causes

- S/s

- complication

- 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

Shock or abrupto placentae: renal concequence; mechanism

Diffuse cortical necrosis of both kidneys

 

Via vasospasm and DIC

79

Ischemic ATN:

Area affected

 

Area = PCT and Thick AL

 

80

Nephrotoxic ATN:

Areas affected:

Causes:

Areas = PCT

 

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

81

Renal papillary recrosis causes

ALL via ISCHEMIA:

sickle or trait

analgesics (NSAIDS)

Acute pyelonephritis

DM

*also recent infection or immune stimulus*

82

Acute renal failure: causes and chart

Prerenal: decreased RBF

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

Post-renal: bilateral outflow obstruction

83

Uremia s/s

Urea crystal skin deposits

encephalopathy

asterixis

nausea and anorexia

functional hypothyroidism

pericarditis/tamponade

platelet dysfunction (bleeding)

84

Associatoins with ADPKD

Berry aneurism

hepatic cysts

MVP

pancreatic cysts

85

ADPKD genes

85% = PDK1 = chrom 16

15% = PKD 2 = Chrom 4

86

ARPDK associations

congenital hepatic fibrosis --> portal hypertension

systemic HTN

renal insufficiency

87

ADPKD and ARPKD at birth

AD = microscopic cysts (but still there)

AR = >1cm

88

Diuretic for altitude sickness with mechanism

Acetazolamide (carbonic anhydrase inhibitor)

 

Decrease oxygen → hyperventilation → decreased CO2 → respiratory alkalosis.

Prevent with drug to induce metabolic acidosis

89

NSAID + specific diuretic

Loops; inhibit their PDE stimulation effects

(so lost their afferent dilation effects)

90

Diuretic for quick (days) relief of HF

Loops

91

Loop drug interactions:

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

Loop AE:

Ototoxicity

Nephrotoxicity (AIN)

Sulfa (use ethacrynic acid as substitute loop)

Gout 

93

Thiazdize AE

Hyper GLUC + sulfa

(glycemia, lipidemia, uricemia, calcemia)

94

—| ENaC

Triamterene

Amiloride

95

Paradoxical aciduria: explanation and causes

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

ACE-I contraindications

Pregnancy - renal malformations

Hereditary angioedema (prevent bradykinin breakdown)

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

97

aliskiren MOA

renin inhibitor

98

Diuretics with sulfa

Acetazolamide

Loops: furosemide, turosemide, bumetanide

Thiazides