Shit - Renal Flashcards
(98 cards)
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*
2
Q
MC site of hydronephrosis in fetus
A
uretero-pelvic junction (last to canalize)
3
Q
COD potters
A
Lung hypoplasia
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
5
Q
JG cell location
A
between afferent arteriole and macula dense (DCT)
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
7
Q
size barrier
A
fenestrated endothelium
8
Q
charge barrier
A
GBM - lost in nephOTIC syndromes
9
Q
Estimating GFR;
normal value
A
**Filtered, but NOT resorbed or secreted**
Estimate = creatinine (slight overestimate)
Better = inulin
GFR = 120ml/min
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%)
11
Q
FF
A
FF = GFR/RPF
FF = 20%
12
Q
Filtered load
A
FL = GFR * plasma []
13
Q
Excretion =
A
excretion = filtered + secreted - resorbed
14
Q
Pregnancy and kidneys
A
Normal pregnancy can decrease PCT resorption of glucose and amino acids –> out in urine
15
Q
glucose and kidney: threshold and Tm
A
Threshold = 200mg/dL
Tm = 375mg/dL
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)
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
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
19
Q
tAL
A
NKCC-T
MG and Ca
20
Q
DCT
A
NaCl-T Ca//Na @ BL to resorb Ca (stim by PTH)
21
Q
PTH locations and actions in kidney
A
Inhibits:
- PCT = Na/PO4
Activates:
- DCT = Na//Ca (@BL)
- PCT = 1-aOHase activity
22
Q
CD
A
Principal:
- ADH @ AQP
- Aldosterone @ Na, K, Na//K
A-intercalated:
- H+ ATPase
- HCO3//Cl- @ BL
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
24
Q
Bartters
A
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
