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Step 1 > Renal > Flashcards

Renal Flashcards

1
Q

ureters and uterine arteries

A

water under the bridge
ureters pass under and behind the uterine arteries (and veins) and the vas deferens

gyn procedures may damage ureter

ureter starts anterior to the internal iliac (in the true pelvis) and then courses posterior to the uterine artery

note: gonadal arteries come off the aorta - below the level of the renal arteries
- first posterior to the gonadal artery
- then medial

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2
Q

JG apparatus

A

mesangial cells + JG cells (modified smooth muscle cells of afferent arteriole) + macula densa (at tip of thick ascending limb)

macula densa - senses NaCl concentration of filtrate

  • decreased in NaCl concentration = not enough fluid was filtered –>
    1) decreases resistance to blood flow in afferent arterioles –> returns GFR to normal
    2) increases renin release
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3
Q

macula densa

A

senses decreased NaCl delivery to DCT –> adenosine release –> vasoconstriction

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4
Q

calcitriol

A

produced by the PCT cells

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5
Q

Cr and eGFR

A

Cr is freely filtered - also secreted to a small extent

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6
Q

afferent arteriole

A

juxtaglomerular cells

more a1 receptors on afferent arteriole

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7
Q

ang 2

A

renin - released in response to DEcreased volume (so decreased BP, decreased Na delivery to macula densa, increased SNS/b1 tone)
- b-blockers (and clonidine) decrease renin secretion

vasoconstricts - efferent and afferent arterioles, low levels increase GFR, high levels decrease GFR
-ang2 protects GFR during vasoconstriction - because efferent arteriole constricts more

stimulates Na/H exchange in PCT - contraction alkalosis

pressor effects - vasoconstricts by acting on AT1 receptors on vascular smooth muscle
-affects baroreceptor function so reflex bradycardia does not occur

aldosterone secretion

stimulates hypothalamus + ADH secretion

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8
Q

PGs

A

E2 and I2 are produced by kidneys
vasodilation of afferent and efferent

activated by stimuli that activate SNS and RAAS - modulate vasoconstriction, which would otherwise lead to renal failure

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9
Q

dopamine

A

acts like a rest and digest hormone at low levels

  • dilates cerebral, cardiac, splanchnic, and renal arterioles
  • constricts skeletal muscle and cutaneous arterioles

can be administered during hemorrhage

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10
Q

adenosine

A

vasoconstricts

ATP, thromboxane also vasoconstricts

other vasoconstrictors: endothelin

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11
Q

Hartnup disease

A

AR - inability to reabsorb tryptophan –> niacin deficiency
- pellagra-like symptoms = 4Ds - diarrhea, dementia (and hallucinations), dermatitis (C3/C4 broad collar rash), hyperpigmentation of sun-exposed limbs, death

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12
Q

urea handling

A

passive reabsorption (with water)

thin descending loop - urea secreted (into the lumen)

  • UT1 transporter is activated by ADH - inserted into inner medullary cortical ducts
  • corticocapillary osmotic gradient increases in the presence of ADH

thick ascending onwards - IMPERMEABLE to urea

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13
Q

morphine

A

organic base

organic acids and bases are excreted in proximal tubule
-treat aspirin OD by alkalinizing urine

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14
Q

resorptive functions of kidney

A

early PCT - NaHCO3- (glucose, aas, acids/etc.), lumen has negative charge (loss of Na+, glucose)
-phosphate, Ca2+

late PCT - NaCl, paracellular Cl- transport, lumen negative (Na+ follows into blood)

thin descending limb - permeable to water and urea (water moves out of tubule, solutes move into tubule)

thin ascending limb - permeable to NaCl, impermeable to water

thick ascending limb - impermeable to water, Na/K/2Cl transporter

  • K+ and Cl- diffuse in blood, some K+ leaks back into lumen (lumen positive)
  • lumen postive!! - drives Ca2+ and Mg2+ reabsorption
  • loop diuretics bind at Cl- site

early DCT - impermeable to water, NaCl transporter

  • thiazides act here
  • there is also an Na/Ca antiporter on the BL membrane - activated by PTH

late DCT and collecting ducts

  • principal cells (Na+ reabsorption and K+ secretion)
  • a-intercalated cells (K+ reabsorption and H+ secretion)
  • aldosterone and ADH (controls permeability of principal cells)

other things:

  • SNS - vasoconstricts afferent arterioles, increased proximal tubule reabsorption
  • ANP (acts via cGMP) - respond to increased volume
    - vasodil and decreased Na+ reabsorption in late distal tubules and collecting ducts
    - dilates afferent, constricts efferent, contributes to aldosterone escape mechanism
  • BNP - responds to increased tension, good negative predictive value for heart failure
    - nesiritide is a BNP analog - used in acute decompensated heart failure
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15
Q

PTH

A

inhibits! Na-phosphate reabsorption
-binds to BL Gs-adenyl cyclase receptor

hallmarks of PTH action - urinary cAMP (travels through luminal channel) and phosphaturia

also decreases reabsorption of bicarbonate

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16
Q

K sparing diuretic

A

dont promote the excretion of K into urine

K- sparing diuretics block all functions of aldosterone
spironolactone - aldosterone antagonist, prevent aldosterone entry into nucleus
amiloride, triamterene - block eNaC

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17
Q

hypokalemia

A

K+ sets resting membrane potential

hypokalemia - insulin, b2 agonists, a antagonists, METABOLIC alkalosis

hyperkalemia - … hyperosmolarity

  • plasma osm > cell osm
  • -> water shifts out of cell and into plasma
  • now, cell K+ concentration has increased significanlty
  • -> K+ moves down its concentration gradient ==> hyperkalemia (of plasma)

thiazides and loop diuretics increase K+ secretion - why?

  • upstream inhibition of Na+ reabsorption + increased urine flow rate
  • more Na delivery to DCT and collecting ducts - drives Na/K exchange
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18
Q

Ca balance

A

99% contained in bone
40% bound to plasma proteins

PCT - Ca2+ transport follows Na+ transport, more Ca2+ absorption during volume contraction

thick ascending limb - paracellular absorption due to lumen positive potential
-loop diuretics inhibit Ca2+ reabsorption

early distal tubule - luminal Ca2+ channel, PTH increases Ca2+/Na2+ exchange – > PTH increases Ca2+ reabsorption
- thiazides increase Ca2+ reabsorption

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19
Q

phosphate balance

A

85% of phosphate contained in bone
phosphate in ECF is a buffer for H+ (phosphate = PO4,3-)

reabsorption in PCT and proximal straight tubule

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20
Q

when plasma osm increases

A

osmoreceptors in the anterior hypothalamus are stimulated

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21
Q

ADH functions

A

1) increases water perm of principal cells (V2 receptors)
2) increases activity of Na/K/Cl transporter in thick ascending limb
3) adds UT1 transporters to collecting ducts of inner medulla

demeclocycline - inhibits V2-ADH receptors

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22
Q

nephrogenic DI

A

treat with thiazides! - how?

1) inhibit Na/Cl transport in early DT
2) decreased Na+ reabsorption –> decreased ECF volume –> decreased GFR
3) decreased GFR causes increased reabsorption in proximal tubule

= less water filtered, more water reabsorbed

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23
Q

reflex bradycardia

A

decrease in heart rate when baroreceptors sense an increased blood pressure
- PSNS - vagus nerve releases Ach - binds M2 receptors –> bradycardia

safety mechanism so abnormal increases in blood pressure dont occur

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24
Q

acetazolamide

A

= sulfonAMIDE
used in urinary alkalinization, metabolic alkalosis/altitude sickness, and increased ICP (pseudotumor cerebri caused by vitamin A tox, glaucoma)

tox - hyperchloremic metabolic acidosis, NH3 tox

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25
Q

mannitol

A

osmotic diuretic - used in DKA, drug OD

tox - pulmonary edema because - it initially increases plasma oncotic pressure and thus VOLUME –> pulm edema

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26
Q

thiazides

A

tox - hypokalemic metabolic alkalosis, hyponatremia, hyperglycemia, HLD, hyperuricemia, hypercalcemia, sulfa allergy

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27
Q

loop diuretics

A

furosemide, bumetanide, ethacyrnic acid

tox- OH DANG

  • ototox, hypokalemia, dehydration, (sulfa) allergy, (interstitial nephritis), gout
  • ethacrynic acid - can cause hyperuricemia

side note - loops also stimulate PG release

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28
Q

ACEI

A

uses - HTN (prevents unfavorable heart remodeling), HF, proteinuria, diabetic nephropathy (decreases intraglomerular pressure, slows GBM thickening)

inhibition of ACE prevents inactivation of bradykinin

contraindicated in C1 esterase inhibitor deficiency –> angioedema

teratogen

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29
Q

ARB

A

blocks binding of ang2 to AT1 receptor

also a teratogen

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30
Q

aliskiren

A

direct renin inhibitor

tox of ACEi, ARB, and alikiren = hyperkalemia, hypotension, decreased renal function

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31
Q

horseshoe kidney

A

associated with ureteropelvic junction obstruction + chromosomal aneuploidy syndromes

32
Q

cystic kidney diseases

A

multicystic dysplastic kidney - NOT inherited, cysts + cartilage (other abnormal tissue)

PKD - cysts in cortex and medulla
ARPKD - associated with hepatic fibrosis + hepatic cysts, portal HTN
ADPKD

Medullary cystic kidney disease - AD, cysts in collecting ducts, parenchymal fibrosis (tubulointerstitial fibrosis –> inability to concentrate urine) + shrunken kidneys

33
Q

Renal tubular defects

A

kidneys put out FaBulous Glittering LiquidS

Fanconi syndrome = PCT failure, occurs with hereditary defects (Wilson’s, tyrosinemia, glycogen storage disease), multiple myeloma, tetracyclines, tenofovir, lead poisoning

Barter syndrome, AR = thick ascending limb, Na/K/2Cl transporter affected

Gitelman, AR = DCT, Na/Cl transporter

Liddle syndrome, AD = collecting tubule, increased activity of ENaC

Syndrome of apparent mineralocorticoid excess - deficiency of 11b-hydroxysteroid dehydrogenase
-can be acquired by licorice consumption

34
Q

casts

A

*bladder cancer and kidney stones present with hematuria and NO casts

RBC casts - Gnephritis, malignant HTN
WBC - inflammation, acute pyelo, transplant rejection
fatty casts - nephrotic syndrome
granular casts - acute tubular necrosis
waxy casts - ESRD, CRF
35
Q

uric acid stones

-cysteine stones

A

radiolucent - visible on CT or US, but NOT on XR

occur in acidic pH urine

side note - cysteine stones are similar - radiolucent, Na Cn nitroprusside test is positive, may form staghorn calculi
-remember - Ammonium Mg phosphate stones (aka struvite) also form staghorn calculi

Am Mg phos stones - form in alkaline environments in the setting of infection with urease-positive orgs

interesting - high dietary calcium reduces the risk for renal stone formation

  • dietary calcium is ingested with oxalate in food –> forms insoluble salts that cant be absorbed –> excreted in feces
  • low dietary calcium –> hyperoxaluria
36
Q

Wilms tumor

A

C11
malignant, blastema –> see primitive glomeruli, tubules, stromal cells

WAGR - Wilms, aniridia (no iris), genital abnormalities, retardation

Beckwith-Wiedemann syndrome - Wilms, neonatal hypoglycemia, muscular hemihypertrophy, organomegaly (tongue!)

37
Q

angiomyolipoma

A

TS

38
Q

renal oncocytoma

A

benign
large eosinophilic cells
painless hematuria

39
Q

RCC

A

men 50-70s - presents as a met
associated with paraneoplastic syndromes

will involve renal vein…

RCC can be sporadic or inherited (AD - RCC + hemangioblastoma of cerebellum)

retroperitoneal LNs

40
Q

uremia

A 
azotemia, encephalopathy with asterixis 
nausea, anorexia
pericarditis
platelet dysfunction (uremia inhibits platelet adhesions and aggregation)
deposition of urea crystals in skin
41
Q

CRF

A

constellation of features:
low GFR - salt and water retention
hyperkalemia with metabolic acidosis
poor phosphate excretion + decreased calcitriol
-hyperparathyroidism –> secondary hyperparathyroidism –> renal osteodystrophy

42
Q

urothelial carcinoma

A

risk factors: smoking (polycyclics, naphthylamine), azo/aniline dyes (hair coloring), cyclophosphamide (cancer, nephrotic syndrome in kids), phenacetin (contained in vicks cold tablets)

flat pathway - associated with early p53 mutations

papillary pathway

43
Q

squamous cell carcinoma

A

lower urinary tract does NOT have squamous cells

risk factors - chronic cystitis, Shistosoma hematobium (young middle eastern male), long standing nephrolithiasis

44
Q

adenocarcinoma of bladder

A

urachal remnant - connects bladder to yolk sac, occurs at dome of bladder

exstrophy - bladder exposed to outside world

cystitis glandularis - columnar metaplasia due to chronic irritation

45
Q

nephrotic syndrome

A

proteinuria - hypoalbuminemia, decreased AT3 (hypercaogulable state), hypogammaglobulinemia
-due to loss of negative charge of glomerular filtration barrier

increased fat - HLD, increased TGs, fatty casts

pathognomic = maltese cross-nephrotic syndrome - free cholesterol in urine

can get spontaneous peritonitis - S pneumo in kids and E coli in adults

fusion of podocytes alway seen in nephrotic syndrome

MCD - kids

  • effacement of foot processes due to cytokines (Hodgkins)
  • treat with steroids, 2nd line is cyclophosphamide

FSGS - Hispanic, AA pts, AIDS, IVDA, pts with pre-existing illness

  • collagen deposition in glomerulus + hyalinosis
  • effacement of foot processes
  • next worst glomerular disease, after RPGN
46
Q

membranoproliferative glomerulonephritis

A
  • membrano- IC deposits –> thickened membrane
  • granular IF
  • also associated with hep

mesangial cell proliferation –> tram tracks through deposits

1) subendothelial deposits - classic tram track, associated with HBV/HCV
- cryoglobulinemia
- polyarteritis nodosa
2) within basement membrane - associated with C3 nephritic factor
- lowest complement levels

*can produce nephritic or nephrotic syndrome

47
Q

systemic nephropathies

A

DM

  • NEG –> BM becomes leaky –> protein leaks INTO BV wall –> hyaline arteriolosclerosis
  • efferent arteriole is more affected… (–> increased eGFR and increased CrCl aka hyperfiltration injury)
  • urine microalbuminuria
  • Kimmelstiel Wilson nodules - large eosinophilic nodules, consist of type 4 collagen
  • ACEIs will slow this (remember ang2 constricts efferent arteriole)

systemic amyloidosis - MM, TB, RA

  • Congo red staining and apple-green birefringence under polarized light
  • “biting into apple, youre bitting into amyloid”
48
Q

lupus + kidney disease

A

membranous nephropathy (idiopathic, phospholipase A2 receptor antibodies, SLE, hepatitis, drugs, NSAIDs)

  • thick basement membrane
  • subepithelial deposits
  • silver stain or EM - supepithelial deposits with spike and dome lesions

**diffuse proliferative glomerular nephritis - wire loop lesions

49
Q

glomerulonephritis

A

glomerular inflammation and bleeding, glomerular destruction –> salt retention (not filtering as much sodium) –> periorbital edema, HTN

  • oligouria
  • by wouldnt have pitting edema and ascites (arent spilling that much protein)

immune complex deposition –> complement, C5a attracts neutrophils –> hypercellular glomeruli
-treat with emergent plasmapheresis

PSGN - hypercellular glomeruli

  • lumpy bumpy (migrating subendo–> supepi –> out complexes)
  • increased anti-DNAse B titers, decreased complement (C3)
  • resolves spontaneously
  • remember group A strep causes pharyngitis +impetigo, SCARLET fever, toxic-shock-like syndrome, nec fasciitis*

RPGN = crescents (fibrin + macrophages + Bowman’s capsule parietal epithelial cells)

  • linear IF - Goodpastures
  • granular - diffuse proliferative GN = wire looping of capillaries, IC deposits
    - presents as nephrotic syndrome too
  • negative - Wegners (cANCA, pR3-ANCA), microscopic polyangiits &Churg-Strauss syndrome (p-ANCA/MPO-ANCA)
    - Wegners aka granulomatosis with polyangiitis
    - Churg-Strauss - associated with eosinophilia, granulomatous inflammation of small/med vessels, and asthma

IgA nephropathy (Berger syndrome) - deposits in mesangium, granular

  • MOST common
  • occurs in Henoch-Schonlein purpura
  • presents after a mucosal infection, presents with renal insufficiency or acute gastroenteritis
  • episodic gross hematuria in kids
  • episodic microscopic hematuria in adults
  • will do damage in 10-20 years

Alport - type 4 collagen defect

  • basket-wave appearance of EM - thinning and splitting of GBM (looks like thick BM with “holes”)
  • presents as isolated hematuria, sensory hearing loss, and ocular disturbances
50
Q

nephritic syndromes

A

PSGN
RPGN (3 subtypes)
IgA nephropathy
Alport

51
Q

isosmotic volume contraction

A

diarrhea - volume of fluid lost is similar to ECF

52
Q

hyperosmotic volume contraction

A

water deprivation - ex sweating
remember - plasma has RBCs, RBCs will experience water shifts so keep that in mind when thinking about increases/decreases in HCT
-in this case - HCT unchanged - ECF volume decreases and RBC volume decreases

53
Q

isosmotic volume expansion

A

infusion of isotonic NaCl

54
Q

hyposmotic volume contraction

A

aldosterone insufficiency

55
Q

hyperosmotic volume expansion

A

high NaCl intake

56
Q

hyposmotic volume expansion

A

SIADH

57
Q

hyperkalemia

A

digitalis (digoxin blocks Na/K ATPase), b-blocker, insulin defiency

58
Q

Winters formula

A

predicts respiratory compensation for MET acidosis
PCO2 = 1.5*HCO3 + 8 (+/- 2)
-otherwise there is a mixed acid-based disorder

59
Q

Non-AG acidosis

A 
HARD-ASS
hyperalimentation - IV supply of nutrients
addison's disease = acute adrenal failure (no aldosterone)
renal tubular acidosis
diarrhea
acetazolamide
spironolactone
saline infusion
60
Q

renal clearance equation

A

Cx = UxV/Px

61
Q

glomerular filtration barrier

A

podocytes make the glomerular basement membrane - so if you damage to podocyte, you damage the basement membrane

heparAN sulfate - strong negative charge

62
Q

linear IF

A

goodpastures

IgG antibodies against type for collagen (in BM) - type 2 HSR

63
Q

granular IF

A

lupus - diffuse proliferative glomerulonephritis

  • pts with lupus will have serum ANA antibodies, rim pattern staining
  • IC = DNA-anti-DNA antibody
  • IC are bigger, charged - will not deposit uniformly, ex can get under endothelial cell (fenestrated) but cant get through BM

post-streptococcal glomerulonephritis
-IC are very small and soluble - will deposit under the epithelial membrane (subepithelial deposit)

IgA nephropathy (Berger disease) - only IgA glomerulonephritis can be ddx by IF, BECAUSE you have you a tag against IgA

  • otherwise IF uses tag against IgG - so you know that ICs exist but you dont know where they are located
  • need EM to determine where complexes are located

membrano-syndromes

64
Q

EPO

A

made in interstitium (?) of peritubular capillary cells

EPO for CKD-anemia
- side effects include increased risk for thromboembolic events and HTN (EPO receptors on vascular endothelium and SMCs)

65
Q

causes of azotemia

A

azotemia is an increase in BUN
BUN nl = 10
Cr nl = 1 mg/dL (sometimes Cr is secreted in the gut)

pre-renal azotemia - low RBF –> decreased GFR –> proximal tubule will have more time to reabsorb urea

  • decreased GFR - CR filtration is decreased
  • BUN increases more than Cr, BUN/CR > 15:1

acute renal failure (oligouria) - filtration of BUN and Cr decreased equally

  • BUN cant be reabsorbed
  • ratio unchanged, absolute values are increased
  • most common cause is ischemic, acute tubular necrosis (will see brown casts and increased serum Cr)
  • most common cause is not treating pre-renal azotemia

ischemic tubular necrosis - issue is that the BM gets damaged

  • when pt recovers from acute tubular necrosis - cant regenerate cell where there is no basement membrane
  • PST and thick ascending segment (in inner medulla) are most susceptible
66
Q

nephrotox drugs

A

nephrotoxic acute tubular necrosis - involves proximal tubule, it is the first part hit by the drug

gentamycin (AG) - proximal tubule, BM remains intact

IV pyelogram (dye for urinary system)

67
Q

renal arteries and veins

A

L1 level

68
Q

UTIs

A

bladder has protections

  • mucosa normally does not allow bacterial attachment - cystitis (fimbriae attach)
  • normal urine is bactericidal (urea, osmolarity) - capsules
  • urine flow

pyelo: risk of hematogenous spread (and risk is greater in hospitalized, elderly)

69
Q

multiple myeloma

A

excess excretion of free light chains (Bence Jones proteins) –> precipitate with Tamm-Horsfall protein –> obstructing CASTS

MM - can cause poor bicarb absorption

70
Q

edema

A

pitting edema:
transudates

non-pitting:
exudates (pus)
lymphedema (mastectomy, Peau de orange inflammatory carcinoma, lymphogranuloma venereum chlamydia, Wuchereria bancrofti)

71
Q

how many liters of isotonic saline do you have to inject into plasma to increase it by 1 L

A

3 L

- 2 L distribute into interstitial space, 1 L into plasma

72
Q

CCBs

A

used for HTN

amlodipine, nifedipine - dihydropyridine CCBs

  • peripheral edema - due to dilation of precapillary vessels –> increased Pc
  • dizziness or lightheadedness, flushing
73
Q

familial hypocalciuric hypercalcemia

A

benign, AD

defective Ca2+ sensing by PTH and renal tubule cells

  • PTH is not suppressed when Ca2+ is high
  • constellation - high PTH, high Ca2+ and lower urinary Ca2+
74
Q

cyclophosphamide and mesna

A

cyclophosphamide = chemo
–> converted to acrolein by kidneys –> toxic to urothelium

mesna - sulfyhydryl compound that binds and inactivates toxic metabolites

75
Q

acid-base disorders

A

metabolic acidosis - Winters

metabolic alkalosis - PaCO2 increases 0.7/1 meQ/L rise in bicarb

acute respiratory acidosis - 1 mEq/L rise in HCO3 for every 10 mmHg CO2

acute respiratory acidosis
2 mEq/L drop in HCO3 for every 10 mm Hg decrease in CO2

76
Q

CKD and drug effects

A

long-acting insulin is cleared by the kidney –> hypoglycemia

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