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BOARDS! > Renal > Flashcards

Renal Flashcards

1
Q

HSP (Henoch-Schonlen purpura)

A
  • pathphys: Ag from infection releases IgA-Ab which deposit in vessel walls and cause an inflamm rxn
  • CP=purpuric rash (palpable purpura on extremities), colicky abdo pain, polyarthralgia (jt pain), hematuria,
  • complication: acute glomerulonephritis
  • who? males 3-11 yo; most common small vessel vasculitis in kids
  • diag: IgA-mediated leukocytoclastic vasculitis (hypersensitivity)
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2
Q

Benign Prostatic Hyperplasia

A

CP: intermittent bladder outlet obstruction and overflow incontinence

>>urinary retention causes increased pressure in urinary tract and reflex nephropathy

stones and renal interstitial atrophy and scarring ensues

>>tx promptly! prolonged obstruction: permanent damage/chronic renal failure

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3
Q

Renal angiomyolipoma

A
  • benign tumor composed of:
    • blood vessels
    • smooth muscle
    • fat
  • bilat renal angiomyolipoma are associated with tuberous sclerosis (AD condition)
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4
Q

Renal (Clear) Cell Carcinoma

A
  • originate from epithelial cells of proximal renal tubules
  • most common type of kidney tumor
  • high lipid content
  • microscopic cells with abundant clear cytoplasm and eccentric nuclei
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5
Q

Unilateral Renal Artery stenosis

A
  • cause of secondary HTN in 2-5% of hypertensive pts
  • affected kidney may become atrophied due to O2 and nutrient deprivation
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6
Q

Horshoe Kidney

A
  • kidneys are fused at the poles
  • isthmus of the horseshoe kidney usually lies nterior to the aorta and posterior to the inferior mesenteric artery (IMA)
  • during fetal development, the IMA limts the ascent of the horseshoe kidney
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7
Q

ascending urinary infection

A
  • clinical:
    • costovertebral angle tenderness
    • flank and abdo pain, fever, shaking chills, N/V
  • diag: UA: pyuria, WBC casts, bacteriuria and hematuria
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8
Q

Minimal Changes Disease (MCD)

A
  • Pathphys:
    • primary defet in immuno function=overproduction of IL-13=direct podocyte damaga
      • seleective albuminuria (FSGS and memb nep are NON-selective)
  • Clinical: most common cause of nephrotic in kids 2-6yo after: URI, immunization, insect bite
  • diag: **EM: diffuse effacement of podocyte foot processes
    • light microscopy: nml glomeruli
    • IF: no deposits
  • Tx: ***STEROID therapy***
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9
Q

RP(crescentic)GN

A
  • Clinical:
    • renal failure, pulm (cough, dyspnea, hemoptysis)
    • URT (upper resp tract…epistasis, mucosal ulceraton, chronic sinusitis)
  1. anti-GBM inhibits lpha 3 chain of type 4 collages
    1. IF: LINEAR GBM deposits (IgG + C3)
      1. Goodpasture;s; hemoptysis (from cross reactivity); CRESCENTS: FIBRIN deposition
  2. IC-mediated;
    1. IF: lumpy bumpy
    2. PSGN, SLE, IgA nephropathy, HSP
  3. “pauci immune”, no Ig IC in BM
    1. ANCA (anti-neutrophil cytoplasmic Ab) in serum
    2. Wegener’s (or idiopathic)
  • Diagnosis: crescents on light microscopy
  • IF: cANCA stain green
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10
Q

Diabetes Insipidus (DI)

A
  • pathphys: unable to concentrate urine in response to dehydration
  • Clinical:
    • ADH deficient=ctl DI
    • complete/partial kidney ro response to ADH=nephrogenic
    • free water loss in urine (dilute urine)
      • low specificity gravity
    • excessive thirst
  • tx: desmopressin (DDAVP); urine osm increase to nml (NOT in complete nephrogenic DI)
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11
Q

Transitional Cell Carcinoma

A
  • Pathophys: gross hematuria in an elderly man
  • Clinical:
    • older male, blood in urine and back pain
  • Hx: smoker or occupied exposure to: rubber, plastics, amine-dyes, textiles, leather
  • diag: most common tumor of UT system: renal calyces, renal pelvis, ureters, bladder
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12
Q

PSGN

A
  • Clinical: **6-10yo (AGE!!)
    • older child, young adult with:
      • edema and HTN
      • hematuria a few wks
      • proteinuria
      • PLUS: malaise, fever, nausea, cola-colored urine
    • after skin or pharyngeal infection
  • Pathphys: inflamm rxn involving all glom in BOTH kidneys
  • Diag:
    • light microscopy: enlarged, hypercellular glom
    • IF: lumpy-bumpy granular deposits of IgG and C3
    • EM: electron-dense deposits on the epithelial side of basal membrane (HUMPS***)
  • Tx: loop diuretics, vasodilators (to help the edema and HTN)
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13
Q

UTI

A
  • CP: female pt post-sex
    • dysuria, freq/urg, pyuria, bacteriuria
      • ** more suprapubic pressure and tenderness
    • fever, chills, N/V, flank/abdo pain, CVA tenderness
  • urine sedimant microscopy: WBC, WBC casts, bacteria=pyelonephritis
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14
Q

Multiple Myeloma

A
  • CP: elderly pts w/:
    • easy fatigability (caused by anemia)
    • constipation (due to hypercalcemia)
    • bone pain-bacl and ribs (from osteoclast activating factor from myeloma cell)
    • RF
  • light microscopy: large, glassy eosinophilic casts (BJ proteins)
  • pathophys: excess excretion of free light chains (Bence Jones proteins)=myeloma cast nephropathy
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15
Q

Acute Interstitial Nephritis (AIN)

A
  • pathophys: **interstitium, edema and infiltration with lymphocytes, macrophages, plasma cells and eosinophils
    • IgE-HSR + cell-mediated rxn
  • CP: fever, maculopapular rash, oliguria (1-3 wks after: beta lactam AB, NSAIDS, sulfonamides, Rifampin, diuretics)
  • Hausel/Wright stain: eosinophilia*
  • tx: STOP the meds!
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16
Q

Acute Tubular Necrosis (ATN)

A
  • PP: most susceptible are proximal tube and thick ascending LoH (outer medulla)
    • severe hypovolemia, shock, and surgery lead to decreased renal perfusion an acute kidney injury
    • ischemic injury affects medulla (cortex gets more blood)
  • CP: increased serum Cr and BUN, nml BUN:sCr, oliguria and muddy brown casts
  • tubular epithelium regenerates, renal fxn nml in 3 wks
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17
Q

Renal stones (Nephrolithiasis)

A
  • urine supersaturation (due to low fuid intake and dehydration)
  • # 1: calcium (oxalate>phosphate): 70-80
  • Mg. Ammonium phosphate (struvite)
  • Uric acid
  • cystine
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18
Q

Renal Papillary necrosis

A
  • pyelonephritis, analgesic (NSAIDS), DM and sickle cell all lead to ischemia
  • CP: abrupt onset gross hematuria (healthy otherwise) and FHx of sickle cell dz
    • gross hem and acute flank pain
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19
Q

What is the most significant RF for UTI?

A
  • duration of catheterization!
  • Avoid/reduce by:
    • eliminating unnecessary catheterization
    • sterile technique
    • remove catheter promptly
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20
Q

Anion-Gap Acidosis vs, nml

A
  • AG acidosis: MUDPILES
    • Methanol
    • Uremia
    • DKA
    • Propylene glycol
    • INH (or iront ablets)
    • lactic acid
    • ethanol
    • salicylate
  • nml: HARDASS
    • Hyperalimentation
    • Addison’s dz
    • renal tubular acidosis
    • Diarrhea
    • Acetazolamide
    • Spironolactone
    • Saline infusion
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21
Q

POMC (proopiomelanocortin)

A
  • polypeptide precursor that goes through enzymatic cleavage and modifcation to produce beta endorphins, ACTH, and MSH
  • means: there may be close physiological relationship between the stress axis and the opioid system
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22
Q

Renal agenesis

A
  • absent kidney formation
  • unilat -or- bilat
    • unilat leads to hypertrophy
  • hyperinfiltration INC r/o renal failure later in life
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23
Q

BILAT renal agenesis

A
  • leads to POTTER sequence (incompatible with life):
    • oligo-hydramnios
    • lung hypoplasia
    • flat face with low set ears
    • developmental defects of the extremities
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24
Q

dysplastic kidney

A
  • NON-inherited
  • congenital
  • malformatoin of renal parenchyma, characerized by cysts and abnml tissue
  • usually unilat
  • when BILAT must be distinguished from inherited polycystic kidney dz
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25
Q

What are the two forms of PKD (polycystic kidney dz)

A
  • AR and AD
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26
Q

ARPKD

A
  • infants
  • CP: worsening renal failure and HTN
  • newborns may present with Potter sequence
  • associated w/:
    • congenital heptaic fibrosis
      • leads to portal HTN
    • –and– hepatic cysts
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27
Q

ADomPKD

A
  • young adults
  • CP:
    • HTN d/t increased RENIN
    • hematuria
    • worsening renal failure
  • PP: mut in APKD1 or APKD2 gene
  • cysts develop over time
  • assoc w/:
    • hepatic cysts
    • mitral valve prolapse (MVP)
    • berry aneurysm-COD
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28
Q

medullaty cystic kidney dz

A
  • AD defects leads to cysts in the medullary collecting ducts
  • parenchymal fibrosis results in shrunken kidneys and worsening renal failure
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29
Q

glutamine in ammoniagenesis

A
  • acidosis stimulates renal ammoniogenesis which is a process by which:
    • renal tubular epithelial cells metabolize glutamine to glutamate
    • generate ammonium that is excreted in the urine
    • generate bicarb that is absorbed into the blood and buffers acids
  • renal ammoniagenesis is a process that is responsible for MAJORITY of renal acid excretion in chronic acidotic states
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30
Q

acid in urine under nml physiologic conditions

A
  • half of acid secreted in the urine is in the form of ammonium
  • other half is excreted as titratable acids (espec inorganic phosphate)
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31
Q

What is almost entirely responsible for the INC in renal acid excretion seen with chronic acidosis?

A

IN ammonium production

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32
Q

What is the role of eosinophils in HD d/r parastic infection?

A
  • Ab are bound to a parasitic organism
  • stimulated eos will destroy parasite vie Ab-dependent cell-mediated cytotoxicity <adcc>
    </adcc><ul>
    <li>using enzymes from their cytoplasmic granules</li>
    </ul></adcc>
  • eos also regulate type 1 HSR
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33
Q

Who all uses ADCC (Ab-dependent cell-mediated cytotoxicity)

A
  • eosinophils
  • macrophages
  • neutrophils
  • NK cells
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34
Q

What symptoms should raise suspicion for multiple myeloma

A
  • easy fatigability (due to anemia)
  • constipation (due to hypercalcemia)
  • back pain (bone lysis d/t production of osteoclast-activating factor y myeloma cells)
  • elevated serum protein (monoclonal proteins)
  • azotemia/renal failure
  • epi: elderly pt
    *
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35
Q

multiple myeloma labs

A

large (glassy) eos casts composed of Bence-Jones (free light chains) proteins are seen in the tubular lumen in myeloma cast nephropathy

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36
Q

Fabry dz pathophys

A
  • XR
  • alpha-galactosidase A deficiency results in acumulation of globo-tria-osyl-ceramide
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37
Q

Fabry dz Clinical features

A
  • neuropathic pain
  • angiokeratomas
  • telangiectasias
  • glomerular dz (eg proteinuria)
  • cerebrovascular dz (eg TIA, stroke)
  • cardiac dz (eg LVH)
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38
Q

Fabry dz general

A
  • lipid storage d/o
  • alpha galactosidase A is a lysosomal enzyme that breaks down Gb3-/ceramide trihexoside a sphingolipid
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39
Q

What causes the adverse manifestations of Fabry dz?

A
  • Gb3 accumulation in:
    • vascular smooth muscle cells
    • glomerular/distal tubule cells
    • cardiac myocytes
    • dorsal root and autonomic ganglia
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40
Q

What are the earliest s/s of Fabry dz and when do they occur?

A
  • neuropathic pain and hypohidrosis (DEC sweating) present during adolescence.
  • late adolescence: angiokeratomas (dark red, non-blanching macule and papules, butt groin umbilicus) and telangiectasias develop on the skin
  • exercise, stress, fatigue=exacerbating factors
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41
Q

What are s/s of Fabry dz in early and mid-adulthood?

A
  • cerebrovascular and cardiac dz=mc cod
  • also: Gb3 buildup in the glomerulus and distal tubules results in protein
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42
Q

What is the correlation between T1diabetics and overflow incontinence?

A
  • diabetic autonomic neuropathy is common in type 1 diabetics
  • it can cause overflow incontinence d/t inability to sense a full bladder and incomplete emptying
  • PVR (postvoid residual) testing with US or catherization can confirm inadequate bladder emptying
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43
Q

saddle anesthesia

A
  • loss of sensation in the perineal area
  • can indicate cauda equina syndrome–commonly d/t epidural cord compression from a malignancy
  • pts usually develop urinary retention late in the course of the disease-usually assocuated with fecal incontinence
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44
Q

what causes tumor lysis syndrome

A
  • when tumors with a high cell turnover are treated with chemotherapy
  • lysis of tumor cells causes intracellular ions to be released into serum
  • prevent with: urine alkalinization and hydration
    • high urine flow and high pH along the nephron rpevents crystallization an dprecipitation of uric acid
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45
Q

acute urate nephropathy

A
  • uric acid=metabolite of tumor nucleic acid
  • uric acid is soluble at physiologic pH
  • UA can precipitate in the normally acidic environment of distal tubules and collecting ducts
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46
Q

renal artery stenosis

A
  • can cause renal hypoperfusion and activation of RAA
  • modified smooth muscle (juxtaglomerular) cells of the afferent glomerular arterioles synthesize RENIN
  • leads to a cascade of effects that include systemic vasoconstriction (angiotensin 2) nd Na and water retention (aldosterone and angiotensin 2)
  • chronic renal hypoperfusion will cause hypertrophy and hyperplasia of the juxtaglomerular cells
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47
Q

juxtaglomerular apparatus

A
  • consists of macula densa and JG cells
  • MD-in distal tubule, monitor salt content and tubular flow rate
    • transmits info to nearby JG cells (modified smooth muscle cells with renin-containing zymogen granules) located mostly in wall of afferent arteriole
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48
Q

What happens with severe, long-term RAS?

A

it auses the JG cells of the affected kidneys to undergo hypertrophy and hyperplasia

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49
Q

HTN in unilat bs. bilat RAS

A
  • even if contralat kidney fxn, secretion of renin by stenotic kid wil cause INC angiotensin 2 and aldosterone leading to systemic vasoCONSTRICTION and retention of salt and water by BOTH KIDNEYS
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50
Q

chronic kidney dz: bilat vs. unilat

A
  • bilat RAS: CKD
  • unilat RAS-will NOT have CKD, nml kideny can still efficiently filter and excrete waste products
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51
Q

What is the mc c/o glomerulonephritis?

who does it affect?

CP?

A
  • IgA nephropathy (Berger dz)
  • older kids and young adults
  • CP: painless hematuria within 5-7 days of an URTI
    • hematuria returns every few months, or with another URTI
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52
Q

PSGN (post-streptococcal slomerulonephritis) cause of glomerular injury

A
  • Ab against streptococcal antigens cross-react with GBM
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53
Q

PSGN (post-streptococcal slomerulonephritis) characteristic biopsy features

A
  • IF: C3 granular staining along GBM
  • EM: SUB-EPITHELIAL HUMPS
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54
Q

Anti-GBM dz characteristic biopsy features

A
  • Light microscopy: glomerular crescents
  • IF: LINEAR STAINING (IgG) along GBM
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55
Q

Anti-GBM dz c/o glomerular injury

A

Ab vs. type 4 collagen in GBM

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56
Q

RPGN c/o glomerular injury

A
  • SEVERE immunolgic injury (eg anti-GBM Ab, immune complex deposition)
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57
Q

RPGN characteristic bx features

A
  • LM: glomerular CRESCENTS
  • IF: fibrinogen in crescent
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58
Q

IgA nephropathy c/o glomerular injury

A
  • deposition of IgA-containing complexes
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59
Q

IgA nephropathy characteristic bx features

A
  • LM: mesangial hypercellularity
  • IF: IgA in mesangium
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60
Q

Alport syndrome

a. c/o glomerular injury
b. characteristic bx features

A
  • defective type IV collagen in GBM
  • EM: lamellated appearance of GBM
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61
Q

signs of atheroembolic diseases

A
  • signs of embolism:
    • blue toe, livedo reticularis (bilek legs) with nml peripheral pulses)
  • following an invasive vascular procedure:
    • angiography, angioplasty, aortic sx
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62
Q

PP of atheroembolic disease

A

PP: cholesterol-containing debris gets dislodged form larger arteries (the aorta during cardiac catheterization) and dislodges in smaller vessels=ischemia

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63
Q

What is the mc presenting symptom of post-procedure atheroembolism?

A
  • acute kidney injury (oliguria, azotemia)
    • frequently seen in elderly pts with pre-existing renal atherosclerosis
  • cholesterol is disolved during tissue prep for microscopic evaluation leaving needle-shaped clefts that partially or completely obstruct the arcuate or intrlobular renal arteries
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64
Q

What does the ureteric bud ultimately give rise to?

A
  • collecting system of the kidney:
    • collecting tubules and ducts
    • major and minor calyces
    • renal pelvis
    • ureters
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65
Q

What does the metanephric mesoderm (blastema) give rise to?

A
  • glomeruli
  • Bowman’s space
  • proximal tubules
  • the loop of Henle
  • distal convoluted tubules
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66
Q

Primary thrombotic microangiopathy (TMA) syndromes

A
  • common clinical and pathologic features
  • result in platelet activation and diffuse microthombosis in arterioles and capillaries
  • CP: hemolytic anemia with:
    • microangiopathic hemolytic anemia with schistocytes
    • thrombocytopenia
    • organ injury (brain, kidneys, heart)
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67
Q

HSRT1 (immediate)

A
  • humoral components: IgE
  • cellular components: basophils and mast cells
  • examples: anaphylaxis and allergies
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68
Q

HSRT2 (cytotoxic)

A
  • humoral components:
    • IgG and IgM auto-Ab
    • complement activation
  • cellular components:
    • NK cells
    • eos
    • neutrophils
    • macrophages
  • examples:
    • auto-immune hemolytic anemia
    • Goodpasture syndrome
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69
Q

HSRT3 (immune complex)

A
  • humoral components:
    • deposition of antibody-antigen complexes
    • complement activation
  • cellular components: neutrophils
  • examples:
    • serum sickness
    • PSGN
    • lupus nephritis
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70
Q

HSRT4 (delayed type)

A
  • humoral components: NONE
  • cellular components: T-cells AND macrophages
  • examples: contact dermatitis and tuberculin skin test
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71
Q

MUDPILES (AG)

A

M=Methanol
U=Uremia
D=Diabetic ketoacidosis
P=Propylene glycol
I=Iron tables, Isoniazid
L=Lactic acidosi
E=Ethylene glycol
S=Salicylates(late)

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72
Q

HARDASS (nml AG)

A

H=hyperalimentation
A=Addisons disease
R=Renal Tubular Acidosis
D=Diarrhoea

A=Acetazolamide
S=Spiranolactone
S=Saline Infusion

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73
Q

retroperitoneal organs

A
  • S: suprarenal (adrenal) gland
  • A: aorta/IVC
  • D: duodenum (second and third part)
  • P: pancreas (except tail)
  • U: ureters
  • C: colon (ascending and descending)
  • K: kidneys
  • E: (o)esophagus
  • R: rectum
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74
Q

suprapubic cystostomy

A
  • in placement of a suprapubic cystostomy, trocar and cannula will pierce the layers of the abdominal wall
  • will NOT enter the peritoneum
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75
Q

PAH clearance

A
  • Para-amino-hippuric acid is freely filtered from the blood in the glomerular capillaries to the tubular fluid in Bowmans space
    • some is also freely filtered by the glomerulus
  • PAH is NOT reabsorbed by any portion of the nephron
  • it is also secreted from the blood into the tubular fluid by the cells of the proximal tubule by a carrier protei-mediated process
  • PAH secretion can be saturated at high blood concentrations
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76
Q

PIGN (post-infectious glomerulonephritis) Prognosis

A
  • kids: mostly recover completely
  • adults: poor prognosis and higher r/o chronic HTN and renal insufficiency
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77
Q

What are the clinical features of ACUTE PSGN (post streptococcal glomerulonephritis)

A
  • can be asymptomatic
  • if symptomatic (onset 1-3 wks after group A strep pharyngitis or skin infection):
    • gross hematuria (tea-/cola-colored urine)
    • edema (peri-orbital, generalized)
    • HTN
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78
Q

What are the lab findings of ACUTE PSGN (post streptococcal glomerulonephritis)

A
  • UA: +protein, +blood, +/- RBC casts
  • serum:
    • DEC C3 and possible DEC C4
    • INC:
      • serum Cr
      • anti-DNase B and AH-ase
      • ASO and anti-NAD (from preceding pharyngitis)
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79
Q

What organ is immediately deep to the tip of the 12th rib?

A
  • the left kidney!
  • left 12th rib overlies the parietal pleura medially and the idney laterally
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80
Q

RIBS-yum

A
  • 1-7=true ribs
    • costal cartilage attaches directly to the sternum
  • 8-12=false ribs
    • costal cartilage does NOT attach directly to the sternum
    • cartilage of ribs 8-10 attaches to the costal cartilage of the upper ribs
    • 11&12 are floating ribs=NOT bound to the anterior rib cage by cartilage
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81
Q

APS and SLE

A
  • antiphospholipid Ab syndrome is characterized by presence of ANTI-phospholipid Ab in the setting of venous or arterial thromboembolism AND/OR recurrant pregnancy loss
  • may be a primary d/o or occur secondary to other a.i dz such as SLE
  • antiphospholipid Ab are present in 10-30% of pts with SLE
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82
Q

what are indications of the presence of circulating antiphospholipid antibodies?

A
  • prolonged activated partial thromboplastin time (aPTT)–in vitro
  • false-positive results of nontreponemal serologic syphilis tests by reacting with cardio-lipin <the>:
    </the><ul>
    <li>rapid plasma reagin (RPR) </li>
    <li>VDRL</li>
    </ul></the>
  • in vivo–produce hypercoaguable state d/t activation of phospholipid-dependent coagulation pathways
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83
Q

What are the clinical features of antiphospholipid antibody syndrome?

A
  • venous or arterial thromboembolic disease
    • DVT
    • PE
    • ischemic stroke/TIA
  • adverse pregnancy outcomes
    • unexplained embryonic or fetal loss
    • premature birth d/t placental insuficiency or pre-eclampsia
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84
Q

Lab findings in ANTI-phospholipid Antibody syndrome

A
  • lupus anticoagulant effect: paradoxical aPTT prolongation
    • not reverse on plasma mixing studies
  • presence of specific antiphospholipid antibodies
    • ANTI-cardiolipin Ab
    • ANTI-beta2-glycoprotein-I Ab
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85
Q

Define selective proteinuria

A
  • albumin loss with minimal loss of the more buky proteins (such as IgG and macroglobulin)
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86
Q

What provides a filtration barrier to protein molecules?

what three components does it contain?

A
  • barrier: glomerular capillary wall
  • 3 components:
    • fenestrated endothelium
    • GBM (glomerular basement membrane)
    • epithelial cells
  • selective to size and charge
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87
Q

filtration barrier-size selectivity

A
  • size selectivity is a features of the dimensions of the pores
  • endothelial cells: fenestrations with 40nm raidus
  • GBM pores: 4nm radius
    • also: slit diaphragms
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88
Q

filtration barrier-charge selectivity

A
  • provided by negtively charged anions on endothelial cells and the GBM
  • repel negatively charged molecules (such as albumin)
    • albummin is small enough to fit through GBM pores
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89
Q

Define tubular proteinuria

A
  • assoc w/ presence of LMW proteins:
    • beta 2-miroglobulin
    • immunoglobulin LC
    • AA
    • retinol-binding protein
  • they are normally filtered by the glomerulus and almost completely reabsorbed in the proximal tubule
  • appear in urine when proximal tubular fxn is disrupted (ex: tubulointerstitial nephritis)
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90
Q

DKA urine chemistry patterns

A
  • decreased serum pH and HCO3-
  • compensatory decrease in pCO2
  • kidneys try to correct metabolic acidosis via 3 major mechs:
    • INC HCO3 reabsorption
    • INC H+ secretion
    • INC acid buffer excretion
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91
Q

What are pts with indwelling bladder catheters at an INC risk for?

A
  • UTI causes by typical and opportunistic organisms
  • typical:
    • E coli
    • Klebsiella
    • S. saprophyticus
    • Proteus mirabilis
  • opportunistic:
    • Pseudonomas
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92
Q

ADH and urine concentration

A
  • ADH acts on the medularry segment of the CD to INC urea and water rebsorption, allowing for the production of maximally concentrated urine
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93
Q

a. what does ADH/vasopressin do?
b. what are the major 2 receptors it acts on?
c. what causes ADH secretion?

A
  • ADH/V is the primary physiologic INHIBITOR or free water EXCRETION (stay here, mufuh)
  • V1R stimulation: vasoconstriction and INC PG release
  • V2R stimulation: anti-diuretic response
  • ADH is secreted in resp to plasma HYPER-osmolarity and (to a lesser extent) depletion of the ECV
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94
Q

What is the region of highest osmolarity in the kidney?

A
  • medullary interstitium of the collecting duct
  • here, ADH increases the number of passive urea transporters=highly concentrated urea diffuses down its concentration gradient
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95
Q

Sirolimus MOA

A
  • binds to the immunophilin FK-506 binding protein (FKBP) in the cytoplasm
  • forms a complex that binds and inhibits mTOR
  • inhibition of mTOR signaling blocks IL-2 signal transduction and prevents cell cycle progression and lymphocyte proliferation
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96
Q

What are the THREE main roles of Angiotensin 2?

A
  • sodium retention (direct effect)
  • aldosterone production
  • vasoconstriction
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97
Q

Who are the main two groups affected by RAS (indicated by marked unilat kidney atrophy)

A
  • elderly d/t atherosclerotic changes in the arterial intima
  • women of childbearing age d/t fibromuscular dysplasia
  • HT and abdominal bruit are often present
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98
Q

What is the state of the tubular fuid in the absence of ADH

A
  • most concentrated at the jxn between the descending and ascending limbs of the loop of Henle
  • most dilute in the collecting ducts
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99
Q

What is the differential diagnosis for urinary incontinence?

A
  • stress, urge, overflow
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100
Q

Stress and Urinary Incontinence

A
  • most common form, typically after 45
  • 2x as common in women b/c EUS trauma or pudendal nerve (innervated EUS) injury is common d/r vaginal child birth
  • etiology:
    • loss of urethral support and intra-abdo pressure>urethral sphincter pressure
  • symptoms:
    • leaking with coughing, sneezing, laughing and lifting (all INC abdo pressure)
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101
Q

Urge and Urinary Incontinence

A
  • etiology: detrusor over-activity
  • symptoms: overwhelming, or frequent need to empty bladder
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102
Q

Overflow and urinary incontinence

A
  • etiology: impaired detrusor contractility and bladder outlet obstruction
  • symptoms: constant involuntary dribbling of urine and incomplete emptying
103
Q

internal and external urethral sphincter

A
  • internal: mainly smooth muscle, controlled by autonomic nervous system
    • sym=contraction, PS=relaxation
  • external: mostly pelvic floor skeletal muscl under voluntary control
104
Q

bladder filling, emptying and continence

A
  • bladder emptying-mainly d/t detrusor muscle contraction
  • continence-maintained by urethral (mainly external) sphincters
  • d/r bladder filling: sympathetic activation closes the internal sphincter and inhibits detrusor contraction
105
Q

What causes an INC in GFR

A
  • higher glomerular hydrostatic pressure
106
Q

What causes an DEC in GFR

A
  • INC bowmans capsule hydrostatic pressure
  • –or–
  • higher glomerular capillary oncotic pressure
107
Q

what is the equation for filtration fraction?

A
  • GFR:RPF ratio; the portion of the RPF that is filtered form the glomerular capilaries into bowman’s space
  • acute ureteral constriction or obstruction decreases the GFR and FF
108
Q

What are the three Schistosoma species?

A
  1. S. haema-tobium
  2. S. man-soni
  3. S. japon-icum
109
Q

Schistosoma haemato-bium

A
  • location:
    • N. Africa, SSA, ME
  • symptoms: Urinary schisto
    • ​terminal hematuria, dysuria, frequent urination
    • hydronephrosis, pyelonephritis, squamous cell carinoma of the bladder
110
Q

Schistosoma man-soni

A
  • location: SSA, ME, SA, Caribb
  • Intestinal Schisto
  • Symptoms:
    • diarrhea and abdo pain
    • intestinal ulceration–>iron deficiency anemia
111
Q

Schistosoma japonicum

A
  • location: Asia (*China, also: Phillipines, Japan)
  • hepatic schisto
  • symptoms:
    • hepato-spleno-megaly
    • peiportal fibrosis and subsequent portal HTN
112
Q

What is the mc c/o HYDAtID cysts in humans?

A

dog tapeworm Echino-coccus granulosus

113
Q

What are the steps of the Potter sequence

A
  • urinary tract anomaly
  • anuria/oliguria in utero (classic finding: bilat renal agenesis)
  • oligohydramnios (severely reduced amniotic fluid)
  • pulmonary hypoplasia (d/t lack of nml alveolar distension by aspirated amniotic fluid), flat facies, limb deformities (club feet)
114
Q

Diabetic Nephropathy

A
  • mc c/o ESRD in the US
  • moderately INC albuminuria (<300mg/day) is the earliest manifestation of diabetic nephropathy
115
Q

Pancreas specific ca RF

A
  • tobacco smoke
  • obesity
116
Q

gastric specific ca RF

A
  • dietary nitrates
  • alcohol and tobacco use
  • H. pylori
117
Q

Liver specific ca RF

A
  • Hep B and C
  • liver cirrhosis (any cause)
  • hemochromatosis
  • aflatoxin
118
Q

CRC specific RF

A
  • hereditary CRC syndromes
  • IBD
  • obesity
  • charred or fried foods
119
Q

Renal specific ca RF

A
  • tobacco smoke
  • obesity
  • HTN
120
Q

Bladder specific ca RF

A
  • tobacco smoke
  • occupational exposures
    • rubber
    • aromatic amine-containing dyes
    • textiles
    • leather
121
Q

Breast specific ca RF

A
  • early menarche
  • late menopause
  • nulliparity
  • BRCA mutations
122
Q

Prostate specific ca RF

A
  • INC age
  • negussss
123
Q

Pyelonephritis Diagnosis

A

WBC casts only form in the renal tubules and are pathognomonic for acute pyelonephritis when accompanied by s/s of acute UTI

124
Q

What happens when the EFFERENT (outgoing) arteriole is constricted?

A
  • constriction of EFFERENT will IMPEDE blood flow through the kidney
  • will DEC RPF
  • INC glomerular capillary hydrostatic pressure as the fluid “backs up” in the glomerulus
  • increased glomerular hydrostatic pressure will cause an INC in the FF
125
Q

RPF

A
  • volume of plasma that is delivered to the kidney per unit time
  • provided by the renal blood flow-delivers BOTH erythrocytes and plasma to the kidney
  • clinically calculated by PAH clearance
126
Q

heavy proteinuria in nephrOtic syndrome

A
  • can cause regional or generalized interstitial edema b/c the DEC in serum albumin and total protein concentrations lowers the plasma oncotic pressure and INC net plasma filtration in capillary beds
127
Q

What are causes of saline-responsive metabolic alkalosis

A
  • vomiting/nasogastric suctioning
  • thiazide/loopdiuretic use
  • –they cause volume and Cl- depletion
128
Q

What causes saline-UN-responsive metabolic alkalosis?

A
  • excess mineralcorticoid activity:
    • primary hyperaldosteronism
    • Cushing dz
    • ectopic ACTH production
129
Q

Where does the majority of water reabsorption occur in the nephron?

A
  • proximal tubule passively with the reabsorption of solutes
130
Q

Which parts of the renal tubule and NON-permeable to water?

A

THICK and thin ascending limbs of Henle’s loop

131
Q

Where is tubular fluid concentration of PAH lowest?

A

Bowman’s space

132
Q

Urachus

A
  • remnant of the allantois that connects the bladder with the yolk sac d/r fetal development
  • failure of urachus to obliterate at birth=patent urachus
  • patent urachus can facilitate discharge of urine form the umbilicus!!
    • excerbated by crying, straining, or prone position
    • local skin irritation can cause erythema
133
Q

what incorporates short RNA primers into replicating DNA?

A

PRIMASE-DNA dependent RNA polymerase

134
Q

what repairs SSB in duplex DNA during DNA replication and repair?

A

DNA ligase

135
Q

GFR and serum Cr relationship

A
  • when GFR is nml, relatively large decreases in GFR result in only small increases in serum Cr
  • when GFR is significantly DEC, small decrements in GFR produce relatively large changes in serum creatine (an L shape ona graph: GFR x-axis, SCr y-axis)
  • **every time GFR halves, SCr doubles
136
Q

What are the three types of transplant rejection reactions?

A

hyperacute, acute, chronic

137
Q

HYPERACUTE transplant rejection rxns

A
  • onset time: minutes to hours
  • etiology: preformed Ab vs. graft in recipient’s circulation
  • morphology:
    • gross mottling and cyanosis
    • arterial fibrinoid necrosis and capillary thrombotic occlusion
138
Q

ACUTE transplant rejection rxns

A
  • onset time: usually <6 months
  • Etiology: exposure to donor Ag induces humoral/cellular activation of naive immune cells
  • Morphology
    • Humoral:
      • C4d deposition
      • neutrophilic infiltrate
      • necrotizing vasculitis
    • Cellular:
      • lymphocytic interstitial infiltrate
      • endotheliitis
139
Q

CHRONIC transplant rejection reactions

A
  • onset time: months to years
  • etiology: chronic low-grade immune response refractory to immunosuppressants
  • morphology:
    • vascular wall thickening + luminal narrowing (ying and yang)
    • interstitial fibrosis + parenchyma atrophy
140
Q

neurogenic bladder in a pt with MS

A
  • pts with MS often develop a spastic bladder a few wks after developing an acute lesion of the SC
  • CP: INC urinary frequency and urge incontinence
  • urodynamic studies: bladder hypertonia
141
Q

Flaccid bladder

A
  • typically occurs in the setting of LMN lesions (cauda equina syndrome)
  • pt w/ flaccid bladder will have a large residual volume of urine after attempted emtying and will typically experience urinary incontinece at the end of the day
  • pressure from a full bladder becomes greater than urinary sphincter pressure
142
Q

CP of a pt with a spastic bladder

A

frequent episodes of urinary incontinence throughout the day d/t urgency

143
Q

Urethritis

A
  • common organisms: N. gonorrhoeae and C. trachomatis
  • symptoms:
    • pain or buring sensation d/r urination
    • –or– frequent urination
  • Lab: UA +WBC
144
Q

Cystitis

A
  • Common organisms:
    • E. coli
    • S. saprophyticus
    • P. mirabilis
    • Klebsiella
    • Enterococci
  • symptoms:
    • may by asymptomatic or symptomatic
    • suprapubic pain and tenderness
    • frequent urination
  • UA&Micro:
    • +Leukocyte esterase
    • +Nitrites
    • +bacteria
    • +WBC
    • +RBC (occasionally)
145
Q

Pyelonephritis

A
  • common organisms (same as cystitis):
    • E. coli
    • S. saprophyticus
    • P. mirabilis
    • Klebsiella
    • Enterococci
  • symptoms:
    • flank pain
    • costovertebral angle tenderness
    • fever
    • chills
    • hematuria with casts
  • UA&Micro:
    • same findings as in cystitis [+Leukocyte esterase, +Nitrites, +bacteria, +WBC, +RBC (occasionally)]
    • may also see WBC casts indicating renal-based pyuria
  • CBC: elevated WBC
146
Q

genetic code-initiation and haltation of protein synthesis

A
  • AUG codon initiates
  • UAA, UAG, UGA codon halts protein synthesis
147
Q

Vesico-ureteral Reflux

A
  • PP: caused by retrograde urine flow into the ureter
  • hydrostatic pressure of refluxing urine along with infections d/t ascending bacteria causes inflammation
  • compound papillae in the upper and lower poles of the kidney are most susceptible to reflux-induced damage
  • gross: dilated calyces and overlying renal cortical scarring
148
Q

signs of recurrent pyelonephritis

A
  • h/o recurrent fever
  • abdominal pain
  • imaging findings with renal scarring
149
Q

ureter and bladder angles

A
  • nml: ureters travel through bladder wall at an oblique angle
  • when bladder fills intramural ureter becomes compressed
  • flap-valve mechanism prevents retrograde flow of urine
  • with VUR (vesico-ureteral reflux), FV mech is fucked because the ureter enters the bladder at a more perpendicular angle
150
Q

What are the consequences of VUR

A
  • higher risk for chronic pyelonephritis
  • if uncorrected, can lead to loss of nephrons and secondary HTN
151
Q

FF, RBF, RPF, GFR

A

FF=GFR/RPF

RPF=RBF*(1-HCt)

152
Q

What are the steps of GFR autoregulation

A
  • DEC arterial pressure
  • DEC RPF (DEC glomerular hydrostatic pressure)
  • DEC GFR (DEC NaCl reaching macula densa)
  • afferent arteriolar dilation AND (via RAS activation) efferent arteriolar constriction
  • restoration of GFR and INC FF
153
Q

HUS triad (MAT)

A
  • microangiopathic hemolytic anemia (MAHA)
    • with schistocytes
  • thrombocytopenia
  • acute kidney injury
154
Q

HUS etiology and epi

A
  • major cause of acute renal failure in young kids
  • most cases d/t: intestinal infection by Shiga toxin (verotoxin)-producing organisms
155
Q

HUS pathophys

A
  • shiga toxin (vero-toxin)-producing organisms
  • toxins injure the endothelium of preglomerular arterioles and glomerular capillaries
  • leads to platelet activation and aggregation and the formation of microthrombi
156
Q

K in the tubular fluid

A
  • Bowmans capsule: 100%
  • proximal tubule: 35%
  • THICK ascending loop: 10%
  • collecting duct: 110%
157
Q

What are some causes for INC K excretion

A
  • High extracellular K levels
  • INC aldosterone
  • alkalosis
  • volume expansion, high sodium intake, or diuretic use (thiazide and loop diuretics)=INC fluid flow through the distal tubule, quickly flush away secreted K
158
Q

What is the mc c/o unilateral fetal hydronephrosis

A
  • inadequate canalization of the URETERO-pelvic jxn, the connection site between the kidney and the ureter
  • undiagnosed NBN CP: palpable abdominal mass reflecting an enlarged kidney
159
Q

IL-who? IL-2!

A
  • produced by helper T cells
  • stimulates the growth of CD4+ and CD8+ T cells and B cells
  • activates NK cells and monocytes
  • INC activity of T cells and NK cells gives IL-2 its ANTI-cancer effect on metastatic melanoma and RCC
160
Q

Alkaptonuria

A
  • AR
  • lack of homogentisic acid dioxygenase blocks the metabolism of tyrosine
  • leads to an accumulation of homogentisic acid
  • CP:
    • black urine color when exposed to air
    • blue-black pigmentation on the face
    • ochronotic arthropathy
161
Q

Eplerenone

A
  • aldosterone antagonist (along with sprinolactone–S and E of SEAT)
  • can be used as medical therapy for Conns syndrome
162
Q

primary HYPER-aldosteronism (Conn’s syndrome)

A
  • CP:
    • HTN
    • hypokalemia
    • metabolic alkalosis
    • DEC plasma renin activity
  • aldosterone causes:
    • resorption of sodium and water + wasting of K and H ions at distal nephron=hypokalemia and alkalossis
    • will also suppress renin activity as pt of a feedback inhibition loop
163
Q

A1AT Deficiency

A
  • AcoD
  • affects lung and liver
  • alpha-1 anti-trypsin=serum protein (produced mostly in liver)
  • inhibits neutrophil elastase (and other proteolytic enzymes), so reduces tissue damage caused by inflammation
  • Histo: reddish-pink, PAS positive granules of unsecreted, polymerized AAT in the periortal hepatocytes
164
Q

What happens in HF in an attempt to maintain effective intravascular volume?

A
  • stimulation of sympathetic nervous system an the RAA system
  • a1 to a2 by endothelial-bound ACE in lungs
  • a2:
    • systemic vasoconstriction to INC bp
    • efferent arteriolar vasoconstriction to maintain GFR
165
Q

What are the main characteristics of nephrotic syndrome?

A
  • massive proteinuria (>3.5g/day adults, >40mg/m2/hr in kids)
  • hypO-albuminemia (<2.5g/dL)
  • generalized edema
  • hyperlipidemia
  • lipiduria
166
Q

pathogenesis of nephrotic syndrome

A
  1. INC permeability of the clomerular capillary wall to plasma proteins leas to massive urine protein loss (mostly albumin, sometime globulins)
  2. drop in colloid osmotic pressure in blood, fluid moves into interstitial tissue=EDEMA
  3. fluid shift=depeltion of intravascular volume=DEC renal perfusion pressure–>triggers RAA=aldo syn and Na retention (and water)=exacerbates edema
  4. liver increases protein syn (incuding lipoproteins)
  5. lipiduria
167
Q

acute interstitial nephritis (AIN)

A
  • CP:
    • fever
    • maculopapular rash
    • symptoms of ARF
    • 1-3wks after beginning tx with: beta-lactam B or other
  • Clinical clues: peripheral eosinophilia and eosinophiluria
  • symptoms resolve completely after cessation of the offending medication
  • glomeruli are usually spared
168
Q

what path damages small renal arterioles?

A

commonly damaged in hypertensive or diabetic nephropathy

169
Q

When does IC vasculitis develop

A

in conditions such as SLE and HSP; can cause a proliferative glomerulonephritis characterized by INC glomerular cellularity

170
Q

Achondroplasia-Mode of Inheritance

A
  • AD d/o
  • results in GOF mut inthe FGFR gene
  • most infected indivs are heterozygous and have 50% chance of transmitting mut to their offspring (Punnett squarezzz)
171
Q

What is the tx choice for DKA?

A
  • tx: IV nml saline and insulin
  • they INC bicarb and Na and DEC serum glucose, osmolality, and K
172
Q

muddy brown casts are pathognomonic for?

A

ATN (acute tubular necrosis)

173
Q

NFKB

A
  • TF with a critical role in the immune response to infection
  • (upregulates transcription of G-CSF and TNF-alpha)
  • normally present in the cytoplasm in a latent, inactive state bound to its inhibitor protein IKB
  • extracellular substances such as LPS can initiate a signal cascade that results in the destruction of IKB and translocation of free NFKB to the nucleus
174
Q

JAK2

A
  • TK involved in the signalling PW for myeloproliferation
  • constituent activation is assoc w:
    • polycythemia vera
    • essential thrombocytosis
    • myelofibrosis
  • does not play a major role in the immune resp to infection
175
Q

Amphotericin B toxicity

A
  • common electrolyte disturbances d/t INC in distal tubular membrane permeability:
    • hypO-kalemia
    • hypO-Mg
176
Q

What is the most toxic antifungal meication, and what is its more dangerous adverse effect

A
  • Ampho B and its nephrotoxicity
    • d/t DEC in GFR and direct toxic effects on the tubular epithelium
    • tox can lead to anemia (DEC EPO production) and electrolyte abnormalities
177
Q

Which part of the nephron is IMPERMEABLE to water

A

thich and thin ASCENDING LoH

178
Q

Which pt of the nephron has high permeability to water?

A

descending limb of the LoH

179
Q

Homocystinuria

A
  • mc cause: defect in cystathionine synthase
  • inability to form cysteine from HOMO-cysteine
  • cysteine becomes essential in affected pts
  • HOMO-cysteine buildup leads to elevated methionine
  • HOMO-cysteine is PRO-thrombic…results in premature thromboembolic events :
    • atherosclerosis
    • acute coronary syndrome
180
Q

What random shit can you tx with Acetazolamide (CAi)

A

relieve intraocular pressure in open-angle and angle-closure glaucoma

181
Q

What are the target organs of m1 receptor?

A

brain

182
Q

What are the target organs of M2 receptor

A

heart

183
Q

What are the target organs of M3 receptors?

A
  • peripheral vasculature
  • lung
  • bladder
  • eyes
  • GI
  • skin
184
Q

Who are the loop diuretics?

MOA?

A
  • Furosemide, Torsemide, Bumatenide, Ethacrynic acid
  • MOA: inhibit Na-K-2Cl cotransporter in THICK ascending LoH
185
Q

Loop diuretic electrolyte abnormalities+clinical indications

A
  • electrolyte abnormalities:
    • hypO-kalemia
    • metabolic ALK-alosis
    • hypO-calcemia
  • Ci: volume-overloaded states (CHF)
186
Q

Who are the thiazide diuretics? MOA?

A
  • Hydrochlorothiazide (HOT), Chlorthalidone, Indapamide, Metolazone
  • inhibits the Na-Cl cotransporter in the early DCT
187
Q

Thiazide diuretic electrolyte abnormalities and clinical indications

A
  • electrolytes:
    • hypO-natremia
    • hypO-kalemia
    • metabolic alkalosis (HYPER-uricemia)
    • HYPER-calcemia
  • Ci:
    • HTN
    • Ca nephrolithiasis prophylaxis
188
Q

carbonic anhydrase inhibitors (Acetazolamide) MOA

A

inhibit CA enzyme in the proximal tubule (ALL)

189
Q

CAi/Acetazolamide electrolyte abnormalities and clinical indications

A
  • refractory metabolic ALK-alosis
  • intracranial HTN
190
Q

Which two drug groups cause HYPER-kalemia and metabolic acidosis…ci?

A
  • sodium channel blockers and mineralcorticoid receptor antagonists
  • ci: often used in synergy with loop and thiazide diuretics to limit potassium loss
191
Q

Sodium channel blockers…who? MOA?

A
  • Amiloride and Triamterene (AT of SEAT)
  • MOA: inhibit the apical ENac channel in the cortical CD
192
Q

mineralcorticoid receptor antagonist…who? MOA?

A
  • Spironolactone and Eplerenone (SE of SEAT)
  • used in synergy with loop and thiazide diuretics to limit K loss
193
Q

ACEi MOA

A
  • reduce A2=cause EFFERENT arteriole dilation=DEC glomerular pressure and filtration rate
  • can precipitate acute renal failure in pts with reduced intrarenal perfusion pressure (…eg..:
    • renal artery stenosis (RAS)
    • CHF
    • hypO-volemia
    • chronic renal dz
194
Q

ACEi SE

A
  • can cause an acute rise in sCr by blocking angiotensin mediated efferent arteriole vasoconstriction
    • leads to a reduction in renal FF
  • in pts dependent on EFFERENT arteriole constriction to maintain renal perfusion (those with RAS), ACEi can be detrimental by precipitating ARF
195
Q

Prostaglanding and Loop diuretics

A
  • loop diuretics stimulate renal PG release
  • this INC RBF, leading to INC GFR and enhanced drug delivery
  • concurrent use of NSAIDS with loop diuretics can result in a decreased DIURETIC response
196
Q

Bradykinin

A
  • important mediator in the bodys inflamm response
  • peptide that stimulate pain, vasodilation, and INC vascular permeability
197
Q

Which K-sparing diuretic causes gynecomastia and anti-androgen effects?

A

Spironolactone

198
Q

Effective discharge planning

A
  • requires collab of multiple disciplines:
    • physician
    • nurse
    • social worker
  • SW can be instrumental in assessing whether the pt has adequte family or caregiver support at home
199
Q

Why is the clearance of inulin used to calculate GFR

A
  • it is neither secreted NOR reabsorbed by the renal tubules
  • filtered amount=excreted amount
200
Q

Renal stone formation

A
  • renal calculi occur when there is an ambalance of the factors that facilitate and prevent stone formation
  • INC concentrations of the following promote salt crystallization:
    • calcium, phosphate, oxalate, UA
  • INC citrate and high fluid intake help prevent calculi formation
201
Q

How does INC citrate have a stone-preventing effect?

A
  • HIGH urine citrate binds to free (ionized) calcium, thus preventing its precipitation and facilitating its excretion
  • K citrate is often prescribed to prevent recurrent calcium stones in adults when dietary modifications are unsuccessful
202
Q

Ethylene Glycol and toxic Tubular necrosis

A
  • proximal tubular cell ballooning an vacuolar degeneration in a pt with acute RF=ATN
  • oxalata crystals in the tubular lumen is suggestive of ethylene glycol poisoning
  • EG found in antifreeze (and fireball, yummm)
  • EG rapidly absorbed from GI tract, metabolized to glycolic acid which is toxic to renal tubules and oxalic acid which precipitate as ca-oxalate crystals
203
Q

Ethylene Glycol s/s

A
  • symptoms of ethanol intoxication
  • signs of acute renal failure 24-72 hr after ingestion:
    • oliguria
    • anorexia
    • flank pain
  • high AG metabolic acidosis and osmolar gap are typically seen
  • UA: tubular casts and oxalate crystals
  • LM: morphologically nml glomeruli with proximal tubular necrosis
204
Q

Give an example of how to help reduce the incidence of medication errors

A

avoid the use of unsafe abbreviations and trailing zeros in medication orders

205
Q

ureter Blood supply

A
  • proximal ureter-branches of renal artery
  • distal ureter-superior vesical artery
  • in between-anastomic, highly variable, possible afferent branches from gonadal, common and internal iliac, aorta, uterine arteries
206
Q

in a kidney transplant operation where is the donor kidney placed

A
  • native kidney are left in place, donor is placed retroperitoneally in the right iliac fossa
  • establish blood supply by anastomosing donor renal artery with the recipients external iliac artery
  • most distal pt of the ureter may be susceptible to ischemia d/t lack of anastomotic connections
    • leakage of urine 5-10 days following transplant
207
Q

Holo-pro-sencephaly

A
  • malformation characterized by a spectrum of fetal anomalies d/t incomplete division of the forebrain (or proencephalon)
  • [malformation=primary, intrinsic defect in the cells or tissues that form a structure leading to a chain of downstream anomalies]
208
Q

define deformations

A
  • fetal structural anomalies that occur d/t extrinsic mechanical forces
  • m/c: pressure applied by the uterus
209
Q

define disruption

A
  • secondary breakdown of a previously nml tissue or structure
  • Ex: rupture of the amnon d/r fetal development may produce amniotic bands which can compress or amputate fetal limbs <amniotic></amniotic>
210
Q

define sequence

A
  • occurs when a number of abnormalities result from a single primary defect
  • ex: oligohydramnios causing Potter sequence etc
211
Q

What are two examples of age-related changes

A
  • presbyopia and skin wrinkles
  • presbyopia: d/t denaturation of structural proteins within the lens
    • leads to loss of lens elasticity
  • skin (rhytides) wrinkles: d/t DEC synthesis (DEC fibroblasts) and INC breakdown of collagen and elastin
    • with age, skin becomes atrophic, fragile, LESS elastiity, LESS subdermal fat
    • dermal and epidermal thinning
    • flatteing of dermoepithelial jxn
212
Q

ADH and Urea Clearance

A
  • vasopressin (ADH) and desmopressin (DDVAP-synthetic ADH analogue) cause a V2 receptor-mediated INC in water and urea permeability at the INNER medullary COLLECTING DUCT
  • resulting rise in urea reabsorption (DECreased urea clearance) enhances medullay osmotic gradient–>allows production of maximally concentrated urine
213
Q

Ca in the tubule

A
  • majority of filtered calcium is passively absorbed in the proximal tubule and ascending LoF
  • further ca reabsorption by the distal and collecting ducts is stimulated by parathyroid hormone
214
Q

RCC

A
  • aka clear cell carcinoma
  • mostly originate from epithelial cells of the proximal renal tubules
  • mc type of kidney tumor
  • HIGH lipid content
  • gross: golden ylw mass
  • LM: large, rounded, polygonal cells with abundant clear cytoplasm and eccentric nuclei
  • detected incidentally at an advanced stage
  • mc site for mets: LUNGS
215
Q

transitional cell carcinoma

A
  • responsible for 90% of the tumors involving the renal pelvis
  • arises from renal pelvis lining
  • tends to multifocal in nature
  • often forms papillary tumors composed of urothelium supported by a thin fibrovascular stalk
216
Q

renal oncocytomas

A
  • v. rare tumors
  • originate from CD cells
  • oncocytes=lage, well-differentiated neoplastic cells
  • contain numerous mitochondria
217
Q

Cystinuria

A
  • AR d/o
  • PP: defective transportation of cystine, ornithine, arginine, and lysine across the intestinal and renal tubular epithelium (COLA shares a common transporter in the intestinal lumen and kidneys)
  • clinical manifestation: recurrent nephrolithiasis
  • UA: pathognomonic hexagonal cystine crystals
218
Q

What are the two types of calcium stones?

A
  • frequency: 70-80%
  • ca oxalate-micro: octahedron (square with an X in the ctr)
  • ca phosphate-micro:
    • elongated, wedge-shaped
    • forms rosettes
    • pH>7
  • both: HIGH radiograph opacity
219
Q

Funerals put stu on the MAP

A
  • Magnesium ammonium phosphate (struvite or triple phosphate)
  • freq: 15%
  • high radiography opacity
  • pH>7
  • micro: rectangular prism (coffin lids)
220
Q

uric acid stones

A
  • freq: 5%
  • pH<7
  • micro: ylw or red-brown diamond or rhombus
221
Q

Cystine

A
  • freq: 1%
  • pH<7
  • micro: flat, ylw HEX-agonal
222
Q

Which thiazide is more potent in lowering bp than the others?

A
  • Chlor-Thalidone..but also has more associated metabolic abnormalities
  • significant hypO-kalemia can cause muscle weakness, cramps, and possible rhabdomyolysis
223
Q

(idiopathic) Membranous Nephropathy (MN)

A
  • white ppl live in MN
  • idiopathic MN is assoc w/ circulating IgG4 Ab to the phospholipase A2 receptor
    • may play a role in the development of the dz
  • The M-type PLA2R is a transmembrane R found in high concentrations in glomerular podocytes
224
Q

Chronic kidney dz with mineral bone disease

A
  • CP: HYPEr-phosphatemia, secondary HYPER-parathyroidism, and DEC calcitriol levels
  • pts can be asymptomatic or develop weakness, bone pain, and fractures
225
Q

what is the most common small vessel vasculitis in kids

A
  • HSP-Henoch-Schonlein purpura
  • affects boys 2-10yo
  • often preceded by viral or streptococcal URTI
  • symptoms develop a few wks after the associated illness resolves
  • PP: Ag from the infection stimulates production of IgA Ab and IgA-containing immune complexes then deposit in vessel walls, induce inflamm rxn
  • –IgA-mediated leukocytoclastic (hypersensitivity) vasculitis
226
Q

In which organs are the effects of vasculitis seen most prominently?

A
  • GI tract-intermittent severe abdo pain, uppper and lower GI bleed, INC r/o intussusception
  • Kidneys-similar to IgA nephropathy in Berger dz…mesangial proliferation and crescent formation
  • Skin-palpable purpura on butt and lower extrmeities, d/t leukocytoclasis of cutaneous vessels
  • Joints-self-limited migratory arthralgias and arthritis; m/c seen in large jts of lower extremities (ankles, knees)
227
Q

Kawasaki dz

a. characteristic findings
b. other symptoms

A
  • a. swollen LN and red eyes
  • b. other s/s: high fevers, strawberry tongue, perioral erythema and fissuring, periungual desquamation
228
Q

What are the clinical features of acute post-streptococcal glomerulo-nephritis

A
  • canbe asymptomatic
  • if symptomatic:
    • gross hematuria (tea-/cola-colored urine)
    • edema (periorbital, generalized)
    • HTN
229
Q

what is the m/c c/o calcium kidney stone dz?

A
  • most common cause: idiopathic HYPER-calciuria!
  • characterized by:
    • nml sCa with HYPERcalcuria
  • other RF:
    • HYPER-oxaluria
    • HYPER-uricosuria
    • low urine volume
    • HYPO-citraturia
230
Q

PAH and Creatinine

A
  • Net tubular SECRETION
  • excreted amt>>filtered amt..more gets added to the shit that has already been filtered
231
Q

Glucose, Sodium, and Urea

A
  • net tubular reabsorption
  • excreted amt<<filtered amt…some of the shit that is filtered out slurped back in>

</filtered>

232
Q

Goodpasture syndrome

A
  • PP: anti-GBM Ab that react with a component of the alpha3-chain of collagen type IV
    • **GBM is composed of TYPE FOUR
  • CP: rapidly progressive glomerulonephritis resulting in acute RF and hemoptysis d/t pulmonary hemorrhage
  • LM: crescent formation
  • anti-GBM Ab cross-react with other basement membranes, especially those in the lung alveoli=pulmonary hemorrhage (hemoptysis)
233
Q

BOO and BPH

A
  • straining on urination in an elderly male suggests BOO (bladder outflow obstruction)
  • BOO usually d/t prostate enlargement
    • m/c cause: BPH
  • as bladder outlet obstruction worsens, pts experience a sensation of incomplete bladder emptying
    • usually signifies urinary retention
    • overflow incontinence=next clinical stage
234
Q

BPH

A
  • combo of epithelial and stromal hyperplasia
  • predom in peri-urethral and transition zones
  • on palpation: rubbery consistency (vs. prostate ca nodular and firm)
  • leads to intermittent BOO and overflow incontinence
  • urinary rtention results in INC pressure in urinary tract and resultant reflux nephropathy
  • ultimately: hydronephrosis and renal interstitial atrophy and scarring
  • prolonged obstruction: permanent damage and chronic renal failure
235
Q

What toxicity occurs with higher dosages of loop diuretics

A
  • ototoxicity occurs with higer dosages
  • usually reversible
  • other ototoxic agents: aminoglycosides, salicylates, cisplatin
236
Q

RPGN can be caused by a number of diseases, what are the three classifications which are based on immunologic findings? (3)

A
  • Anti-GBM RPGN
    • liner GBM deposits of IgG and C3 found on IF
    • some pts: anti-GBM Ab cross-react with pulmonary alveolar BM=pulmonary hemorrhages (Goodpasture syndrome)
  • IC RPGN
    • “lumpy bumpy” granular pattern of staining for Ab (IgG & IgA) and complement on IF microscopy
    • can be a complication of post-strep GN, SLE, IgA nephropathy, or HSP
  • pauci-immune RPGN
    • no BM deposits
    • ANCA in serum
    • assoc w/: granulomatosis w/ polyangitis or microscopic polyangitis
237
Q

What are the most potent diuretics?

A
  • LOOP DIURETICS
  • MOA: inhib Na-K-2Cl cotransporter in the medullary and cortical thick ascending limb of LoH–>INC Na, Cl, and H20 excretion
  • Ci: used as first-line for rapid relief of symptoms in pts with acute decompensatd HF
238
Q

Beta-blockers effect on RAAS system

A
  • beta-adrenergic blocking dx INHIBIT renin release by blocking Beta-1 receptor-mediated regulation of the RAAS
  • =reduced plasma renin activity
  • =reduction in A1, A2, and aldosterone levels
  • (RAA is all: omg lets INC bp…beta blockers are all: simmer tf down)
239
Q

What are the THREE major components that regulate RAAS

A
  • macula densa (distal tubule sodium sensor)
  • intrrenal baroreceptors
  • beta-adrenergic receptors
    • mediated through sympathetic stimulation of beta-1 receptors on JG cells
    • have no affect on ACE activity=do NOT affect bradykinin levels
240
Q

medication review

A
  • medication-related falls are a common problem in elderly nursing home pts
  • optimal management should include careful me review AND discontinuation of agents assoc w/ INC fall risk
241
Q

Phospho-inositol second messenger system

A
  • begins with ligand-receptor binding and Gq-protein activation
    • exchange of GDP for GTP on the alpha-subunit of Gq
  • Gq alpha subunit conformation change leads to activation of phospho-lipase C (PLC)
  • PLC hydrolyzes phos-phatidyl inositol bisphosphate (PIP2) and forms diacylglycerol (DAG) and inositol triphosphate (IP3)
  • finally: IP3 activates Protein kinase (PKC) via an INCREASE in intracellular Ca2+
242
Q

Which hormone receptors exert their intracellular effects via the PI system (phospho-inositol)

A
  • alpha-1 adrenergic
  • M1 and M3 cholinergic
  • V1 (vasopressin)
  • H1 (histamine)
  • oxytocin
  • Angiotensin 2
  • TRH
  • GnRH
243
Q

ACEi Effect on RAAS

A
  • prevent conversion of A1 to A2
  • leads to DEC levels of A2 and aldosterone
  • INC plasma renin and A1 d/t inhibition of negative feedback (inhib the inhibitors)
  • INC level of bradykinin (ACE is a kininase, degrades bradykinin)
    • responsible for coughing seen in treted pts
244
Q

ARBs effect on RAAS

A
  • block the action of A2 on AT1 receptors
  • leads to INC levels of renin and A1&A2
  • no effect on bradykinin levels
245
Q

How can you reduce the risk of progression of diabetic nephropathy in pts with proteinuria

A
  • appropriate glycemic and bp control
  • ACEi and A2RB are the preferred anti-hypertensive agents d/t their bp-INDEPENDENT antiii-proteinuric effects
246
Q

CKD-MBD

A
  • pts with CKD may develop renal osteodystrophy (abnormal bone path) from secondary hyperparathyroidism (caused by hyper-phosphatemia and hypo-calcemia)
247
Q

Lithium-induced Diabetes Insipidus

A
  • result of Lithium’s antagonizing effect on the action of vasopressin on principial cells within the collecting duct system
  • s/s:
    • psych hx+polydipsia, polyuria, inappropriately low urine specific gravity after 8hr of water restriction
  • Li reduces the ability of the kidneys to concentrate urine by antagonizing the action of vasopressin (ADH) in collecting duct and tubules
  • can be permanent if yrs of chronic use
248
Q

Trisomy 21

A
  • Down syndrome
  • meiotic NON-disjxn
  • assoc w/:
    • DEC maternal alpha-fetoprotein
    • INC nuchal translucency (via US)
  • mc gi complication: duodenal atresia
    • CP: first few days w/ bilious emesis and DOUBLE-BUBBLE sign <dilated></dilated>
249
Q

Physical Features of Down syndrome

A
  • epicanthic folds (eyes)
  • upslanting palpebral features
  • low-set small ears
  • flat facial profile
  • short neck with excess skin
  • furrowed tongue
  • sandal-toe deformity
  • hypoplastic incurved 5th finger
  • single transverse palmar crease
  • brushfield spots
250
Q

ACEi SE w/ RAS

A
  • pts with evidence of diffuse atherosclerosis may have bilat RAS
  • GFR is therefore dependent on A2-mediated efferent arteriolar vasoCONSTRICTION
  • ACEi or A@RBs cause efferent arteriolar vasoDILATION that causes the GFR to fall and may lead to the development of acute renal failure
251
Q

RF for nephrolithiasis (diseases)

A
  • primry HYPER-parathyroidism (–>hyper-calciuria)
  • Crohn dz (–>hyperoxaluria)
  • distal RTA (–> hypocitraturia)
  • gout (–>hyperuricosuria)
252
Q

RF for nephrolithiasis (dietary intake)

A
  • low fluid (dehydration)
  • low calcium
  • high oxalate (spinach, rhubarb)
  • high protein
  • high sodium
  • high fructose
253
Q

what are the three phases for the clinical course of ATN

A
  • initiation
  • maintenance (oliguric)
  • recovery: re-epithelization of tubules

BOARDS! (14 decks)

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