Save
Busy. Please wait.
Log in with Clever
or

show password
Forgot Password?

Don't have an account?  Sign up 
Sign up using Clever
or

Username is available taken
show password


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.
Your email address is only used to allow you to reset your password. See our Privacy Policy and Terms of Service.


Already a StudyStack user? Log In

Reset Password
Enter the associated with your account, and we'll email you a link to reset your password.
focusNode
Didn't know it?
click below
 
Knew it?
click below
Don't Know
Remaining cards (0)
Know
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how

Path 20 Kidney

LECOM Path Ch 20 Kidney

QuestionAnswer
4 stages of renal failure Deminished renal reserve, Renal insufficiency, Chronic renal failure, End-stage renal disease
Progression to renal failure usually ensues when GFR is reduced to 30-50% of normal
Acute Nephritic, after infection, Sub-epithelial humps, granular IgG and C3 in GBM, diffuse proliferation PSGN
Diffuse nephritis, global hypercellularity, Granular IF PSGN
Rapidly progressive glomerulonephritis, Linear IgG and C3 and/or fibrin crescents, proliferative, maybe crescenteric Goodpasture
RPGN Type I mediated by Anti-GBM
RPGN Type II mediated by Immune complex
RPGN Type III mediated by Pauci Immune
Type I RPGN that cross reacts with lung BM Goodpasture
Elevated titer in Type III RPGN ANCAs
Ruptures of the GBM on EM, inflammatory and parietal cell proliferation in Bowman space RPGN/ cresenteric
Escape of this into bowman’s space is a leader in crescent development fibrinogen
MCC of nephrotic syndrome in children Minimal-Change Disease
Nephrotic syndrome Dx with >3.5g of daily proteinuria
Membranous Nephropathy mediated by chronic immune-complex mediated
Nephrotic, Diffuse thickening of capillary walls, tubular epithelial cells with protein reabsorption droplets, diffuse GBM granular staining, sub-epi deposits on EM membranous Nephropathy
Pathognomonic finding of spikes on GBM w. silver stain Dx? Membranous Nephropathy
Membranous nephropathy vs Minimal Change disease: difference in onset Minimal change is selective proteinuria and responds to corticosteroids
Nephrotic, Diffuse effacement of podocytes on EM, but look normal on light microscopy. Dx? Minimal-Change Disease
Most characteristic thing about Minimal-Change disease is it’s response to corticosteroid therapy
Effacement of podocytes with normal glomeruli Dx? minimal change
MCC of nephrotic syndrome in adults in the US is Focal Segmental Glomerulosclerosis (FSGS)
MC location of lesion is FSGS juxtamedullary glomeruli
Disease states that can cause FSGS (5) HIV, IV drug use, Sickle Cell, morbid obesity, loss of renal tissue
Hylinosis and sclerosis of some viewed glomeruli and only some of the capillaries FSGS
Retraction of entire glomerular tuft, proliferation and hypertrophy of glomerular visceral epithelial cells. Dx and most characteristic lesion of? Collapsing glomerulopathy of FSGS and in HIV-nephropathy
MC lesion in HIV nephropathy collapsing variant of FSGS
Alteration in the GBM, proliferation of glomerular cells, and leukocyte infiltration membranoproliferative glomerulonephritis (MPGN)
Other name of Type II primary MPGN dense-deposit disease
Type I MPGN is Dx when finding immune complexes in the glomerulus and activation of both compliment pathways
Type II MPGN is Dx when finding decreased serum C3 but normal C1 and C4
Is there IgG deposits found in Dense Deposit Disease? no, only C3 and properdin
70% of Pts w/ DDD have this circulating antibody C3NeF
“Tram-tracking” or duplication of the basement membrane is seen in what disease MPGN
Large hypercellular glomeruli, GBM thickened, IgG and C3 in granular pattern in subendothelial location. Dx? MPGN Type I
Large hypercellular glomeruli, dense-ribbon like GBM, C3 in basement membrane granular or linear, and circular rings of C3 in mesangium. Dx? MPGN Type II aka DDD
Causes of Secondary MPGN (all type I)(7) SLE, HBV, HCV, HIV, alpha 1 antitrypsin, leukemia or lymphoma
Frequent cause of recurrent gross or micro hematuria, probably MC glomerulonephritis worldwide IgA nephropathy
Which subclass forms Ab in IgA nephropathy IgA1
Which pathway is activated in IgA nephropathy alternative compliment pathway
2 causes of secondary IgA nephropathy celiac disease and liver disease
Teen presents with gross hematuria after respiratory infection a week before. Dx and outlook? IgA nephropathy, variable
Classic findings in IgA nephropathy mesangial widening with IgA and C3 in the mesangium
Hematuria with progression to renal failure, eye disorders Dx? And what else will be found with sensitive testing Alport Syndrome and hearing deficiency
Cause of Alport Syndrome defective collagen IV synthesis; a5 in X-linked variety
On EM of 2 brothers glomeruli: irregular foci of thickening alternating with attenuation of the GBM, splitting and lamination of the lamina densa “basket weave” appearance. Dx? Alport syndrome
2 diseases linked to defective type IV collagen Alport and Thin Basement Membrane Lesion/Benign Familial Hematuria
Gross appearance of kidneys in Chronic glomerulonephritis symmetrically contracted, diffusely granular cortical surface
Findings in a dialysis kidney (5/6) arterial intimal thickening, calcifications, calcium oxalate crystals, cystic disease, increased renal adenomas and adenocarcinomas
Purpuric skin lesions on extensor surfaces of arms and legs and buttock; abdominal pain, GI bleed; non-migratory arthralgias; renal abnormalities Henoch-Schonlein Purpura
Mesangial proliferation, IgA and C3 deposition in the mesangium. 2 DDx and what would differentiate IgA nephropathy or Henoch-Schonlein Purpura; subepidermal hemorrhages and necrotizing vasculitis of small vessels, and GI manifestation
Arteriolar manifestation of diabetic nephropathy hylanizing arteriolar sclerosis
Capillary basement membrane thickening, diffuse mesangial sclerosis, nodular glomerulosclerosis diabetic nephropathy
Normal or enlarged kidneys with deposition of AL or AA type chains. Dx? amyloid kidney
MCC of acute renal failure AKI or ATN
4 types of ATN/AKI: due to ischemia, Direct toxic injury, Acute tubulointerstitial nephritis from drug hypersensitivity, urinary obstruction
2 critical events in AKI tubule cell injury and persistant/severe disturbance in blood flow
In AKI, loss of cell polarity causes what abnormal ion transport, increase Na+ to distal tubules, causes vasoconstriction
What causes luminal obstruction in AKI detached injured cells
Patchy tubular necrosis, in short lengths around straight segments of proximal tubule and ascending limb of Loop of Henle. Type of AKI? Ischemic
Extensive necrosis along proximal convoluted tubule. Type of AKI Toxic AKI
2 areas most susceptible in ischemic AKI straight portion of proximal tubule and ascending thick limb in medulla
Area most susceptible to toxic AKI proximal convoluted tubule
3 stages of AKI initiation, maintenance and recovery
Findings in initiation phase of AKI slight decline in urine output and rise in BUN
5 findings of maintenance phase of AKI sustained decrease in urine to 40-400ml/d; salt/water overload; rising BUN; hyperkalemia; metabolic acidosis
6 Findings in recovery stage of AKI increased urine output; loss of large amounts of water, sodium and potassium(hypokalemia); increase infection risk;BUN/Creatinine return to normal
Acute vs Chronic tubulointerstitial nephritis: interstitial edema, eos and neuts, focal tubular necrosis Acute
Acute vs Chronic tubulointerstitial nephritis: mononuclear leukocytes, interstitial fibrosis, widespread tubular atrophy chronic
(4 bugs) MCC of UTI (85%) gram neg bacilli; E.coli; Proteus; Klebsiella; Enterobacter
MCC of clinical pyelo ascending infection
Acute pyelonephritis with reflux: damage is mostly seen where? upper and lower poles
Patchy interstitial suppurative inflammation, intratubular aggregates of neutrophils, and tubular necrosis Dx? acute pyelonephritis
3 complications in Acute Pyelo and their special circumstances Papillary (coag)Necrosis: in Pt’s with DM and obstruction; Pyonephrosis: complete obstruction; Perinephric abscess: extension through renal capsule
What finding differentiates kidney from bladder Infx? leukocyte casts
Cause of emerging pyelonephritis in transplant Pt’s polyomavirus
Only 2 tubulointerstitial diseases that affect the renal calyces chronic pyelonephrosis and analgesic nephropathy
2 types of chronic pyelo reflux and obstructive
MC type of chronic pyelo reflux
Asymmetric scarring of kidney with coarse, discrete corticomedulary scars overlying blunted or deformed calyces, with flattened papilla chronic pyelo
What do tubules look like in chronic pyelo atrophy in some and hypertrophy or dilation in others
Foamy macrophages with plasma cells, lymphs and PMN cells in large yello/orange nodule in kidney. Not renal cell carcinoma. Dx and w. what Infx? Xanthogranulomatous pyelonephritis; Proteus infx
Acute Drug induced interstitial nephritis: common drugs(3) and onset synthetic penicillin, diuretics, NSAIDS, 15 days after drug exposure
Kindey injury in acute drug induced nephritis is cause by IgE and/or cell mediated immune reaction; not the drug ie dose independent
Kindey interstitium edema and mononuclear infiltration; eos and neuts in clusters with plasma cells, normal glomeruli Dx? acute drug induced interstitial nephritis
Analgesic nephropathy is cause by what 2 events, in order papillary necrosis, then cortical tubulointerstitial nephritis from urine obstruction
2 drugs causing Analgesic Nephropathy and their action acetaminophen/phenacetin depletes glutathione causing ROS damage and aspirin inhibits vasodialation by PG
Normal or slightly small kidneys, cortical atrophy over papillary necrosis which are in various stages Dx? Analgesic nephropathy
Cancer associate w/ analgesic pephropathy transitional papillary carcinoma of the renal pelvis
Pink/blue tubular casts, angulated and/or fractured, surrounded by macrophages. Dx? Bence-Jones proteinuria / Myeloma Kidney
Normal or slightly shrunken kidneys, leather grain on the outside Benign nephrosclerosis
Medial and intimal thickening of small arteries in kidney with hyaline arteriosclerosis, microscopic subcapsular scars with sclerotic glomeruli benign nephrosclerosis
Pts with malignant HTN with show what type of arterial disease in the kidney malignant /accelerated nephrosclerosis
Early malignant nephrosclerosis shows (3) fibrinoid necrosis of arterioles and small arteries, swelling of vascular intima, intravascular thrombus
Typical arteriopathy in malignant HTN that causes further narrowing of the lumen hyperplastic arteriolosclerosis
“flea bitten kidney” Dx? malignant nephrosclerosis
This finding represents an acute event in a person with HTN fibrinoid necrosis of arterioles
Interlobular arteries and arterioles with proliferation of concentric smooth muscle cells, collagen, and clear layers Dx? 2 names and what it correlates with onion-skinning, hyperplastic arteriolitis; renal failure
Initial cause of HTN with constriction of renal artery is due to increased plasma renin
MCC of renal artery stenosis plaque at the origin
MC location, age and sex for fibromuscular dysplasia of renal artery medial thickening, 20-40yo, women, distal or medial portion of the artery
Typical HUS is most often associated with consumption of food with Shiga-like toxin
MCC of TTP deficiency of ADAMTS13, which regulates vWF
2 MCC of Atypical HUS mutation in compliment-regulatory proteins; or acquired endothelial injury
Initiating event in TTP vs HUS TTP: platelet aggregation by vWF multimers; HUS: endothelial injury
What is usually present and causative in the majority of TTP Pts? antibodies to ADAMTS13
Child Diarrhea then Sudden onset of bleeding, hematemesis, melena, severe oliguria, hematuria, microangiopathic hemolytic anemia, thrombocytopenia and HTN Dx? typical HUS
MC deficiency in atypical HUS factor H, compliment regulatory protein
How to differentiate TTP and HUS? normal ADAMTS13 in HUS
Better outcome typical or atypical HUS? typical
Fever, neurologic symptoms, microangiopathic hemolytic anemia, thrombocytopenia, and renal failure. CNS involvement is a dominant feature TTP
Massive necrosis after an obstetrics emergency is usually limited to where? Dx? cortex; diffuse cortical necrosis
Renal infarcts are usually of what type white
Wedge shaped area of gray white color, depressed scar on cortex Dx? renal infarct
Adult Polycystic Kidney Disease: Inheritance, cyst locations, outcome AD; large multicystic kidneys, liver cysts, berry aneurysms; chronic renal failure at 40-60yo
Childhood Polycystic Kidney Disease: Inheritance, cyst locations, outcome AR; enlarged, cystic kidneys at birth; variable, death in infancy or childhood
Medullary Sponge Kidney: Inheritance, cyst locations, outcome none; medullary cysts on excretory urography; benign
Familial Juvenile Nephronopthisis: Inheritance, cyst locations, outcome AR; corticomedullary cysts, shrunken kidneys; progressive renal failure starts in childhood
Adult-Onset medullary cystic disease: Inheritance, cyst locations, outcome AD; Corticomedullary cysts, shrunken kidneys; chronic renal failure in adulthood
Simple Cysts: Inheritance, cyst locations, outcome none; single or multiple cysts in normal sized kidney; benign
Acquired Renal Cystic Disease: Inheritance, cyst locations, outcome none; Cystic degeneration in end-stage kidney disease; Dialysis dependant
MC mutation in ADPKD PKD1
Better or worse prognosis with PKD1 mutation in ADPKD? worse
Gene affected in ARPKD PKHD1
Bilaterally Enlarged kidneys with smooth external appearance; numerous small cysts on section with dilated elongated channels at right angles to the cortex Dx? ARPKD
Extra-renal disease with ARPKD liver cysts with portal fibrosis
Extra-renal disease with ADPKD cysts in the liver, intracranial berry aneurysm, mitral valve prolapse
Multiple cystic dilations of the collecting ducts in the medulla Medullary sponge kidney
MC malignant kidney tumor in adults renal cell carcinoma
MC malignant kidney tumor in children Wilms tumor
On autopsy small tumor with the cortex, pale yellow, discrete, well circumscribed nodules, complex branching cuboidal cells Dx? Renal Papillary Adenoma
Angiomyolipomas are present in 25-50% of Pts with tuberous sclerosis
Clinical importance of angiomyolipoma? likes to spontaneously hemorrhage
Solitary tumor in kidney, tan/brown, well-encapsulated, large eosinophilic cells, small round benign nuclei, lots of mitochondria. Dx? And what cell they come from Oncocytoma; intercalated cells
Most significant risk factor for renal cell carcinoma tobacco
MC type of renal cell carcinoma Clear Cell Carcinoma
Loss of VHL on 3p leads to what tumor hereditary and sporadic Clear Cell Carcinoma
Trisomy 7 leads to what renal tumor sporadic and hereditary Papillary carcinoma
Mutated/activated MET leads to what renal tumor sporadic and hereditary Papillary carcinoma
Renal tumor with pale eosinophilic cells, perinuclear halo, in solid sheets. Dx? Chromophobe renal Carcinoma
Renal tumor: nest of malignant cells enmeshed within a prominent fibrotic stroma. Typically in the medulla Collecting duct / Bellini Duct carcinoma
Created by: csheck
Popular Science sets

 

 



Voices

Use these flashcards to help memorize information. Look at the large card and try to recall what is on the other side. Then click the card to flip it. If you knew the answer, click the green Know box. Otherwise, click the red Don't know box.

When you've placed seven or more cards in the Don't know box, click "retry" to try those cards again.

If you've accidentally put the card in the wrong box, just click on the card to take it out of the box.

You can also use your keyboard to move the cards as follows:

If you are logged in to your account, this website will remember which cards you know and don't know so that they are in the same box the next time you log in.

When you need a break, try one of the other activities listed below the flashcards like Matching, Snowman, or Hungry Bug. Although it may feel like you're playing a game, your brain is still making more connections with the information to help you out.

To see how well you know the information, try the Quiz or Test activity.

Pass complete!
"Know" box contains:
Time elapsed:
Retries:
restart all cards