nephrology

Question 1

diagnostic method of kidney

Answer 1

most chronic diseases r asx so picked up incidently on urine analysis or abnormal renal aprameters (creatinine, uric acid, BUN). blood test (ESR,anemia, proteinuria). deranged electrolyte balance.

Question 2

history of patient

Answer 2

good history outlines: questioning & evaluating sx, Socrates to evaluate PAIN (SITE, ONSET, CHARACTERISTICS ,RADIATION, association Factor, time, exacerbating and relieving factors.
pMH, RF’s, FMhx and social hisotry.

Question 3

hsigns and symptoms of kidney dsiease

Answer 3

urination changes (poly/oligo or anuria). foamy/ hematuria.
peripheral oedema -> fluid overload, nephrotic syndrome, hypercholesterlimenia / hypoalbunisim.
hypertension (increased intravascular pressure due to renin). dyspnea (fluid in chest)/ angina.
other signs: difficulty sleeping / fatigue (increased toxin, secondary anaemia).
muscle spasm/twitching: electrolyte imbalance, low Ca 2+,high phosphates (erythropoetin-> stimulate RBC production).
uremia: in R-> uremic pericarditis, uremic encepalopathy (ALS< confusion), asterixis (tremor flap bilateral), pruritis (dry skin).
N+ V (anoreixa, Wt loss)- decreased appetitie
platelet dysfunction (thrombocotyopenia, gingivial bleeds, cutaenous bleeds, epistaxis, petechiae/ purpura, easy bruising).

Question 4

physical exam

Answer 4

inspect for bruises, edema, uremic tinge, vasculitis rash (indicitive for autoimmune vasculitis HSH) . plpation (PCKD enlarged), percuss (R. kidney below 12th ICS-> liver ). pain indicate urolithiasis and pelonephirits (flank P).
ascultation- renal bruits (RA stenosis).
CVAT- tenderness if pain reported on hit).
kidney: 5-6 cm, 125-10 g. from t12 to L3.

Question 5

uroanalysis/ quality of urine.

Answer 5

painless hematuria (malignancy!), hemogloinuria (severe intravascular hemolysis) polyuria (DM, DI, overhydration), persistent hematuria (vesicular or supra/vesicular cause), hematuria on 1st or last part of voiding (urethral damage).
terminology:
polyuria > 2 L/ day in adults.
oliguria (< 500/ ML day) indicate obstrution, renal parenchymal disease).
anuria < 100 ml (stones/ tumor, HTN).
* HTN causes poly/anuria*.
isosthenuria - loss of ability to concentrate / dilute urine-> CKD. specifci grvity 1.010 SG
glycosuria - DM.
proteinuria -1/3 g/l AGN (acute GN) (light) 0.3- 1.5 g/L , mild = 1.5-4 g/l & severe > 4 g/L.
SG: 1.005-1.030 (dehydrated-> 1.030) and lots of fluid (1.001).
urinalysis : presence of blood, protein, glucose, ketone, nitrate, leukocyte, pH, osmolarity- dipstick.

Question 6

urinalysis continued

Answer 6

urine microscope or flow cytometry detect Er (dysmorphic RBC nephritis), RBC casts -> glomerular disease. crystals -> urolithiasis.
leucocytes+ bacteria + white casts-> pyelonephritis.
urine pH (RT acidosis).
collect urine over 24 hrs-> assess calcium oxalate+ urate (renal stone disease) e.g catheterization.
blood values -> serum creatinine ( 53-106 normal) only rises if eGFR < 50% (indirect indicator).
creatinine clearance -80-180 mL/min
U+V/P
if 700-800 begin dialysis.
BUN >/= 20:1 prerena (dehydration).</=10:1 (renal damage.
10:1-2: 1 (normal or post renal cause).
uric acid: metabolite of purine bases.

Question 7

other investigations for diagnosing kidney diseases

Answer 7

USS and biopsy -> nature and extend of disease.
imaging: X ray-> renal size, diff b/w tumors/ casts. dilution of UT.
IVU-. x ray taken via IV bolus injection-> visualise renal parenchyma-> stones, papillae, urothelial malignancy.
CT- lesions, stones.
radionuclide-> cortex, size, function of each kidney

Question 8

nephritic syndrome/AGN

Answer 8

inflammation to glomerulus. microscopic/ macro hematuria, proteinuria, glycosuria (sterile), HTN. extra -renal _> alveolar hemorhage, rash.
AGN causes nephritic syndrome.
damage to bowman capsule causes leaks-> RBC (acanthocytes/ dysmorphic)
podocytes cause proteinuria (<3.5 g/24 hr).
Neu recruited and leak (sterile pyouria).
inflammation reduces eGFR -> oliguria and AKI creatinine increase).
azotemia (increase urea).
RAAS activation (HTN)- Na+ and water retention.

nephrotic if >3.5 g/24 hr.
compexes: rapidly progressive GN, anti GBM antibody (good pasutre), ANCA ( vasculitis), imune complex mediated GN (IgA nephropathy, SLE, PSA), membranoproliferative GN.

Question 9

rapidly progressive GN

Answer 9

aka crescenteric GN. its caused by other GN disease - anca, immune complex or anti GBM.
loss of 50 % GFR.
ruptured capilary wall-> accumulate immune complex, fibrin and fibroblasts, paritetal epithelial cells & leak. proliferate paritetal cell (severe injury)
on biopsy see crescenteric shape on MS.
trx: treat underlying cause.

Question 10

anti GBM ( good pasture)

Answer 10

Ab-Ag mediated inflammation against GBM.
crescent formation and 90% have RPGN.
targets NC1 domain of alpha 1 chai of type 4 collagen (also present in lungs). linear deposition along the GBM. on immunoflourescent.
alveolar haemorrhage (seen 60%) or sometimes isolated.
anti GBM -> plasma phoresies, corticosteroids, cyclophosphamide (immune suppressant agent)
ANCA-> no immune deposit on electron MS and immunofluorescent. account for majority of cases .
pANCA and cANCA against myeloperoxidase and proteinase 3 Neu-> lysosomes and Neu granules activated-> vasculitis.
systemic: prodrome of flu like sx and AKI sx manifest, myalgia, malaise, arthalgia.
Neu-> infiltrate, cause inflammation & necrosis.
monocyte infiltrate-> scarring/ fibrosis.
Trx: steroids, immunosuppressant, azithroprim (12 month till stability).

immune complex-> immunofluorescent seen deposit in GM. histological and
IgA nephropathy. (mesangial and GC IgA deposits)
post strep-> sub-epithelial hum, anti strep Ab.
lupus nephritis: full house IgG, IgA, c3, c1q,

• pathophysiology: activate classical complement pathway (inflammation) associated with low c3, c4 levels.

Question 11

Membrano-proliferative GN

Answer 11

immune complex ediated MPGN and complement mediated mPGN.
causes -idiopathic and secondary is autoimmune, paraproteinaemoa, infection.

complement- decreased serum c3+c4. genentic (complement dysregulation) activates alt. pathway. low c3 and normal c4 levels.
changs: mesanglial expansion, thick BM, tram tracking of BM.

Question 12

extra notes

Answer 12

divided into KD: glomerulopathies (bilateral) and interstitial disease. AGN (post strep 90%) affects children.
primary classification: AGN, CGN, rapid, minimal change GN, membranous and igA nephropathy.
secondary: systemic/ hereditary ( lupus, DM, amyloidosis, wegener’s (angitis), good pastures.
etiology: B-hemolytic infection (most strains r nephritogenic).
other agents include staph, pneumococcus, ricketssia. virus (mumps, small pox, hepatitis.
ma: kidney symmetrically enlarged, petechaie on surface ‘flex-bitten kidney’.
mi- diffused endcapilayr GN.
exudative: cells present, glomeruli hyperaemia-leaky.
proliferative:l structural changes.
sg urine increases 1.001-1.040.
isosthenuria reflects damage to tubules/medulla.
triad of volhard complex (IMPORTANT)
edema (face/periorbital) , slight HTN, haematuria (macroscopic).
urinary syndromes: oliguria/anuria, proteinuria, duiresus, sediment (hematuria).
edematous syndrme: nephrotic?
HTN + CVS syndrome=> retention.
neurological: brain edema seizures.
normal urine protein (1-3 g/L).

Question 13

associated real function loss with AGN

Answer 13

low Egfr, brief azotaemia (BUN elevated).
high Sg.
dx: hx (previous infections, sore throat), bloods (elevated wbc, anemia, increased protein aplha 2 and sigma, fibrinogen increase.
immunological test: ast, decreased complement, increased circulating immune complex.

Question 14

treatment of AGN

Answer 14

penicillin (3-4 ml) 10-14 days.
ampicillin 3-4 g/ 24 hrs.
special cases: erythromycin, cephalosporin.
prophylaxis= benzacillin 200,000 iu.
calcium gluconium 10% twice day.
vit c : 500 mg/2x daily.
diureitcs, anti -hTN (nifedipine) , cardiac failure and treat brain edema’s.
extra notes: nephritic (edema, mild proteinuria, hematuria).

Question 15

chronic GN

Answer 15

progresive GN lasting for more than 3 months. slow cumultative damage and scarring (inflammation) result in nerotic/ neprhtic syndrome. its irreversible.
tubulointersitial fibrosis small size kidney, scarring. reductin in GFR, retention of uremic toxin, electorlyte imbalance, protein, anameia, calcium imbalance.
idiopathic cause, strep, viral hep B,C , HIV/aids, autoimmune disease SLE and oter vasculitis. most commmon in RPGN
focal glomueruloscrlosis is high.
CGN (hardening of arteries)-> scarring/contracted-> severe damage-> RF.
sx: foamy+ cola like hematuria urine, edema, face, legs edema, ascites, PE, anemia, dyspnoea, decreased alertness (uremic).
malaise, HTN secondary, oliguria, uric seizures, cramps, N+ V (electrolyte imbalance/ cerebro-edema).
urameic frost (sweating out stinky crystal uremic).
heavy proteinuria: DM, amylodiosis, membranous, focal sclerosis, minimal changes.
+hematuria: memrbanoproliferative, endocarditis, HSP, lupus.

predominantly haematuria: acute strep, RPGN, HUS.

AGN disappear and re-appear as CGN.

AGN-> CGN-> RF.

Question 16

investigations of CGN

Answer 16

history, systemic investigation (PE),
blood test; thrombocytopenia, high BUN, CK high, HB, pancytopneia, leukopenia, cast present, proteinuria, hypocalcemia, Na,K,ph changes as disease progresses.
KUB, CT, USS- see size of kidney.
biospy-> etiology (few case)
antibody (immunoflorescence) suppress immune system, hep C+ B.
CXR (pericardium check).
abdomen, IVP, urinalysis, HCO3 checked and increased PTH.
managemnet: symptomatic, immunosuppression (teroid, MTX, cyclophsophamide, treat complication, blood transfusion, EPO IV, protein intake, phosphate levels decreased and calcium supplement,
trx: renal replacement, pharmacological, diet and activity (physiotheraphy-> BMI, exercise).
diuretics (furosemide -> fluid, HTN treated.
lifestyle-> restrict na+ and water intake, restrict potassium, po4-, mg2+, cut down protein (uric cut down), maintain weight.

Question 17

CGN

Answer 17

acidosis is common.
end stage-> high mortality.
idioapthoc nephrotic syndrme: minimal change, focal segmental and mesangial prolif.
-BM intact, epithelial foot changes, deposit of IgM.
-all share nephrotic syndrome.
immune- humoral/cell mediated (cytokine GF), complement/ alt pathway.
humoral- insitu (ab-ag complex localised to tissue).
CIC-> trapped and cause glomerulus injury (no specificity).
cell mediated once localised can release ROS, and other harmful metabolite (amplify exisiting immune response)- direct injiry or denature glomerular proteins.

classifications (bulgarian)
INS (mentioned above)
mebraneous prolfierative:
mesanglial igG, igM, C3 depsoits
mix of both

Question 18

acute pyelonephritis

Answer 18

RF same as lower UTI (obstruction, female,catheter, sex,DM). upper (kidney and ureter.
VUR-> retrograde urine, failure of orifice - congenital or bladder outlet obstruction.
urinary stasis.
ascending- e.coli, proteus, enterobacter (bowel flora).
hematogenous- disseminated (less common)
staph, ecoli.
unilateral - acteria adhere to tubular epith-> neu attracted-> interstitial disease.
urinalysis-wbc (casted in shape of tubule).
leukocytosis, fever, chills, N+ V-> costovertebral angle pain.
systemic.
trx;# hydrated, antibiotic-> renal abscess. recurrent-> chronic-> papillary necrosis (poor prognosis).

Question 19

chronic pyelonephritis

Answer 19

chronic- tubulointerstitial tissue leading to scarring of pelvis, renal parenchyma and calyces.
-causes ESRD.
- congenital VURS, superimposed urinary infection.
uni/ bilateral
chronic obstructive pyelonephritis-> recurrent infx superimposed on obstructive lesion-> inflammation, atrophy and scarring.
gross- atrophy (scar-> upper/lower lobes) well defined and coarse scar.
calcyx irregular and thickened, papillae flattened.
tubules-.chronic infiltrates-> atrophy, hypetrophy and dilution.
thryoidization-> diluted-> esophilinic hyaline material resembles thryoid colloid,
hyaline arteriosclerosis, endoarteritis obliterians.

xanthogranulomatous -> unusual, rare form, proteus infx.
gross: cut surface, large orange nodules.
stag horn calculi. confused with RCC
foamy macrophage, plasma, lymp
c/f: back/ flank pain, fever, bacteriuric, pyuris.
honeymoon cystitis- frequent vaginal intercourse
endocrinological distubrnace-low EPO, vit D , low calcium, low PO4-.
classification: non symptomatic bacteriuria, acute and chronic pyelonephritis.

Question 20

treatment: gentacmin or aminoglycosides. tobramycin (1-2 mg/kg. ) for 10 days

Answer 20

aid in regimen, diet and treat in hospital. diet rich in protein.

Question 21

features of CPN

Answer 21

asx or w/ headache, wekanes,s dry mouth, dysuria, polyuria (2L/ 24 hr), nocturia, fever, wt loss, uti n childhood. additiona sx (palpable pain anemia, HTN).
labs: low spg, proteinuria, decreased tubular clearanc (acidosis), USS changes.
xray- low size, salt loosing, haemuatric .

Question 22

features of CPN

Answer 22

asx or w/ headache, wekanes,s dry mouth, dysuria, polyuria (2L/ 24 hr), nocturia, fever, wt loss, uti n childhood. additiona sx (palpable pain anemia, HTN).
labs: low spg, proteinuria, decreased tubular clearanc (acidosis), USS changes.
xray- low size, salt loosing, haemuatric .

Question 23

treatment of CPN

Answer 23

scheme-> etiolgical treat-» abx (10 days), suphonamide- biseprol-tmp/smx (10 ) & quinolone- 10 days.
abx ( 10 days) clarithromycin, aminoglycosides, gentamicin (2mg/kg), no strep.
b-lactam-cephalo.

Question 24

RPGN

Answer 24

most severe, cellular proliferation of BC._> crescent shape.
RF shortly after.
rapid GFR via 50%.
nephrotic syn, HTN, sclerosis -> filtered-> RF.
post strep.
classification- type 1 - anti GMB detected (good pasture/ idiopathic).
type 2: immunw complex -1gA nephropahty (1) and 2 type -SLE< HSP.
immunoflorescent pattern-> granular sub.epi/endothelial deposit of c3 and ig3.
type 3: non mediated, 60 %.
ANCA (Ab against eutrophils.
1- idiopathic
2- wegener, polyangitis, churg straus syndrome/
pathophysiology-bm damange, protein, inflammaotry, cytokines (fever, inflammation), fibrin clots, hematuria, other immune component.
check C-anca and p - anca (p-anca -> mciroscopic polyangitis whereas C-anca associated with wegener).
CF: proteinuira, nephrotic or nephritic, rbc cast edema, HTN, myalgia, arthalgia, N+V.

dx: resistant HTN treatment, rapid CRF, pulmo hemorhage seen, biopsy confirms.
lower salt and fluid intak. corticosteroids. methylpredisone 10.g/kg.
suppress
plasmapheresis-> remove circulating Ab, blood TFN.

Question 25

notes for analgesic nephropathy

Answer 25

tubular dysfunction, w. electrolyte, proteinuria mod, renal impairement.
classification: if chronic then anlagesic nephropaty, balkan endemic disease, metal and radioation nephritis, chronic PN, gout.
PG; edema, compress vessels-> hypoperfusino of intersititum->ishcmeia-> dysfunction.

toxic: polyuria, hyosthenuria, high BUN if ischemia (papillae necrosis)
CF: weight gain (retention), hematuria, oliguria (sometimes) .
usually non-oliguric.
cause: hypersensitivty to drugs like sulfonamide, floroquionolones, rifampicin, nsaid, phenytoin etc.
infection- ecoli, strep, cmv, trep pallidium, (fever) if drug then rash.
immune- lupus, sarcoidiosis, sjoren syndrome.
anti-tubular BM disease, TINU (anti.uveitits infection w/ AKI).
drug and microbes depost and immune reaction.
asx or systemic (malaise, NV , flank).
sterile pyruria, wbc cast, subneprhtoci range, esophinilia, microscopic hematuria.
trx: dialysis, urinalysis , bloods, biopsy (definitive), clinical. corticosteroid key, remove offending age.

Question 26

ddx:

Answer 26

2-2.5 g/L proteinuria, creatine 0.6-1.2 mg/dl.
USS (enlarged), biopsy (inflammatin).
hx.
2-3 mg/kg then reduce to 0.8 mg/kg. high dose start of methypredisolone.
chronic IN: intoxication chronic, acute IN.
CF: CKD< HTN, small kidney, moderate-> hyperkalaemia, acidosis (stage 3).
salt losing nephropahty- hypotension, polyuria, dehydration, impaired urine conc ability.
chech volume + sg of urine (zimnitsky test (3hr for 24 hr). 1020 normal
if no oedema, HTN, advanced CRF, pregnant then volhard concer test (dry food , no fluid for 36 hr-> conc should reach 1028 sg).
trx: vit C 2-3 x /day and calcium gluconate, correct defciit

analgesic nephrophaty: chronic IN after excssive analgesic + NSAIDS>
if >6 / day for 3 years (phenacetin source)-> papillary necrosis.
pieces in urine seen , dark/ brown urine, pain in bavk.
same dx as IN, HTN, urinalysis.
tx: anemia reliefed, treat acidosis, dialysis if severe, HTN treat, lower analgesic.

Question 27

myeloma manifestatin of kidney

Answer 27

IG: labda and kappa free chain 9light ) and heavy chain.
myeloma-> produe mix , whole or just ligt chain.
-500 mg normal, normal to see in urine, catalizd via PT.
bens johns protein if myeloma persists in excess. 40-50 % affected, dialysis.
depost in glomerulus.
light chai deposition disease or amyloidosis.
if in DT-> cast nephropahty-obstructive (myeloma kidney), fanconi syndrome.
volume depletion- dehydration, sepsis (suppressed), hypocalcemia, meds toxicity, infection related, nsaid related.
CRAB - hypercalciu,, rneal disease, anemia, lesions (npehrotic impaired function, micro hematuria,tubular dysfunction).
do ESR, FBC -anaemia , serum ablumin blood picture, BJP urinalysis, lytic lesions, hypercalcemia.
dx: biospy.
high cut off dialysis- membranr to reduce FLC clearance.

Question 28

HTN / diseasee

Answer 28

uncontrolled HTN cause CKD an HT can be 2 to kidney.
hTN-> thicken and reduce lume-> ischmeia-> fibrosis and changes.
malignant HTN -> more damage since presure recieved directed va glomerulus (hyaline arteriosclerosis).
management: low salt diet, control BP WELL.
stenosis RA: renin-> angiotensin-> aldosteorne-> h20 and salt retnetion-> fluid overload.

Question 29

Diabetic nephropahty

Answer 29

poorly controlled diabetes (check retinopahthy)

type of nephrotic syndrome (lupus and amylodisos also causes it).
lose oncotic-> oedema.
hyperproteinemia > 4 g/day in urine and hypoproteinemia in serum.

nephrotic-MCD, FSGC, SLE,MM, HSP, good pasture.
diabetes destroy efferent arteriole then afferent and cause hyperfiltration injury (mesangial sclerosis), nodular glomerulosclerosis.
affect papillae-necrosis.
renal pelvis -P PN.
glucose damage protein, fat-> BM destroyed.
ace I destroy angio 2 -> decrease GFR, decrease injury.
hyaline arterioscloeriss.
trx: manage DM.
aceI-> HSP, DM and scleroderma (contraindicated in preg)

Question 30

lupus nephritis

Answer 30

SLE: 1/2 patients -> nephritis.
anti-nuclear ab attack , poor clearance-> attack and deposit-> inflammaton (type 3 hypersensitivity)
deposit in capillary wall, mesngial, BS, BM space.
can be focal or diffuse.
nephrotic syndrome.
hypoalbumenia.
hyperlipidemia and lipiduria.
can present a nephritic: hematuria.
location of lesion and extent of AKI determiens which 1.
dx: biospy, wire loop and crescent shaped swelling, BM.
immune maekers, complement and iG markers-> stain.
corticosteroid, suppress.
damage to mesangium secrete cytokine.

Question 31

nephropathies in pregnancies and multiple myelomas.

Question 32

CF of DM nephropathies

Answer 32

sevre tiredness, headache, N+ V , appetite reduced, pruritis, leg swelling.
DM is 1 of CKD complciation.
dx;urinalysis, screening -> urine albumin; creatine ratio. USS-> hypertrophy.
nodula wimmelstial wilsons disease (type II DM)
stage:
stage 1: v early signs of GFR (normal).
2: microalbuminemia (30-300 mg/24 hrs)
3. clinical proteinuria
4.nephortic syn+ HTN -> (5) renal impairement-> stage 6 final (ESRF).
lupus: skin UV damage-> DNA damage-> attack immune-> deposit in organs -> inflammation.

Question 33

CF of lupus

Answer 33

etiologiy: genetic susceptibility+ environmental triggers (autoimmune) complexes deposit.
fever, wt loss, LN, malar rash, SCLE (erythema cutaneous), arthritis, raynauds, , CVS manifestaion,
LN: nephrotic manifestation or nephritis (microscopic hematuria)
mesangial and sub-epithelial damage->inflammation + nephritic synd.
stages:
class 1:minimal mesanglial lupus nephritis-> no change in biopsy, few deposits
class 2: proliferation.
class 3: focal LN-> sclerosis + necrosis.
class 4: diffuse LN, hyper cellularity, necrosis, proliferation changes etc.
class 5: membraneous LN - expansion , deposit in sub-epithelial area.
6: advanced sclerosing LN - glomerulosclerosis.
dx: immunofluorescent-> C3, IgG, m, A seen, lumps and bumps. ANA detected, esr, anemia, leukocytopenia/ thrombocytopenia.
Trx: normal renal function. analgesic, NSAIDS, hydroxychloroquine (200-40- mg/day).
corticosteroids+ immunosuppressant.
acei?ARBS.

Question 34

pregnancies and renal disease

Answer 34

egfr picks up 80% in 1st trimester and little bit in 3rd trimester.
pre-eclampsia-> HTN and proteinuria.
susceptible to UTI, pyelonephritis due to stasis, VURS etc.
ARF: hypoperfusion? HEELPS, eclampsia, haemorrhage delivery.
CF: v. young vs older, multiple preg, DM.
L. platelets, vision disturbance, epigastric P, LDL low. hallmark (swollen intra-capillary endothelial CELLS in glomerus)
trx: MDT -abx= vancomycin, sulfonamide.

pyelonephritis: treat w/ ceftriaxone +hospitalization.
-severe: iv ticarcillin -clavulante or piperacillin tazobactam (oliguria/ immunocompromised).

end stage= infrequent cycle, ovulation, hormone imbalance.DM: use CCB instead like nifedipine.
Asx: UTI high, more nutrient in urine.
microvasculature fibrin aggregate.
1- HUS (post partum)-damage to SV in kidney (damaged RBC clog kidney filtration).
thrombocytopenia, neurological disturbance- (small clots all over)> thrombocytopenia purpura (antepartum).
acute fatty liver -> hepatocytes infiltrated.

MM: hypercalcemia - kidney damage.
uromodulin (abdundant uroprotein), hyperuricemia due to obstruction.
- Tamm-horsfall proteins (reno -original and in thick ascending limb).
monoclonal Ig deposit -> other organs-> nodular GS.
CF systemic: fever, fatigue, night sweat, wt loss, anemia.
tubular pathology-acidosis-> inability to concentrate (cannot acidify-> accumulate).
Fanconi syndrome- disorder of tubes-> faulty genes or kidney damage, 0 reabsorption.

Question 35

CF

Answer 35

hypercalcameia-> falconi. inadequate reabsorption in proximal tubule.
clinical form
1.ARF 2. CRF.
3. falconi.
dx: bone scans, BJ urinalysis etc.
Trx: transplant, Dialysis doesn’t WORK unless special.
maintain diuresis.
deranged electrolytes: hypercalcaemia, hypercaluria, hyperphosphaturia, glycosuria.

Question 36

amyloidosis

Answer 36

irregular misfolded protein-> deposit in organs.in tubule, glomeruli,
localised vs systemic (poorer prognosis).
primary-> MM (AL )
2nd-> familiar meditterea disease, RA< TB, MM, chronic sepsis (CHONIC INFLAMMATIODN)
classificaition based on precursor protein->
Ig light chain (AL)- MM.
serum Amyloid-> 2 to inflammation e.g RA.
manifestation: nephrotic, nephrotogenic DI, retro-peritoneal fibrosis.
cf; nephrotic syn (2-20 g/24hr), biospy to dx, glycosuria, t.acidosis, uremicemia.

Congo red and immunofluorescent, ben-johns protein, eosinophilic, apple green bifringence in plane polarised light.
proteasomes should remove it, faulty genes-> amyloidosis.
Trx: diuretic, cs, dialysis, transplant, immunosuppressant in fmf -colchine-> prevention.
find it: arteries, glomerular tuft, capillary wall, mesangial, interstitium.

Question 37

gout

Answer 37

primary: meat and purine consumption.
secondary: to CKD.
clinical
1. after chemo-. crystallisation-> obstruction-> AKF.
2.chronic interstitial nephritis- salts in tubule-> deposit in joints, interstitial etc.
CF: conc urine polyuria, nocturia, anemia early), acid base disbalance.
nephrolithiasis-uric calculi-chronic pyelonephritis-> CRF.
CF: H. creatinine, oliguria.
acute: malignant hemopathies and tumors.
cellular disease-> hyperaemia, tubular damage + obstruction.
chornic nephto-> obese (hyperlipidemia), HTN, polydispia, micro hematuria.

dx: renal stones, joint pain (clinical)
allpurinol inhibits hypoxanthine-> xanthine-> UA metabolism, diuretic-> clear urine, diet (low red meat).

Question 38

PKD

Answer 38

genetic autosomal (adult- PC affected)/ recessive disease (infant/ neonates-> fibrocystein affected)
tubular epith expand-> calcium influx-> water follow-> cyst enlarge-> compress vessel-> ischemia.
RAA activated-> HTN (2nd).
autosomal on cellular elvel becomes recessive (guarantee faulty in healthy protein for polycystin).
copy 1- severe, earlier onset.
copy 2: later, less severe.
see cyst in seminal vesicle, liver fibrosis-> PTN -> varices/bleeds/ hemorrhoids etc.
choestasis->cholangitis.u
potters sequence due to oligohydraminosis (oliguria intrauterine)-> pulmo hypoplasia, RF, deformities (uterine wall compress),clubbed feets, flattened nose.
berry anuerysm-> subarachnoid hemorrhage, pancrease, aortic root dilution-> CHF.
trx: urosodiol for bile issues, portocaval shunt,liver and kidney transplant.
cf: hematuria, flank pain, RF insufficiency.

Question 39

more

Answer 39

> 5 cysts bilateral kidney.
50% chance of having it.
polycystein 1: ca2+ transport.
polycystein 2: voltage-linked ca2+ channel.
neoplastic theory= cysts due to embryological deficit, nephron don’t connect-> blind ends-> filtrate accumulate-> distend and cyst forms.
associated with diverticular disease, hernia/ abnormal vascular.
normal kidney-15-.170 g. PKD 1-5kg.
pregnancy: nerphopathia gravidum UTI’s.
dx: >5 cysts, bilateral, fhx.
2nd: complciation: cyst in liver, enlarged kidney, USS cyst >4mm. IV pyelography, other imaging techniques.

Question 40

polydipseabalkan endemic nephropathy

Answer 40

balkan countreis-,acedonia, bulgaria, romania, serbia.#chroic bilateral fibrosis of kidneys w/ atrophy.
intersitital nephritis.
etiology: genetic-> small kidney 3-4 cm and weight 50g.
40-50 years,
terminal and slow RF.
fibrotic CT, intersistial fibrosis, flattened PT. glomerulosclerosis.
polydipsia, polyuria, nocturia, anemia,HTN, porteinuria, glucosuria, urothelial tumors?
functional: impaired concentration, clearance etv
4 stages 1. latnt (asx)-biopsy only.
2. mid and subclinical
3. clinical, fatigue, headahce, dizziness, tumor redce weight, renal colic, hematuria, backpain
clinical / decomensaption-terminal.
xathochromoia-> copper in palms and poles (red).
trx: same , reduce portien, dialysis, furosemide, tumor removal.

Question 41

nephrolithiasis

Answer 41

kidney stone.
85% calcium-hypercalcuria, hypocituria since ccitriate inhibit calcium being free.
10% uric acid-acidic (pH<55)
2% cystin
struvite-bacteria, proteus, klebisella.
sx: severe colic pain lasting for 20 min cyclic.
N+V. flank pain cannot sit still-> shifting, diaphresis.
dx: urinalysis to exclude other test CT abdo, hx since remission high.
imaging (not x-ray since most stone are radio-luscent).
obtain- analysis (chemical composition - prevention and treatment).
Trx: analgesia (morphine).
medical expulsive therapy -> a receptor blocker like Tamsulosin to dilute.
calculus removal.
1. non-invasive-> lithotripsy.
invasive- endoscope surgery (larger than 1 cm).
meds: ca2+ (resorption-> thiazide diuretic).

Question 42

chornic kidney disease

Answer 42

acute< 3 months kidney decrease Egfr.
chronic> 3 month.
age, diseases and co-morbidities reduce Egfr
100-120 ml/ min, les in females
make hormones, regulte, remove water.
hypertension: walls thicken-> narrow lumen-> ischemic injury- foam cells-> growth facotrs-> mesangial - mesangioblasts-> glomeruloscleroiss-> ckd.
diabetes: excess glucose to porteins - efferent stiff+ narrow (Hyaline)- hyperinfiltration-> structural matrix increaes to support-> glomerulosclerosis.
other causes: systemic disase, infection (HIV), tobacco, nsaids.
urea-> axotemia (blood, nausea/loss of appeitite)-> encepalopathy-> coma & death-> pericarditis-> decrease in platelet aggregation-> uremic frost in skin.
eletrolyte deficiency.
hyperkalemia- cardiac arrythmia.
less vitamin D- ca2+ absorption-_> PTH rleeased-> resorbed from bone-> bone weakens.
renin released-> secondary HTN.
erythropoetin-> reduction in RBC-> anemia.
dx; 90 ml/min.
irreversible if <60ml.
biospy to assess hisoltogy changes.
trx: symptomatic, transplant, dialysis.

Question 43

CKD notes

Answer 43

etiology: GN, PN, AKD, nephropathies, DM, gout, amylodiosis, systemc diseases, esential HTN.
pathogenesis=> decrease in mass-> hyeprtrophy compensatory of surviving nephrons-> undergo sclerosis.
intia; increase of EGFR then decrease. oliguria/anuria.
fluid retention-> increase BP+ oedema.
not to use k+ sparing diuretic since k+ increase causes muscle weakness.
distal failure of na/k+ pmp-> K+ retention.
metaboloc acidosis->bone decalficiation
decrease calcitorl.
uremia-> headahche, hicupds, headache, peripheral neuropahty.
reproduction-impotent.
skin changes-> pruritis > depost urea. kussmauld breathing, melanosis
CV system-> edema, HTN.
anemia- hematuria.
classification: normal 70-120 lower in females. urea is 2.5-8. ceatinine clearance 75-125.
grade 1
2: 150-350, 8-15 urea levels, 40-20
3: 350-700, 15-30, 20-16
4:00-1300,30-50, 10-5
5>1300, >50, <5.
goes fro hyposthenuria-> isothenuria.
from excess osmalitariy and low spg to either high or lowe rthna protein free plasma 1.008-1.012..
diuresis: polyuria-> anuria.

Question 44

labs

Answer 44

abnormal hyperphosphatemia, hypocalcmeia, anaemia, proteinuria.
USS-> small kidneys bilateral.
<400 mg/day- oliguria
<100 g/day: anuria
hosphatemia-> ectoic calcification (depost ca2+ in tissues).
increase Mg-> confusion.
haematuria
ckd: stage 1 (normal ranges)
stage 2: mild loss rf < 60, proteinuria.
stage 3: mild-seere loss 30-59.
stage 5: < 15 ml/min. ESRF.
trx: increase fluid.
decrease sodium, protein. maintian 500 Ml of na 2+ and water.
furosemide.
correct acidoiss. insulin dextrose and bicarbonate infusion.
allopurinol to control gout
gie ca2+ and vit D supplements
anemia-recombinant EPO humans.
HTN-> ace I combination.