R3 Flashcards
Things to do in patients with LUTS and BBH?
Urinalysis
Serum PSA(asses risk of PCa)
serum creatnin especially in a patient who has another risk for RF like HTN and DM
Renal ultrasound: especially when they have raised Cr(AKI) —-used to assess the presence of hydronephrosis/other obstraction cause and planing for catheterization.
Cystoscopy use in BPH?
Used to assess bladder for signs of chronic obstruction.
But indicated only if the patient fails initial managment.
Indication for prostate biopsy inpatient with prostatic enlargement?
asymmetric enlargement
Having nodule/nodularity
persistent PSA elevation > 4ng/dl
How we now cause anion gap metabolic acidosis?
to see associated clues like osmolar GAP
Presence of Osmolar GAP indicate?
Methanol(Blindness)
Ethylin Glycol(Urinary Ca oxalate crystal)
Propylene Glycol
Osmolar GAP calculation?
Measured serum osmolarity - Calculated serum osmolarity
Normal is < 10
Calculated serum osmolarity?
2xNa + Glucose/18 + BUN/2.8
Hyperglycemia + Urine Ketone?
DKA
Uremia(rise in BUN)
AKI
Hypoperfusion?
Lactic acidosis
Drugs?
Salicylates (early Respiratory alkalosis)
Isoniazid
Iron
Anion Gap metabolic acidosis cause?
MUDPILES
The benefit of ACE/ARB in DM?
the slow progress of diabetic nephropathy( DN is evidenced by raise in urine albumin/Cr ratio)
By lowering Glomerular Hyperfiltration(caused by raise in glomerular CHP in the disease process)–Which prevents the risk of glomerular capillary sclerosis(DN).
SGLT-2 inhibitors(canaglifinozine) benfit in DM?
lower the progress of DN by an unknown mechanism.
progression of DN?
First 5 years-Glomerular HyperthrophyRise in GFR
5-15 year(incipient DN)–mesangial expansion, GBM thickening, and arteriolar hyalinosis—moderate Proteinuria and HTN
>15 years (overt DN)–mesangial nodule/KWN/ and tubulointerstitial fibrosis–overt proteinuria(NS) and reduced GFR
Renal and electrolyte complication of anorexia nervosa?
Decrease urine concentrating ability
Dehydration
Electrolyte depletion
analgesic nephropathy>
MCC of drug-induced CKD
Common in older women
Combination increase more risk
2-3 Kg ingestion of indexed drug required
Papillary necrosis and tubulointerstitial nephritis is the pathogenesis
Microscopic haematuria, Sterile pyuria(reduced kidney concentrating capability), Mild proteinuria(NS in advanced disease)
HTN, polyuria, and flank pain
Increase risk of premature aging, atherosclerosis VD, and UT cancers.
Clues that indicate amyloidosis as a cause of nephrotic syndrome?
Presence of chronic inflammatory disease(MC: RA)
Enlarged kidney
Enlarged Liver
Amyloid stain by congo red
Amyloid deposit in BM, BV, and interstitium(may be seen as thin fibrils by E.Microscopy)
apple green birefringence by polarized light
Hyalinosis of the afferent and efferent artery will be seen in?
Hypertensive nephropathy
Screening for diabetic nephropathy?
randome urine albumin/Cr ratio
can detect >30mg/g protinuria erlier
Factor increase DN risk?
Long-standing(5-10 year) DM
Presence of other microvascular complication
Uncontrolled HTN
Poor Glycemic control
Protinuria coplication?
Increase risk of CV mortality
Increase risk of macrovascular complication
Metabolic S/E of thiazides?
Hyperglycemia(impair insulin production and impair pheripherial glucose uptake)_-mostly by chlorthalidone but have a CV mortality benefit.
High triglyceride and LDL
Hyponatremia.hypokalemia and hypomagnesemia
Hypercalcemia
Hyperuricemia (impair UA excretion)–Gout
Cause of AKI in the transplanted kidney?
Acute transplant rejection BK vires reactivation Pyelonephritis Calcineurin inhibitor toxicity urethral obstruction
Acute transplant rejection?
Occur in first 6 month
Arteritis (endothelial edema) and lymphocyte infiltration of the intima and tubulointerstitial pattern
Due to T mediated response to antigen in graft
Usually asymptomatic
Present as fever, decrease UO, and graft tenderness
Occurrence decrease by the immunosuppressant
Usually reversible with high dose IV glucocorticoids but needs immunosuppressant dose increament after
BK virus?
Intranuclear inclusion
Mixed lymphocyte and neutrophil infiltration
Interesticial nephritis feture
Acute Calcineurin inhibitor toxicity?
Present as Prerenal AKI(BUN/Cr >20)
the renal biopsy usually unremarkable
due to efferent and afferent renal artery vasoconstriction
Hypertension
Urethral obstruction?
Due to ureter necrosis–stenosis
Consider in unremarkable renal biopsy
familial hypocalciuric hypercalcemia presentation?
Usually asymptomatic
Normal high PTH level
High serum ca
Low urine Ca
pathogenesis?
Autosomal dominant
Defect in Ca sensing receptor in parathyroid and kidney—PT need high serum ca for suppression and kidney increase Ca absorption
How to D/T from primary hypertyroidism?
PHTS–Will have High urine Ca
Differentiate using urine calcium /cr ratio
urine calcium /cr ratio?
Ca urine/Ca serum/Cr urine/Cr serum
if <0.01 FHH
if >0.02 FHPT
How the other causes like MM, RCC, Sarcoidosis, and it D toxicity?
low PTH level
managment of renal cyst?
Depend on whether benign/malignant
when to say benign?
common in old thin, smooth, regular wall unilocular homogenous no septation absence of contrast enhancement usually asymptomatic
benign managment?
no, follow up needed
ureter stent if there is a sign of obstruction
inspiration if large, painful and infection sign
malignant fetcher?
biopsy
uric acid stone risk factor?
Increase UA excretion(MPD and Gout)
Decrease urine PH(chronic diharoa(BC loss) and Dm/metabolic syndrome)
Increase urine consentration (DHN)
patophysiology?
Acidic urine favours uric acid(insoluble) formation to that of urate(soluble)
supersaturation increase precipitation
Clinical menifetation?
Radiolucent stone
UAS crystal(rhomboid(rosette) on urine
Uine PH < 5.5
Managment?
Alkalanise urine by potasium citrate to 6-6.5
Alopirinol for resistant one with hyperuricemia
Low purine diet
Renal calcuoi symptom?
Intermitent sever flank pain
Intermitent high voulume diuresis(when obstraction relived)
AKI for patient with single kidney
Post diuresis hypokalemia
Acid base diserdor and electroyte disturbance in vomiting?
Metabolic alkalosis(loss of H and Increase HCO3 reabsorbtion. Hypokalemia(GI loss,High aldosteron and intracelular shift due to alkalosis) Hypocloremia(GI loss)
aproch to metabolic alkalosis?
asses urine cloride
Low urine chloride(saline responsive MA)?
vomiting
Ng tube aspiration
diuretic overuse
High urine chloride(saline unresponsive)?
Normo/hyoertensive—Bartner/Getilman syndrome
Hypertensive—PHA,Cushing disease and ectopic ACTH production?
HiV associated nephropathy (HIVAN) CM?
Rapidley progresive
Heavy protinuria
AKI
Common in advaced HIV patients
Subseharan are at risk B/C of APOL1 gene mutation
patient may have edema,hematuria and hypertension
pathogenesis?
Direct infection of tubular and glomerular cell
Diagnosis?
Collapsing Focal segmental glomerulosclerosis on renal biopsy
Tubuloreticular inclusion on EM
managment?
ART ACE inhibitor(treat protinuri and HTN) Poor prognosis(develop to CKD eve with theraphy)
lab finding in rhabdomyolysis?
Hyerkalemia/hyperphosphatemia–release from damaged muscles
Hypocalcemia–Ca deposition in damged muscles
High AST/ALT ration due to high amount of AST in muscle
How sedative risk for rhabdomyolysis?
Prolonged immobilization
Ischemic muscle injury duto prolonged stay in dependent position.
managment of rhabdomyolysis?
exesive hydration
NaHCO3 in some cases
drug induced rhabdomyilysis?
Direct myotoxicity(statine,fibrates,cholchicine,cocaain and ethanol) Vasoconstrictive ischemia(Cocain and amphitamine) Prolonged immobilization(compression ischemia)--sedatives
How to improve Survival in ESRD?
Transplantation(living donor has more mortality benifit to that of diseased donor)
type(changing) of dialysis have not d/c survavial effect
alchol induced myophty?
Preferentialy affect lower extremity
cause pain,swelling and weekness