Nephrology Flashcards
DIDMOAD for Wolfram Syndrome
Causes of Central and Nephrogenic DI
DI
Diabetes Mellitus
Optical Atrophy
Deafness
How to conduct a Fluid Deprivation Test and Interpret it
Whats the treatment for Central and Nephrogenic DI and why
Investigations and Management
Central
Infection (Meningitis)
Infiltrative (Sarcoidosis)
Trauma
Wolfram Syndrome (DIDOAD)
Histiocytosis X and Sarcoidosis
Vascular (Sickle Cell Crisis)
BINGE DRINKING (inhibit Posterior Pituitary)
Congenital nephrogenic DI (AVPR2 gene) - Mutation in Aquaporin Channel
Nephrogenic
CKD
Post Obstructive Uropathy
Intrinsic Kidney Disease - (Casts . Hematuria)
HyperCal , HypoK
DM
Fluid Depriviation Test (2 micorgram IM)
MRI Head + Posterior Pituitary Function
Serum ACE
bHCG (Pineal Germinomas
Stop Offending Drugs
Desmopressin (Central) and Thiazide / NSAIDs (Nephrogenic)
Thiazide Diuretics –> inhibit Prostaglandin Synthesis which cause Volume Contraction and reduce EGFR so less urine goes to Distal Tubule and more solutes are absorbed in the Proximal hence concentrating Urine
Which Diuretic Acts where ?
Acetazolamide - Proximal - Carbonic Anhydrase Inhibitor
Loop Diuretic - Ascending Loop of Henle by Na/K/2Cl symporter
Thiazide - Distal Na/Cl Symporter
Spironolactone - Cortical Cells in Collecting Duct Na/K ATPase
Amiloride - blocks the epithelial sodium channel in the distal convoluted tubule
Explain Plasma Aldosterone / Renin Ratio combinations
Liddle / Bartter (Asociation ?) / RAS / Primary Hyperaldosteronism / Gitelman (association?)
HYPERtension with Hypokalemia differentials
NORMOtension with Hypokalemia differentials
-BOTH high ? > renal artery stenosis with HYPERTENSION but if NORMOTENSIVE then it Bartter Syndrome
-both low ? > liddle’s syndrome (Liddle’s syndrome = L = LOW for both )
-high aldosterone and renin is low : primary hyperaldosteronism
Primary Hyperaldosteronism > overproduction of aldosterone > excessive sodium and water reabsorption in the kidneys > negative feedback onto renin > reduced Angiotensin I and II > attempts to suppress aldosterone but due to primary hyperaldosteroninsm, keeps secreting inappropriate amounts of aldosterone
Liddle - Gain of function of sodium channel in the DCT (Gitleman is Loss of Function here —> Hypomagnesemia) > excessive sodium reabsorbed, regardless of renin/aldosterone > causes negative feedback suppression of renin and aldosterone > low for both.
Bratters > impaired Na/K/2Cl in thick ascending loop > low sodium low water low bp > stimulates renin > stimulates aldosterone > high renin high aldosterone
Bartter – > Hypercalciuria (Due to Paracellular Transport of Mg and Ca blocked due to a lack of positive charge from K+ being kicked out)–> Nephrolithiasis
Hypertension with hypoKALEMIA :
Better spot a cushy little con
Better = 11 beta hydroxysteroid dehydrogenase deficiency
Cushy= cushing syndrome
Little = Liddle’s
Con = Conn’s
——————————-
Normotension and hypokalaemia:
Bartering gits can die vomiting
Bartering= Bartter’s
Gits= Gittleman’s
Die= Diuretics
Vomiting= Vomiting
Kidney Stone Management
Renal stones
watchful waiting if < 5mm and asymptomatic
5-10mm shockwave lithotripsy
10-20 mm shockwave lithotripsy OR ureteroscopy
> 20 mm percutaneous nephrolithotomy
Uretic stones
< 10mm shockwave lithotripsy +/- alpha blockers
10-20 mm ureteroscopy
Stone Prevention for Calcium Oxalate Stones and Uric Acid Stones
Oxalate stones
cholestyramine
pyridoxine
Uric acid stones
allopurinol
urinary alkalinization e.g. oral bicarbonate
ADPKD management
ACEi / ARB for HTN
Cyst Hemorrage - Nephrectomy
Cyst Infection - Ciprofloaxacin
Symptomatic or >10mm anuerysm - Surgical Intervntion
Tolvaptan - CKD 2/3 & rapidly growing
Which HLA shows high risk of rejection of transplant
HLA DR > B > A
Risk Factors for secondary FSGS
and
Light Microscopy and Electron Microscopy findings
HIV
PVB19 via Hemolytic Anemia’s - Sickle Cell or B Thalassemia
Heroin (THE ADDICT)
SLE
Charcot Marie Tooth Disease - Congential
Focal Segmental Sclerosis + Hyalinosis in Light
Podocyte Effacement in Electron
Risk Factors for Secondary Minimal Change Disease
Recent Infection / Vaccination
Hodgkin Lymphoma
NSAIDs / Rifampicin
Infectious Mononucleosis
Risk Factors for Membranous Nephropathy
Light and Electron Microscopy Findings
Syphillis / SLE (Type 5)
HBV / HCV
Malaria
Schistosomiasis
NON Hodgkin
Cancer
Gold
Light - Thick GBM
Electron - SubEPITHELIUM Spike and Dome pattern due to immune complex deposition
FSGS Selective or Non selective proteinuria ?
Non Selective
Only MCD is SELECTIVE
What antibody is associated with Membranous Nephropathy ?
Anti PLAR2 (Spike and Dome Subepithelial on Electron)
Prognostic Factors for MGN ?
Female Good for MGN
Male Poor for IgA
ADPKD Type 1 and Type 2 Chromosome and Genes ?
ADPKD T1 (Chromosome 16) PKD1 Gene - Severe but 85% common
ADPKD T2 (Chromosome 4)
PKD 2 Gene - Less Severe but 15%
Prognostic Markers for IgA
markers of good prognosis: frank haematuria
markers of poor prognosis: male gender,
proteinuria (especially > 2 g/day),
hypertension,
smoking,
hyperlipidaemia,
ACE genotype DD
Non Seminoma Types
non seminomas (Peak 25)
Cu—choriocarcinomas
Y yolk sac
T teratomassS
E embryonal
Factors that increase risk of Pulmonary Hemorrhage ?
smoking
lower respiratory tract infection
pulmonary oedema
inhalation of hydrocarbons
young males
Nephrogenic DI causing Drugs
DR. FLAG
D - Demeclocycline
R - Rifampicin
F - Foscarnet
L - Lithium
A - Amphotericin B
G - Glibenclamide
Side effects of Erythropoietin
Side effects of Erythropoietin
A- accelerated HTN
B- Bone aches
C-Cellular Aplasia of RBCs
D- Deficiency of Iron
E- Exaggerated Skin symptoms ( Rashes , Urticaria)
F- Fistula Thrombosis due to Raised PCV, Flu like symptoms
Which Kidney Stones are Radio-opaque and which are radio-lucent
all the ones that are OOOOOpaque contain an o (phosphate (incl stag horn), oxalate)
all the ones that are radiolucent don’t (urate and xanthine) - just have to remember that cystine are semi-opaque (the c looks like half an o)
High Anion and Normal Anion Gap Causes ?
Methanol
Uremia
DKA
Paraldehyde
Iron, Isoniazid
Lactic Acidosis
Ethyl Glycol
Salicylate
Carbon Monoxide
Aminoglycosides
Theophylline
Normal Anion Gap MA
FUSEDCARS
Fistula (biliary, pancreatic), Ureterogastric conduit, Saline administration, Endocrine (Addison disease, hyper-PTH), Diarrhea,
Carbonic anhydrase inhibitor,
Ammonium chloride,
Renal tubular acidosis, Spironolactone
What is the diagnostic investigation for Recurrent UTI in Peads ?
MCUG for Reflux Uropathy and DMSA later for Renal Scarring
Fibromuscular Dysplasia
Female
Flash Pulmonary Edema
AKI after ACE
Uncontrollable HTN
ACEI in CKD - a decrease in eGFR of up to 25% or a rise in creatinine of up to 30% is acceptable
ACEI for HTN - a decrease in eGFR of up to 15% or a rise in creatinine of up to 20% is acceptable - if more than that - HOLD drug and suspect Renovascular dx