Urology/Nephro IM Flashcards
How does CKD cause hyperparathyroidism?
Defect in the activation of vitamin D in the kidneys due to chronic kidney disease (CKD) leads to hypocalcemia and hyperphosphatemia, causing compensatory increase in parathyroid hormone production and causing secondary hyperparathyroidism.
Which type of Metabolic Acidosis occurs in CKD?
Acidosis usu develops by Stage 4 CKD. Initially, loss of NH4+ excretory capacity leads to a NAGMA. As CKD progresses towards ESRD, uremic toxins accumulate and AG widens.
Eventually HAGMA w/wo NAGMA.
RIFLE criteria for AKI?
Risk
Injury
Failure
Loss
ESRD
RIF not used anymore, replaced by AKIN criteria
In “Loss”, persistent ARF = complete loss of renal function for >4 weeks
AKIN criteria for AKI?
Divided into Creatinine criteria and Urine Output Criteria.
Stage 1-3.
In Stage 3, Cr rises by 3 times + UO falls below 0.3ml/kg/hr for 24hrs
Top 3 causes of ESRD?
- DM
- Glomerulonephritis
- Chronic HTN
On PE of renal transplant, how to tell if new kidney is still working?
If pt is on dialysis (signs of active CVC or other catheters), then u know the new kidney failed.
Can ESRD cause HyperPTH?
Yes. Look for signs of parathyroidectomy which shows neck scar + implant signs in deltoids.
Role of Calcitriol?
Calcitriol is synthesized renally, stimulated by PTH.
Calcitriol raises CaPO4 reabsorption in kidney and GI.
What causes RAAS activation in Renal artery stenosis?
Low glomerular perfusion
Types of urinary incontinence?
Urgency incontinence: This is the inability to hold urine long enough to reach a restroom. It can be associated with having to urinate often and feeling a strong, sudden urge to urinate.
Stress incontinence = leakage of urine during exercise, coughing, sneezing, laughing, lifting heavy objects or performing other movements that put pressure on the bladder.
Functional incontinence = Urine leakage due to difficulty reaching restroom in time cuz of physical conditions, such as arthritis, injury or other disabilities.
Overflow incontinence = Leakage occurs when the quantity of urine produced exceeds the bladder’s capacity to hold it.
Haematuria with red cell casts and dysmorphic RBCs point to?
Glomerulonephritis
What biochemical diagnostic is good to screen for diabetic nephropathy
Urine albumin to Creatinine ratio
Can GN cause hypertension? How
Yes. Chronic GN patients become salt sensitive and consequent renal ischemia causes stimulation of RAAS system, causing HTN.
For nephrotic range microalbuminuria, what to use?
For lower range, what can be an option?
Use pred for nephrotic range microalbuminuria
Lower range = Lisinopril is an option.
Triad of AIN?
Fever
Rash
Eosinophilia
Common causes of temporary albuminuria?
Dehydration
Intense exercise
Infection/fever
Heart failure exacerbation
Common causes of chronic albuminuria?
DM (poor control)
HTN
Heart disease
Glomerular disease
Abx of choice for recurrent UTIs? NOT piptazo anymore!
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Meropenem is 1st choice
Most common pathogen for Pyelonephritis?
E. Coli
4 types of Renal Tubular Acidosis?
Type 1 = Distal tubular acid secretion
Type 2 = Proximal tubular bicarb wasting
Type 3 = carbonic anhydrase deficiency
Type 4 = Aldosterone resistance
Causes of T4 RTA?
HypoALD = Addison’s disease, diabetic nephropathy
Aldosterone resistance
Drugs e.g. NSAIDs, ACE-I, spironolactone
Symptoms of T4 RTA?
Renal insufficiency -> polyuria, polydipsia, dehydration
Impaired growth in children
Features of hyperK
Pathophysiology of Type 1 RTA?
Symptoms?
Treatment?
Alpha-intercalated cells of distal tubule unable to secrete H+
Calcium excretion rises, can cause bone demineralization
A/w kidney stones
Treat with alkali therpay with NaCO3 or Sodium citrate (Shohl solution)
Pathophysiology of Type 2 RTA?
Symptoms?
Treatment?
PCT cells are unable to resorb bicarb ions.
Calcium excretion normal
Can cause Vit D-resistant hypoPO4 rickets/osteomalacia
Treat with oral Potassium citrate
Pathophysiology of Type 3 RTA?
Symptoms?
Treatment?
Combination of T2 and T3 RTA = Cannot secrete H+, with bicarb wasting
Calcium excretion is higher. Can cause osteopetrosis.
Treat with Shohl’s solution
Consequences of CKD?
- Volume overload
- Low excretion of waste products
- Metabolic acidosis
- electrolyte imbalances
- HyperPTH
- Anemia due to EPO deficiency
- CKD MBD
- Hypogly due to reduced gluconeogenesis
How do kidneys show on US in CKD?
Small shrunken kidneys
Increased echogenicity
Define CKD-Mineral Bone Disease
Systematic disorder of mineral and bone metab due to CKD with manifestation by at least one of:
1. Abnormal Ca, PO4, PTH or Vit D metab
2. Abnormal bone turnover, mineralization, volume, linear growth or strength
3. Vascular or other soft tissue calcification
Consequence of MBD?
Immediate = Serum PO4/Ca disequilibrium
Delayed = renal osteodystrophy, atypical fractures, vascular calcifications
High Ca a/w CVS-specific mortality
Mx of MBD?
Target EITHER HyperPO4 or HyperPTH!
Phosphate binders for hyperPO4
Activated Vit D or Calcimimetics for hyperPTH
Definitive treatment is Parathyroidectomy.
Ravine criteria for ADPKD?
any 1 of the following:
At least 2 renal cysts or 1 cyst in each kidney for <30 years
At least 2 cysts in each kidney for 30-60 years
At least 4 cysts in each kidney for >60 years
Manifestation of ADPKD?
Local cystic complications e.g. rupture, infection, mass effects
Flank pain
Arterial HTN
Progressive kidney disease
Renal manifestations = Gross haematuria, recurrent UTI, kidney stones, signs of CKD
Cysts in other organ
ADPKD a/w berry aneurysms and mitral regurg
Diagnostics of ADPKD?
1st line US showing anechoic masses
Confirm diagnosis with genetic testing = PKD1/PKD2 gene
Screen berry aneurysms with MR angiography
What is HUS-TTP?
Thrombotic microangiopathy where microthrombi consistingn mainly of platelets occlude microvasculature
Triad of Hemolytic Uremic Syndrome?
Thrombocytopenia
MAHA
Impaired renal function
Classic presentation of HUS?
Triad is Impaired renal function, thrombocytoenia, MAHA
Diarrhoea (usu bloody) for 5-10 days precedes onset of HUS symptoms.
Mostly kids <5 years.
Typical pt is kid with diarrhoea for 5-10 days and comes in with petechiae, jaundice, oliguria
Pentad of Thrombotic Thrombocytopenic Purpura?
Thrombocytopenia
MAHA
Impaired renal function
Fever
Neurological symptoms
Classic pt of Thrombotic thrombocytopenic purpura?
Previously healthy adult with fever, petechiae, fatigue, pallor, mental state changes.
Lab tests will show hemolytic anemia and possibly AKI
Top causes of AKI in SG?
DM
HTN
Glomerulonephritis
Adult PKD
Pre-renal causes of AKI?
Volume depletion = Can be haemorrhage, GI loss, renal loss e.g. diuresis/DI, skin (burns).
Decreased effective circulatory volume = reduced CO, systemic vasodilation e.g. sepsis, liver failure.
Functional = NSAIDs, ACE-Is, ARB. These drugs lower intraglomerular pressure. ACE-Is and ARB affect afferent arterioles, NSAID affects afferent arterioles.
With prolonged ischemia, pre-renal AKI becomes ATN.
How to differentiate pre-renal AKI vs ATN?
In Pre-renal, glomeruli and tubules still functional. Can use RAAS to restore perfusion.
In ATN, pt loses ability to concentrate urine
Diagnostic criteria for ATN?
- Muddy brown granular casts on urinalysis
- FeNa > 2%
- Poor response to fluid resusc
- Hx of severe hypoperfusion or toxin exposure
- Gold Standard is renal biopsy
Primary causes of nephrotic syndrome?
Kids = Minimal Change Disease (commonest)
Adults = Focal Segmental Glomerulosclerosis
Secondary causes include Diabetic nephropathy
Triad of Nephritic syndrome?
Hematuria
HTN
Azotemia
Mx of nephrotic syndrome?
For edema = sodium restriction <3g/day, fluid restriction <1L, diuretics
For proteinuria = RAAS inhibitors
Treat underlying cause
Compares symptoms of urethritis vs cystitis?
Urethritis usu no frequency or urgency.
Cystitis will have irritative symptoms like that.
