on 15-Apr-2016 (Fri)

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#nephrology

Question

Approach to AKI

Answer

Causes:
1) pre-renal
2) renal
3) post-renal

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#nephrology

Question

What are pre-renal causes of AKI?

Answer

↓ renal blood flow d/t:

1) ↓ ECF volume (volume depletion)
2) ↓ effective ECF volume (volume overloaded - CHF - but not getting to kidneys; fluid shift to interstitial space - liver ds)
3) disruption of hemodynamics/autoregulation​
-drugs (NSAIDs, RAAS blockers)
-endogenous mediators (accumulation of vasoactive compounds in liver failure - hepatorenal syndrome)

NB: could be losing Na or ↓ intake

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Question

What is a renal cause of AKI?

Answer

inj d/t dysfn of renal parenchyma.

look for:
-systemic ft's (ds could also be affecting kidneys)
-HTN (NB: hypo for pre-renal)
-mild to mod ECF volume overload
-anemia/thrombocytopenia
-***abn urine sediment (RBC, WBC, protein, abn casts)***

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#nephrology

Question

What is a cause of post-renal AKI?

Answer

inj secondary to not passing urine from kidneys (urine backs up)

dx = imaging (kidney & bladder u/s)

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Question

What are 2 methods of urine evaluation?

Answer

1) dip stick → **alb, Hg, WBC**, others (glu, pH, urobilinogen, specific gravity)
2) microscopy → cells, crystals, casts

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Question

What are 3 types of renal AKI causes?

Answer

1) tubulo-interstitial → acute tubular necrosis (atn), allergic/acute interstitial nephritis (ain), tubular obstruction
2) glomerular → prolif ds, non-prolif ds (rarely causes aki)
3) vascular → arteries (renal a stenosis, vasculitis), arterioles (atheroembolic ds, vasculitis), capillaries (thrombotic microangiopathies, vasculitis), veins/venules (thrombosis)

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Question

pre-renal aki vs atn:

Test	pre-renal	atn
urine dipstick	[...]	[...]
urine microscopy	normal	hemegranular casts
urinary [Na]	<20mmol/L	>20mmol/L
FENa	<1%	>1%

Answer

pre-renal aki vs atn:

Test	pre-renal	atn
urine dipstick	normal	Hg +/- alb
urine microscopy	normal	hemegranular casts
urinary [Na]	<20mmol/L	>20mmol/L
FENa	<1%	>1%

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#nephrology

Question

pre-renal aki vs atn:

Test	pre-renal	atn
urine dipstick	normal	Hg +/- alb
urine microscopy	[...]	[...]
urinary [Na]	<20mmol/L	>20mmol/L
FENa	<1%	>1%

Answer

pre-renal aki vs atn:

Test	pre-renal	atn
urine dipstick	normal	Hg +/- alb
urine microscopy	normal	hemegranular casts
urinary [Na]	<20mmol/L	>20mmol/L
FENa	<1%	>1%

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#nephrology

Question

pre-renal aki vs atn:

Test	pre-renal	atn
urine dipstick	normal	Hg +/- alb
urine microscopy	normal	hemegranular casts
urinary [Na]	[...]	[...]
FENa	<1%	>1%

Answer

pre-renal aki vs atn:

Test	pre-renal	atn
urine dipstick	normal	Hg +/- alb
urine microscopy	normal	hemegranular casts
urinary [Na]	<20mmol/L	>20mmol/L
FENa	<1%	>1%

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#nephrology

Question

pre-renal aki vs atn:

Test	pre-renal	atn
urine dipstick	normal	Hg +/- alb
urine microscopy	normal	hemegranular casts
urinary [Na]	<20mmol/L	>20mmol/L
FENa	[...]	[...]

Answer

pre-renal aki vs atn:

Test	pre-renal	atn
urine dipstick	normal	Hg +/- alb
urine microscopy	normal	hemegranular casts
urinary [Na]	<20mmol/L	>20mmol/L
FENa	<1%	>1%

Tags

#exam #nephrology

Question

What is ATN (acute tubular necrosis)?

Answer

• 2nd most common cause of AKI
• d/t ischemia/toxins
• look for signs of ↓ volume (pre-renal hypotension can cause ATN)
• **hemegranular casts** = dx

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Question

What is allergic/acute interstitial nephritis (ain)?

Answer

interstitial inflm d/t:

• usually allergic rxn to drugs (abx, NSAIDS, PPIs, etc)
  • usually present 7-10d post-exposure
  • urine → RBC, WBC, protein, **WBC casts**
• autoimmune ds
• inf's

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Question

What is prolif glomerulonephritis?

Answer

• too many cells in glomerulus so can't filter → AKI
• present w/:
  • rapid ↓ in GFR
  • ​HTN, anemia
  • ↑ inflm markers
  • other systemic ft's (if 2ndary)
  • ECF volume full/mildy overloaded
• urine → **RBC casts** (nephrologic emerg)

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Question

What is non-prolif glomerular ds?

Answer

structural problem - rarely causes AKI - just see proteinuria

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Question

What are causes of renal artery stenosis?

Answer

• athrosclerosis
• ​fibromuscular dysplasia

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Question

What are causes of thrombotic microangiopathies?

Answer

TTP, hemolytic uremic syndrome (HUS), hypertensive emerg

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Question

How do you manage AKI?

Answer

general

• prevent additional nephrotoxins (drugs, contrast)
• rx ECF volume status
• avoid complications
  • ECF volume overload (↓Na intake, ↑ diuretics)
  • avoid ↑K (↓ intake, diuretics, laxatives, shift into ICF)
  • renally dose meds

​pre-renal aki

• improve hemodynamics
  • ↑ ECF w/ IV fluids
  • ↑ cardiac output

​renal AKI

• ATN → time
• AIN → remove offending agent, consider corticosteroids
• glomerulonephritis → maybe immunosuppresive therapy (urgent)

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#nephrology

Question

What is the 7 step approach to drugs in nephro?

Answer

1. What is the individual’s GFR? → no adjustment until <60ml/min (Cockcroft ‐Gault Equation)
2. Is the drug effective in the setting of a reduced GFR? → e.g. thiazide doesn't work
3. Is the drug safe in CKD? (metformin, bisphosphonates, meperidine)
4. Is the drug itself nephrotoxic? (aminoglycosides, amphotericin B, NSAIDS)
5. Is an immediate effect desired or needed? → loading dose will often be same but usually ↓ maintenance dose or ↑ interval to maintain the drug level at a safe therapeutic level
6. Is the drug extensively eliminated by the kidney? (aminoglycosides, penicillins, cephalosporins, digoxin, vancomycin, lithium)
7. Does the drug have an active / toxic metabolite that is renally eliminated? (meperidine)

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Question

Drugs with Renal Effects

Answer

• Renin‐Angiotensin‐Aldosterone System (RAAS) blockers
• Diuretics
• Antidiuretic Hormone (ADH)

Question

Angiotensin II stimulation causes:

Answer

↑ aldo
vasoconstriction
↑ Na reabsorption

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Question

Direct renin inhibitors (i.e. aliskiren) do what?

Answer

Blocking Renin Action

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Question

ACE inhibitors do what?

Answer

Blocking Angiotensin II production

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Question

Angiotensin receptor blockers do what?

Answer

Blocking Angiotensin II action

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Question

Spironolactone/Eplerenone does what

Answer

Blocking action of Aldosterone

NB: spironolactone = K+ sparing diuretic

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Question

Diuretics do what?

Answer

• ↓ Na to ↓ ECF volume
• can cause over-diuresis
• if acts prox to CCD = K wasting
• if acts @ CCD = K sparing

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Question

Weak diuretics..

Answer

• work at prox tubule
• carbonic anhydrase inhibitors (not used much as diuretics) - blocks reabsorption of HCO3 (Na stays out with it)

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Question

Potent diuretics..

Answer

loop diuretics (furosemide, bumetanide)
work on asc limb of loop
blocks NKCC2
can add to thiazide diuretics

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Question

Thiazides..

Answer

hydrochlorothiazide (HCTZ), Chlorthalidone, Indapamide, Metolozone
works on DCT (distal convoluted tubule)
imp s/e:

• Dyslipidemia
• Hyponatremia
• Hyperuricemia
• Hypercalcemia

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Question

Potassium Sparing Diuretics..

Answer

weak
2 mechanisms:

• block aldosterone from binding its receptor (spironolactone, epeleronone)
• bind ENaC

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Question

ADH..

Answer

aquaporin insertion in CD
VAPTANS (new)

• Competitive inhibitors for ADH

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Question

Nephrotoxic drugs contributing to pre-renal AKI

Answer

diuretics → ↓ ECF volume d/t ↑ Na loss
RAAS blockade → Block either the formation or action of AngII (which maintains GFR) → efferent vasodilation
NSAID → Inhibit the formation of prostaglandins (which vasodilate afferents)

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Question

What are tubulo-toxic drugs causing ATN?

Answer

Aminoglycosides Antibiotics (Gentamicin, Tobramycin, Amikacin)
Amphotericin B (antifungal)
Cisplatin (chemo)
IV radiocontrast dye

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Question

medications implicated with AIN

Answer

Acute interstitial nephritis:

• NSAIDS
• abx
• PPI
• allopurinol

Chr interstitial fibrosis:

• lithium (most common), etc

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Question

What would you check on hx to differentiate AKI and CKD?

Answer

• Review of Systems (Is this acute?)
– Symptoms during urination (stones, UTI, obstruction)
– Recent infections (post‐infectious GN)
– Skin rashes or arthritis (Connective tissue ds)
– Risk for transmitted infections (HIV, Hepatitis B and C)
• Chronic Diseases
– Hypertension, diabetes
• Past Medical History
– Abnormal urinalysis in the past
– Problems with pregnancies
– Urologic procedures
• Any NEW medications
• Family History
– Polycystic kidney disease

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Question

u/s in CKD shows:

Answer

small shrunken kidneys

↑ cortical echogenicity

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Question

Chronic kidney disease (CKD) is defined by:
– The presence of [...] or an eGFR < 60 ml/min/1.73 m^2
– AND Present for ≥ 3 months
– AND Not treated with dialysis or transplant

Answer

Chronic kidney disease (CKD) is defined by:
– The presence of kidney damage (hematuria, proteinuria, or anatomic abnormalities) or an eGFR < 60 ml/min/1.73 m^2
– AND Present for ≥ 3 months
– AND Not treated with dialysis or transplant

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Question

Chronic kidney disease (CKD) is defined by:
– The presence of kidney damage (hematuria, proteinuria, or anatomic abnormalities) or [...]
– AND Present for ≥ 3 months
– AND Not treated with dialysis or transplant

Answer

Chronic kidney disease (CKD) is defined by:
– The presence of kidney damage (hematuria, proteinuria, or anatomic abnormalities) or an eGFR < 60 ml/min/1.73 m^2
– AND Present for ≥ 3 months
– AND Not treated with dialysis or transplant

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#nephrology

Question

Chronic kidney disease (CKD) is defined by:
– The presence of kidney damage (hematuria, proteinuria, or anatomic abnormalities) or an eGFR < 60 ml/min/1.73 m^2
– AND Present for [...]
– AND Not treated with dialysis or transplant

Answer

Chronic kidney disease (CKD) is defined by:
– The presence of kidney damage (hematuria, proteinuria, or anatomic abnormalities) or an eGFR < 60 ml/min/1.73 m^2
– AND Present for ≥ 3 months
– AND Not treated with dialysis or transplant

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#nephrology

Question

Chronic kidney disease (CKD) is defined by:
– The presence of kidney damage (hematuria, proteinuria, or anatomic abnormalities) or an eGFR < 60 ml/min/1.73 m^2
– AND Present for ≥ 3 months
– AND Not treated with [...] or [...]

Answer

Chronic kidney disease (CKD) is defined by:
– The presence of kidney damage (hematuria, proteinuria, or anatomic abnormalities) or an eGFR < 60 ml/min/1.73 m^2
– AND Present for ≥ 3 months
– AND Not treated with dialysis or transplant

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Question

What are the most common causes of CKD?

Answer

DM + vasc ds
(glomerular ds can also cause it)

NB: CKD has 5 stages

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Question

6 steps to slowing progression of CKD:

NB: Remember CHD risk equivalent

1. [...] or [...] (slow progression to ESRD with additional advantages over blood pressure lowering alone)
2. Tight blood pressure control
Multiple antihypertensive medications and dietary sodium restriction may be required
Targets: < 140/90 mmHg without DM, < 130/80 mmHg with DM
3. Use of a statin in patients with dyslipidemia (target LDL < 2 mmol/L) - shown to prevent CV events and may slow the rate of decline
4. Recommend smoking cessation (independent risk for development/progression of CKD)
5. glycemic control in patients with diabetes mellitus (HbA1C < 7%)
6. Patients with eGFR <60 ml/min/1.73m2 should avoid NSAIDS, COXIBs and other nephrotoxins such as intravenous contrast if possible

Answer

ACE inhibitor
Angiotensin receptor blocker

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#exam #nephrology

Question

CKD and Indications for dialysis

Answer

•**Persistent metabolic disturbances refractory to medical therapy
– Hyperkalemia
– Metabolic acidosis
• Fluid overload refractory to diuretics
• Progressive uremia
– Encephalopathy
– Persistent nausea and vomiting
– Evidence of malnutrition
• Pericarditis**

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Question

Goals of Dialysis

Answer

Solute/toxin removal (“blood purification”)

Salt and water removal (“ultrafiltration”)

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Question

CKD & transplant:

living donor = [...] y kidney survival
deceased donor = [...] y survival

Answer

living donor = 15-25y kidney survival
deceased donor = 5-15y survival

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Question

Sodium [...] determines [...]
Sodium concentration determines intracellular fluid (ICF) volume
Sodium concentration does NOT predict ECF volume status

Answer

**Sodium content determines extracellular fluid (ECF) volume status
Sodium concentration determines intracellular fluid (ICF) volume
Sodium concentration does NOT predict ECF volume status**

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Question

Sodium content determines extracellular fluid (ECF) volume status
Sodium [...] determines [...]
Sodium concentration does NOT predict ECF volume status

Answer

**Sodium content determines extracellular fluid (ECF) volume status
Sodium concentration determines intracellular fluid (ICF) volume
Sodium concentration does NOT predict ECF volume status**

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#exam #nephrology

Question

Sodium content determines extracellular fluid (ECF) volume status
Sodium concentration determines intracellular fluid (ICF) volume
Sodium [...] does NOT predict [...]

Answer

**Sodium content determines extracellular fluid (ECF) volume status
Sodium concentration determines intracellular fluid (ICF) volume
Sodium concentration does NOT predict ECF volume status**

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#nephrology

Question

normal [Na] = [...]

Answer

normal [Na] = 140mmol/L

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Question

Na balance:

input (determined by diet)

output
--small extrarenal loss
--Renal excretion controlled by [...]
• Activation of RAAS results in [...]

Answer

**Renin‐Angiotensin‐Aldosterone System (RAAS)

sodium retention**

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Question

RAAS is activated by:

Answer

↓ BP activates the baroreceptors

↓ GFR → lower NaCl delivery to the juxtaglomerular apparatus

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Question

H2O balance:

input (thirst → intake)

output
--extrarenal loss small
--Renal excretion controlled by [...]
• Release of ADH results in [...]

Answer

**antidiuretic hormone (ADH)
water retention**

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Question

What triggers ADH release?

Answer

• Hypernatremia (osmotic stimulus)
• Non‐osmotic stimuli (inapproriate)
– Low volume states: real or “effective”
– Stress states: surgery, pain
– SIADH states: cancers, drugs, brain or respiratory disease
– Other states: Pregnancy, low cortisol, low thyroid

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Question

Rx of ECF volume expansion (heart failure)

Answer

Reduce sodium content:
1. Decrease intake
2. Promote excretion
– Use of diuretics
3. Remove stimulus for RAAS activation (if possible)

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Question

Rx of ECF volume depletion (diarrheal illness)

Answer

Oral rehydration
Isotonic saline (154 mmol/L NaCl)

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Question

Hyponatremia ALWAYS a result of [...]

Answer

**Hyponatremia ALWAYS a result of relative water retention**

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Question

Why is there H2O retention in hyponatremia?

Answer

**ADH** (main cause)
no kidney fn/GFR
no osmoles to excrete in urine

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Question

Hyponatremia presentation

Answer

If rapid onset then cell swelling can occur
– Biggest concern is cerebral edema (Headaches, Confusion, Seizures, Death)

If slow onset (over days) then often asymptomatic as brain can adapt

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Question

hyponatremia rx

Answer

• Restrict fluid/water intake
• Remove underlying cause (ADH)
• If acute and symptomatic → rapid partial correction to reduce cerebral edema (can use hypertonic saline)
• If chronic and severe (<120 mmol/L ) treat slowly as rapid correction can cause devastating brain injury

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Question

Causes of hypernatremia

Answer

Failure to drink fluid:
– Infancy
– Elderly (reduced thirst, dementia, stroke, nursing home, bed‐bound etc.)
– Coma, impaired consciousness, surgery

Excess losses (frequently present but not required)
– Hyperglycemia
– Diabetes insipidus (no ADH)

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Question

Presentation of hypernatremia

Answer

presentation = confusion, ↓ LOC (brain cell shrinkage)

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Question

normal [K] = [...]

Answer

normal [K] = 3.5-5 mmol/L

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Question

Hypokalemia causes

Answer

1) Decreased intake (not major)
2) Shift into cells → insulin, B2 agonists (salbutamol)
3) Excess loss:
• Renal → high aldo + high flow to collecting duct
– Diuretics (thiazides, furosemide)
– Vomiting (driven by bicarbonaturia)
– Primary hyperaldosteronism (hypertension)
• GI (diarrhea)

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Question

K excretion & Aldo

Answer

(1) Aldosterone stimulation leads to insertion of epithelial sodium channels (ENaC) in the luminal membrane of collecting duct
(2) Na+ reabsorbed faster than Cl‐, leaving a net negative charge in lumen
(3) K+ secretion due to net negative charge

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Question

S&S of hypokalemia (<3.5mmol/L)

Answer

--weakness (hyperpolarized msc)
--cardiac arrhythmias

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Question

Hypokalemia mgmt

Answer

• Acute:
– Oral KCl (pills or liquid)
– Intravenous KCl – important to limit the concentration and amount to prevent hyperkalemia
• Chronic/prevention:
– High K+ foods – fruits, vegetables
– K+ sparing diuretics (amiloride, spironolactone)

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#nephrology

Question

Causes of Hyperkalemia

Answer

(1) Increased intake

(2) Shift of K+ out of cells
--Insulin deficiency – DKA, hyperglycemia
--Muscle necrosis – rhabdomyolysis
--Hemolysis (red cell destruction)

(3) Failure of renal excretion of K+
--Low flow to CCD (↓ ECFV, very low GFR)
--Low aldosterone:

• Adrenal disease (rare)
• ACE inhibitors, angiotensin blockers (common)
• K‐sparing diuretics (common)
• Tubular dysfunction (advanced renal failure)

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Question

hyperkalemia s&s

Answer

• Muscle weakness, stiffness (cells are depolarized)
• ECG changes:
– Small or absent P waves
– Broad QRS
– Peaked T‐waves
• Arrhythmias
• [K+] > 7.0 mmol is life‐threatening

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Question

Treatment of Life‐Threatening Hyperkalemia

Answer

**Four principles of management:
(1) Stabilize myocardium
--Give Calcium Gluconate IV

(2) Shift potassium into cells
--IV insulin
--IV or inhaled beta2‐agonist

(3) Potassium excretion
--90% renal - ↑ ECFV w/ IV saline to promote flow to CCD, then give IV furosemide
--10% GI - promote diarrhea (cation exchange resins) - avoid post-op use

(4) Hemodialysis - if above insufficient**

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Question

pH = [...]
plasma CO2 = 40mmHg
plasma HCO3 = 24mmol/L
plasma anion gap = 12mEq/L

Answer

pH = 7.40
plasma CO2 = 40mmHg
plasma HCO3 = 24mmol/L
plasma anion gap = 12mEq/L

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#exam #nephrology

Question

pH = 7.40
plasma CO2 = [...]
plasma HCO3 = 24mmol/L
plasma anion gap = 12mEq/L

Answer

pH = 7.40
plasma CO2 = 40mmHg
plasma HCO3 = 24mmol/L
plasma anion gap = 12mEq/L

Tags

#exam #nephrology

Question

pH = 7.40
plasma CO2 = 40mmHg
plasma HCO3 = [...]
plasma anion gap = 12mEq/L

Answer

pH = 7.40
plasma CO2 = 40mmHg
plasma HCO3 = 24mmol/L
plasma anion gap = 12mEq/L

Tags

#exam #nephrology

Question

pH = 7.40
plasma CO2 = 40mmHg
plasma HCO3 = 24mmol/L
plasma anion gap = [...]

Answer

pH = 7.40
plasma CO2 = 40mmHg
plasma HCO3 = 24mmol/L
plasma anion gap = 12mEq/L

Tags

#exam #nephrology

Question

Four Primary Acid‐Base Disorders:

Metabolic acidosis: pH [...] and [...]
Metabolic alkalosis: pH [...] and [...]
Respiratory acidosis: pH < 7.4 and ↑PCO2
Respiratory alkalosis: pH > 7.4 and ↓PCO2

Answer

Four Primary Acid‐Base Disorders:

Metabolic acidosis: pH < 7.4 and ↓[HCO3‐]
Metabolic alkalosis: pH > 7.4 and ↑[HCO3‐]
Respiratory acidosis: pH < 7.4 and ↑PCO2
Respiratory alkalosis: pH > 7.4 and ↓PCO2

Tags

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Question

Four Primary Acid‐Base Disorders:

Metabolic acidosis: pH < 7.4 and ↓[HCO3‐]
Metabolic alkalosis: pH > 7.4 and ↑[HCO3‐]
Respiratory acidosis: pH [...] and [...]
Respiratory alkalosis: pH [...] and [...]

Answer

Four Primary Acid‐Base Disorders:

Metabolic acidosis: pH < 7.4 and ↓[HCO3‐]
Metabolic alkalosis: pH > 7.4 and ↑[HCO3‐]
Respiratory acidosis: pH < 7.4 and ↑PCO2
Respiratory alkalosis: pH > 7.4 and ↓PCO2

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Question

metabolic alkalosis is usually associated with [...]

Answer

low serum potassium

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Question

Five Steps to Solving Acid Base Problems

Answer

(1) Look at the pH: Acidemia vs Alkalemia

(2) What is the primary problem?:
Compare HCO3 vs pCO2

(3) Is there adequate compensation?
met acid = 1:1 (pCO2)
met alk = 1:0.7 (pCO2)
R acid A = 1:10 (pCO2)
R acid C = 3:10 (pCO2)
R alk A = 2:10 (pCO2)
R alk C = 5:10 (pCO2)

(4) a) What is the Anion Gap?
AG = Na – (Cl + HCO3)
--Normal is 12 +/‐ 2 mmol/L

b) Is there an Osmolar Gap?
Osmolar gap = Osm(meas) – Osm(calc)
Osm(calc) = 2Na + Urea + Glucose
--Normal is upto 10 mosm/kg

(5) Is there another metabolic disorder?
Does the Δ AG = Δ HCO3?
Δ AG = Δ HCO3 (only AGMA)
Δ AG < Δ HCO3 (AGMA + met alk)
Δ AG > Δ HCO3 (AGMA + NAGMA)

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Question

met acid causes w/ ↑ AG

Answer

**• Lactic acidosis
• Ketoacidosis
--diabetic
--alcoholic
--starvation
• Toxins
– Methanol
– Ethylene glycol
– Salicylates
• Severe chronic kidney disease**

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Question

met acid causes w/ normal AG

Answer

**NaHCO3 Loss
– GI (Diarrhea)
– Renal (Low urine NH4+, Seen in chronic kidney disease or renal tubular acidosis)**

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Question

"What type of dog is this?"

Answer

"You're welcome."

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#nephrology

Question

What are the 2 clinical presentations of glomerular ds?

Answer

nephrotic syndrome

nephritic syndrome (emerg)

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Question

What is nephrotic syndrome a constellation of?

Answer

Constellation of:
• Hypoalbuminemia
• Edema
• Lipiduria and Hypercholesterolemia
• Proteinuria > 3.5 g/day

Typical Pathology:
• Non‐proliferative Disease (structural abn - glomerulonephropathy)

Nephrotic Syndrome can ONLY be caused by a glomerular disease

No RBC cast

Tags

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Question

What is nephritic syndrome?

Answer

Constellation of:
• Hypertension
• Hematuria
• Proteinuria
• Acute Kidney Injury

Typical Pathology:
• Proliferative Disease (prolif of cells in glomerulus - glomerulonephritis)
--renal emerg - May progress to end‐stage renal disease within days to weeks
--RBC casts

Other parenchymal diseases can present with “nephritic syndrome”

Tags

#nephrology

Question

What causes prolif glomerular ds?

Answer

Deposition of Immune Complexes
• E.g. Post‐infectious, Systemic Lupus Erythematosus (SLE), HCV/HBV/HIV related

Antibody Deposition within the glomerulus
• E.g. IgA Antibodies, Anti‐GBM Antibodies, ANCA, circulating paraproteins

Dysregulation of the complement system

Idiopathic

NB: look for immune complexes, Ab, complement dysregulation on w/u

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Question

What are the different cell types noted in pathology of prolif glomerular ds?

Answer

mesangial cell prolif (better)

endothelial cell prolif

epithelial cell prolif (worst)

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Question

What is the ddx for mesangial cell prolif in glomerulonephritis?

Answer

IgA nephropathy (most common)

SLE

HSP (henoch-schonlein purpura)

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Question

What are IgA nephropathy associated ds's?

Answer

Cirrhosis
HIV Infection
Celiac Disease

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Question

How is IgA nephropathy dx?

Answer

renal bx

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Question

What is the mgmt for IgA nephropathy?

Answer

Blockade of the Renin‐Angiotensin‐Aldosterone System (RAAS)
+/‐ Corticosteroids (↓ inflm)
+/‐ Other immunotherapy (e.g. azathioprine, cyclophosphamide) (↓ IgA formation)

Tags

#nephrology

Question

What is the ddx for endocapillary prolif? (glomerular ds)

Answer

Proliferative Lupus Nephritis
Post‐infectious Glomerulonephritis
(above 2 are most common)
Membranoproliferative Glomerulonephritis

N.B. Endocapillary Proliferation is usually also associated with mesangial proliferation

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Question

How do you dx endocapillary prolif?

Answer

renal bx

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Question

What is the mgmt for endocapillary prolif?

Answer

Corticosteroids

Immunosuppression
• Mycophenolate Mofetil (MMF)
• Cyclophosphamide
• Azathioprine

Tags

#nephrology

Question

How do you dx epithelial prolif (crescentic glomerulonephritis)?

Answer

etiology based on immunofluorescence (IF) on bx

• linear GBM staining → anti GBM ds
• coarse/granular staining → SLE nephritis, post-inf GN
• little/no staining (Pauci immune) → ANCA vasculitis

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#nephrology

Question

What is the mgmt for crescentic GN?

Answer

Treatment of underlying disease
• Immunosuppression (commonly d/t autoimmune ds) - High dose (“pulse”) steroids, Other agents (cyclophosphamide, MMF, Azathioprine, Rituximab)
• Consideration of plasma exchange - Rapid removal of inciting factor (e.g. Anti‐GBM Ab)

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#urology

Question

How can you adjust PSA?

Answer

normal = <4.0ng/mL

age-adjusted PSA
PSA density
PSA velocity
free:total (<0.10 = dangerous; ≥0.25 = safe)

Tags

#urology

Question

What are PCa risk factors?

Answer

genetics → ≥1 fam member = ↑ risk
race → black ↑, asian ↓
diet → high fat diet, obesity (↑ risk for higher grade PCa)

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#urology

Question

What are s&s of PCa?

Answer

usually asx

if adv/mets: bone pain, kidney failure, anemia, urinary sx

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#urology

Question

How do you dx PCa?

Answer

transrectal u/s guided bx

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#urology

Question

PSA screening should not be offered to [...]

Answer

men >75y/o

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#urology

Question

annual PSA/DRE is offered @ age [...] or [...] if high risk
it is repeated [...]

Answer

50, 40
q2-4y

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#urology

Question

How is PCa staged?

Answer

DRE+PSA

bx pathology (gleason score)

staging imaging (CT, bone scan)

TNM - T1 (most common - only via bx), T2 (palpable)

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Question

What is the PCa risk stratification?

Answer

low: ≤ gleason 6 + ≤ T2a + PSA <10ng/mL → no imaging

intermed: gleason 7 or T2a or PSA 10-20ng/mL → CT scan

high: gleason 8-10 or ≥T2c or PSA>20ng/mL → CT + bone scan

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Question

What are the mgmt options for PCa?

Answer

1. watchful waiting
2. active surveillance
3. radical therapies (radiation/surg)
4. androgen deprivation therapy (met rx for ~3y)
5. others

Tags

#exam #urology

Question

What are the complications of prostatectomy?

Answer

peri-op: anesthetic risks, bleed/transf, UTI, wound inf, MI, DVT/PE, bowel/rectal/bladder/ureteric injury, etc

post-op: erectile dysfn, stress urinary incontinence, urethral strictures, LUTS, PCa recurrence

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Question

What are risk factors for kidney stone ds?

Answer

diet: ↓ fluid, ↑ Na/animal proteins
hot environment
medical: DM, obesity, chr diarrheal states (IBD), hypercalcemia, gout, UTI + urea-splitting organisms

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Question

What are the kidney stone types?

Answer

Ca oxalate (80%) - radioopaque
uric acid (10%) - radioluscent
struvite (10%) - radioopaque
rare - cystine (faintly radioopaque), matrix, med stones

Tags

#urology

Question

What are kidney stone promotors and inhibitors?

Answer

promoters: concentrated urine, ↑ urine Ca/oxalate/uric acid, urinary stasis, inf

inhibiters: citrate, Mg, pyrophosphate, glycoprotein

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Question

What are the causes of Ca oxalate stones?

Answer

hypercalciuria (most common)
--renal Ca leak (↓ tubular reabsorption)
--Ca leach from bone (hyperparathyroidism, immobilization, malig, steroids)
--↑ GI Ca absorption

hyperoxaluria (5%)
--bile salts & fatty acids ↑ GI absorption

Tags

#exam #urology

Question

How do you prevent Ca stones?

Answer

Diet
--**↑ fluid
--↓ animal protein, Na, oxalate, EtOH
--do NOT ↓ Ca intake (Ca binds oxalate)**

meds
--hydrochlorothiazide (hypercalciuria) - promote Ca reabsorption
--K citrate (↑ pH & citrate lvl in urine)

Tags

#exam #urology

Question

What causes struvite stones?

Answer

inf w/ urea-splitting bugs (proteus, klebsiella, pseudomonas) → alkaline urine (pH>7.5)
--**NOT ECOLI**

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Question

Uric acid stones are always associated with [...] , and often associated with [...]

Answer

↓ pH (<5.5)
gout

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Question

What causes cystine stones?

Answer

d/t aa transport problem (autosomal recessive defect)
--↓ reabsorption of COLA (cystine, ornithine, lysine, arginine)

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Question

stones are sent to lab for:
[...]
[...]
[...]

Answer

Chemical analysis
X-ray crystallography
Infrared spectrometry

NB: tells us stone type

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#urology

Question

What metabolic w/u would you do to define cause of kidney stone?

Answer

All patients who pass a stone
– Serum creatinine, calcium, and uric acid
– Urine R&M
– Urine C&S

Recurrent stone formers / high risk patients
– Full metabolic work up

• TWO 24 hr. urine collections (Volume, pH, Cr., K+, Na+, Ca++, phosphate, uric acid, oxalate, Mg++, citrate)
• ​Serum (Ca++, PO4, uric acid, creatinine, electrolytes – PTH if hypercalcemic)

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#urology

Question

What is the clinical presentation of kidney stones?

Answer

• Severe pain (“renal colic”):
– Stone obstructs kidney → Causes hydronephrosis
– Capsular distension → constant flank pain
– Ureteral spasm → pain radiating from flank to groin

• Nausea and vomiting (ileus)

• Urinary frequency and urgency – Due to irritation of bladder by stone near the ureteral orifice (bladder)

• Hematuria

Tags

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Question

DDx of renal colic

Answer

**• Acute ureteric obstruction (other causes)
– UPJ obstruction
– Sloughed papilla
– Clot colic from gross hematuria
• Pyelonephritis (fever, pyuria, flank pain) without a stone
• Acute abdominal crisis: appendicitis, diverticulitis, biliary colic, bowel obstruction, pancreatitis
• Ruptured abdominal aortic aneurysm (AAA)
• Gynecological: ectopic pregnancy, torsion / rupture of ovarian cyst
• Radiculitis (L1) – herpes zoster, nerve root compression**

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Question

Renal colic investigation

Answer

urinalysis (pH, RBC, WBC, crystals) + culture (if +WBC)

blood tests (CBC (WBC), Cr (renal function), electrolytes)

non-contrast spiral CT (abdo + pelvis) = best

KUB (abdo xray) - can combine with u/s if can't do CT

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Question

Acute Management of Renal Colic

Answer

Medical:
– Analgesia (narcotics: morphine)
– Anti-emetics (Gravol)
– NSAIDs (lower intra-renal pressure; must stop 48h prior to SWL)
– Antibiotics if evidence of UTI (NOT routine)
– IV fluids (if dehydrated) – may increase pain
– Medical expulsive therapy (alpha blockers help facilitate stone passage)

Tags

#exam #urology

Question

Indications for admission or urgent intervention in kidney stone ds

Answer

**– Pain not controlled with oral analgesics
– Fever and urinary tract infection with obstructing stone
– Refractory vomiting
– Solitary kidney with obstruction OR bilateral obstructing stones → RENAL FAILURE
– Severe hematuria**

Tags

#urology

Question

Emergency Management of kidney stone ds

Answer

Patient requires urgent drainage if:
• Persistent high grade obstruction
• Solitary, obstructed kidney
• Bilateral ureteral obstruction
• Persistent uncontrolled pain
• Continued fever after 24 hr. antibiotics

NB: via Ureteric Stent/Percutaneous nephrostomy tube

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#urology

Question

Definitive Management of ureteral stones

Answer

1) Stones < 5mm: conservative management (75% will pass spontaneously within 2 weeks)
2) Medical Expulsive Therapy (MET):
--α blocking agents (tamsulosin) increase the chance of spontaneous stone passage by 20 to 30%
3) Uric acid stones – alkalinization of urine to pH 6.5 to 7 (with sodium bicarbonate or potassium citrate)
4) Urological therapy for those that fail conservative and medical therapy (shockwave lithotripsy, ureteroscopy)