Renal path, phys, pharm
Terms
undefined, object
copy deck
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? - Microvillus transformation, foot process effacement --> MCD
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What classes of drugs should be used to treat hypertension in:
CHF - Thiazide diuretic, beta-blocker, ACEi, ARB, aldo antagonist
- What glomerular disease is hepatitis C associated with?
- Membranoproliferative glomerulonephritis
- What happens when you give an isotonic NaCl injection?
- Remains almost entirely extracellular, causing an increase in the overall ECF volume.
- What RTA is characterized by high urine pH, hypercalciuria, hypocitraturia, and calcium phosphate stones?
- Type I RTA (Distal)
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What substances can cause nephrotoxicity activity at:
Afferent arteriole - NSAIDs, sulfonamides
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What would the urinalysis reveal in:
Pre-renal ARF -
minimal protein
no cells or casts
Uosm > 500 (kidneys are functioning well)
FENa < 1 % -
? - FSGS
- What are causes of Type I RTA?
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Mutation in proton ATPase on alpha-intercalated cells
Mutation in carbonic anhydrase
Mutation in Cl-HCO3- exchanger on BL membrane -
What classes of drugs should be used to treat hypertension in:
Post-MI - Beta blocker, ACEi, aldo antagonist
- What happens when you give a hypertonic NaCl injection?
- Some isotonic expansion of the ECF and some increase in osmolality, resulting in the extraction of water from the ICF.
- What is the morphology of MPGN?
- Large glomeruli, proliferation of mesangium and leukocytes. Lobular appearance. Thick GBM, often with double contour (subendothelial deposits)
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What substances can cause nephrotoxicity activity at:
Glomerulus - Metals, NSAIDs
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What would the urinalysis reveal in:
Acute tubular necrosis -
Mild protein
Casts
Uosm < 350
FENa > 1% -
? - FSGS
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What classes of drugs should be used to treat hypertension in:
High CVD risk - Thiazide, beta blocker, ACEi, calcium channel blocker
- What glomerular disease shows sausage-like immune complex deposits in mesangium and capillary loops?
- MPGN
- What happens when a hypotonic NaCl injection is given?
- Some isotonic increase in ECFV, proportional increases in ICFV and ECFV with reductions in ICF and ECF osmolalities.
- What RTA is characterized by appropriately acidified urine, hyperchloremic acidosis but in acid balance, and bicarbonaturia when alkali is administered?
- Type II RTA (Proximal)
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What substances can cause nephrotoxicity activity at:
Proximal tubule - Metals, pigments (protein), antineoplastics (Cis-platin), antibacterials, cyclosporine, rampamycin
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What would the urinalysis reveal in:
Acute interstitial necrosis -
Mild protein
RBCs, WBCs,
Uosm < 350
FENa > 1% -
? - Collapsing glomerulonephropathy
- What causes Type II RTA?
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Impaired HCO3- reabsorption in proximal tubule (sometimes associated with Fanconi syndrome)
Caused by faulty Na-HCO3- cotransporter on BL membrane -
What classes of drugs should be used to treat hypertension in:
Diabetes mellitus - Thiazide, beta-blocker, ACE-i, ARB, CCB
- What entities can cause crescentic GN?
- Anti-GBM (idiopathic or Goodpasture’s), immune complex (idiopathic, SLE, post-infx, HSP, IgA, MPGN), or pauci-immune (idiopathic, Wegener’s granulomatosis, or microscopic polyarteritis)
- What happens when you give IV mannitol?
- Stays in ECF, acts like NaCl. Used to relieve cerebral edema.
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What substances can cause nephrotoxicity activity at:
Distal tubule - cis-platin, glycols (deposition)
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What would the urinalysis reveal in:
Glomerulonephritis -
Protein, blood
RBC casts
Uosm > 500 (this is weird)
FENa > 1% -
? - Spikes and holes --> membranous GN
- What are the two main features of pauci-immune GN?
- Fibrinoid necrosis and crescents
- What causes generalized edema? Localized?
- Drop in plasma oncotic pressure. Increase in interstitial oncotic pressure.
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What classes of drugs should be used to treat hypertension in:
Recurrent stroke prevention - Thiazide, ACEi
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What happens if you give bicarb to someone with:
Distal RTA (Type I)
Proximal RTA (Type II) -
Distal: serum HCO3- goes up, urine pH doesn't change much
Proximal: can't reabsorb any more HCO3-, so urine pH goes up, and serum HCO3- doesn't change much -
What substances can cause nephrotoxicity activity at:
Collecting duct - Obstruction by anticholinergics, bromocriptine, quinolones, sulfonamides
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What would the urinalysis reveal in:
Post renal ARF -
minimal protein
varied microscopy
Uosm < 350
FENa > 1% -
? - Spikes and holes --> membranous GN
- How does CHF result in edema?
- Reduced CO and systemic BP from left heart --> retention of NaCl and water. Expand vascular volume, mostly on venous side, increasing Pc.
- How does toluene result in nephrotoxicity?
- Causes myoglobinuria --> acute tubular necrosis
- What are the two types of ANCA associated with?
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C-ANCA - proteinase 3 – Wegener’s, occasionally idiopathic or MPA
P-ANCA – myeloperoxidase – MPA and idiopathic, occasionally Wegener’s
So basically this tells you nothing. -
What classes of drugs should be used to treat hypertension in:
Benign prostatic hypertrophy - Alpha-blockers
- What is a lab hallmark of pre-renal ARF?
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Elevated urea concentration out of proportion to creatinine elevation
because more filtrate is reabsorbed proximally, where urea is permeable - What RTA is characterized by acidic urine, hyperchloremic acidosis, and hyperkalemia?
- Type IV - Hyporenin-Hypoaldosteronism
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? - Spikes and holes (see red deposits in GBM) --> membranous GN
- How does acetaminophen cause nephrotoxicity?
- metabolite is a free radical that produces damaging protein adducts in liver and kidney
- How does glomerulonephritis result in edema?
- Retention of NaCl and water is primary (due to decreased GFR). Expand vascular space, resulting in (1) increased venous return from veins--> increased EDV --> increased BP --> inhibits renin release (2) Blood accumulates on venous side --> increased Pc --> transudation --> edema. Increased venous pressure stimulates release of ANP --> inhibit sodium reabsorption and promote diuresis
- How does hypoaldosteronism lead to acidosis?
- Hypoaldo --> hyperkalemia --> inhibits glutaminase and NH3 generation --> lack of buffer to accept protons --> backleak --> acidosis
- What drugs can cause reduced perfusion, resulting in ARF?
- NSAIDs, ACEi, cyclosporine
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What is the mechanism of:
Spironolactone -
Aldosterone antagonist in cortical collecting duct
(Aldo's effects are to increase Na/K ATPase, K+ secretion, mitotic growth factor, upregulation of ENaC) - What is the therapy for pauci-immune GN?
- Immunosuppressive
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? -
Acute post strep GN
See neutrophils, some obliterated capillary lumina - How do aminoglycosides cause nephrotoxicity?
- Magnesium and potassium wasting due to tubular damage
- How do diuretics lead to metabolic alkalosis?
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Loss of NaCl -> decreased EABV --> AII and aldo
AII--> increased HCO3- reabsorption in PT because there's a Cl- deficiency
Aldo --> increased H+ secretion in CCD - How does liver disease cause edema?
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(1) cirrhosis – fibrosis leads to increased R --> increased Pc in acini --> ascites
(2) other liver disease – reduced production of albumin--> lowers oncotic pressure --> fluid leaks out of capillaries -
What are the adverse reactions to:
Spironolactone -
Hyperkalemia
Metabolic acidosis
Gynecomastia - What drugs can cause direct tubular toxicity, resulting in ARF?
- Aminoglycosides, contrast, pigment, heavy metal
- What kind of proteinuria is there in MCD?
- Selective – albumin
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? - Humps - pathognomonic for acute post strep GN
- How does hyperaldosteronism lead to metabolic alkalosis?
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Aldo stimulates intercalated cells to excrete H+
This is not Cl responsive! - How does the nephrotic syndrome result in edema?
- Loss of urine protein > 3.5 g/day --> decreased plasma oncotic pressure --> fluid leaks into interstitium
- How is the therapeutic index calculated?
- TD50/ED50
- What aldo blocker does not cause gynecomastia?
- Eplerenone
- What drugs can cause allergic interstitial nephritis, leading to ARF?
- Antibiotics, NSAIDs, phenytoin
- What is the mechanism of MCD?
- T-cell mediated and cytokines. Mutated nephrin.
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? -
IgA nephropathy
See mesangial hypercellularity, normal capillary loops on left.
Right - more severe, with some endocapillary and extracapillary proliferation (crescents) - Freebie
- Thanks.
- How do you differentiate between MCD and other renal disorders?
- Good response to corticosteroids.
- How is the margin of safety calculated?
- LD1/ED99
- What drugs can cause tubular obstruction, resulting in ARF?
- Acyclovir, sulfa
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What is the mechanism of:
Loop diuretics - Inhibits Na/K/2Cl transporter in TALH
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? - Double contours (not specific for IgA)
- How does acetaminophen induce toxicity?
- Metabolte free radical produces damaging protein adducts in liver and kidney.
- How is urea handled in the nephron?
- Freely filtered at glomerulus. 1/2 is passively reabsorbed in proximal tubule. The rest is impermeable except for the deepest part of the CD, where permeability is increased when ADH is present.
- In what conditions is spironolactone used?
- High aldo states (CHF, cirrhosis, hyperaldosteronism)
- What are the mechanisms of decreased GFR in ATN?
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Tubular cell damage
Obstruction from cell debris --> increased Pt
Loss of cell polarity and disruption of cell jxns --> backleak
Activation of tubuloglomerular feedback because of decreased proximal reabsorption of Na - Where are the deposits in membranous GN?
- SubEPIthelial
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? - MPGN - see GBM thickening, abnormal lobulation of glomerulus, capillary lumens may be occluded
- How do COX inhibitors cause toxicity?
- Vasodilate afferent arteriole, compete with aldosterone --> hyperkalemia
- How is creatinine handled in the nephron?
- Freely filtered at glomerulus.. Not reabsorbed. Some is secreted. Estimates GFR because the secretion makes up for overestimation of plasma creatinine inherent in measurement methodology.
- In what conditions are loop diuretics useful?
- CHF, nephrotic syndrome, cirrhosis
- What is the EM appearance of membranous GN?
- Subepithelial deposits along GBM, separated by spikes
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? - Double contours - in this case, it's MPGN, but it could also be IgA)
- How do aminoglycosides and sulfonamides cause toxicity?
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Aminoglycosides: magnesium and potassium wasting due to tubular damage
Sulfonamides: poor sulubility causes obstruction, also hypersensitivity vasculitis - How do you calculate GFR from creatinine levels?
- GFR= (Ucr x urineflow)/Pcr
- What are the ADRs of loop diuretics?
- Hypokalemia, metabolic alkalosis, deafness
- What is the IF appearance of membranous GN?
- Granular deposits of Ig and complement along GBM
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? - MPGN - sausage-shaped (semi-linear) deposits of IgG and C3
- How is glucose handled in the nephron?
- Freely filtered at glomerulus, actively reabsorbed in proximal tubule by a mechanism that has a transport maximum, which is about 370 mg/min --> glucose does not normally appear in urine if plasma glucose is normal
- What are examples of loop diuretics?
- Furosemide (Lasix), bumetanide, torsemide, ethacrynic acid
- What kind of proteinuria is in FSGS?
- Non-selective
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? - MPGN - subendothelial and rare subEPIthelial deposits
- Does FSGS recur after transplant?
- Yes – suggests circulating factor.
- What are three effects of PTH?
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1) Promotes osteoclastic activity, mobilizing Ca2+ from bone
2) Increases activity of renal vitamin D3 1a-hydroxylase, which is required for synthesizing calcitriol, which increases intestinal reabsorption of Ca2+
3) Increases Ca2+ reabsorption from nephron and reduces the maximal transport for Pi, increasing Pi excretion - What is the mechanism of thiazide diuretics?
- Inhibits Na/Cl transporter in distal convuluted tubule
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? -
Idiopathic pauci-immune
Fibrinoid necrosis without proliferation
Also crescents - Summarize the handling of Na+.
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Oh goody.
Proximal tubule: 70% of Na is actively reabsorbed, Cl and water follow passively
Ascending limb of loop of Henle: 20% is reabsorbed by the Na/K/2Cl cotransport (impermeable to water)
Distal tubule: 5% Na is reabsorbed (Na/Cl cotransport), impermeable to water
Collecting duct: 3-5% reabsorbed by electrogenic Na channel pumps that are aldo regulated (ENaC). Variably permeable to water with regulation by ADH
If there is low aldo (from high blood pressure) – you get decreased Na reabsorption in CD - What are the ADRs of thiazides?
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Hypokalemia,
metabolic alkalosis,
gout (more UA absorbed with Na in proximal tubule under influence of AII),
glucose intolerance (hypokalemia impairs insulin release) - What is the morphology of FSGS?
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Increased mesangial matrix, collapsed GBMs, deposition of hyaline masses and lipid droplets
IgM in the areas of hyalinosis -
If you're thinking of either idiopathic pauci-immune GN or anti-GBM, what does this tell you? - This is anti-GBM, because you don't see immune complex deposits in pauci-immune.
- What are examples of thiazides?
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Hydrochlorothiazide
Chlorthalidone
Metolozone - What are the effects of hypoaldosteronism?
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Na loss, hypovolemia, decreased CO, decreased RBF
K+ retention, hyperkalemia, cardiac arrhythmias
H+ retention, metabolic acidosis - What is the morphology of acute post-strep GN?
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LM- uniform increase in mesangial and endothelial cells, inflammatory infiltrate, thrombi in capillaries. Crescents – bad prognosis
EM – humps
IF – IgG and complement, subENDOthelial -
? -
Malignant hypertension
Top - Fibrous thrombosis
Bottom - Mucoid intimal hyperplasia and onion skinning - What is diabetes insipidus?
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Either no synthesis of ADH (central) or ADH receptors in CD are resistant (nephrogenic)
Leads to inability to reabsorb water, leading to diuresis - What is the mechanism of acetozolamide?
- Carbonic anhydrase inhibitor (decreased ability to exchange Na for H+) --> diuresis
- What nephropathy occurs 1-2 days after a nonspecific upper respiratory infection?
- Berger’s disease (IgA nephropathy)
- How is H+ handled in the nephron?
- Very low concentration in plasma. H+ is actively secreted by nephron, mostly in proximal tubule, 10% in CD. Most titrates HCO3- in tubular fluid, some reacts with ammonia, and some with other buffers (e.g. phosphates)
- What are the ADRs of acetozolamide?
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Metabolic acidosis (decreased HCO3- absorption)
Hypokalemia - What are the clinical manifestations of Alport’s syndrome?
- Nephritis with nerve deafness and eye disorders, hematuria and proteinuria.
- What are the clinical signs of diabetic nephropathy?
- Microalbuminemia, grdual increase in proteinuria. Eventually Cr increases, renal failure. Retinopathy is indicative.
- How is H+ secretion stimulated?
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a) Respiratory acidosis leads to increased H+ secretion and therefore increases plasma HCO3- (renal compensation)
b) Aldo-increased Na reabsorption in CD causes H+ secretion to maintain electrical balance
c) Na+ reabsorption is balanced wither by passive K+ secretion or active H+ secretion. If K+ is in short supply, H+ secretion is stimulated. - What are other examples of K+ sparing diuretics?
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Amiloride
Triamterene
(Block ENaC in collecting duct) - What are the pathological features of diabetic nephropathy?
- Mesangial glomerulosclerosis - increased thickness in capillary walls, increase in mesangial matrix.
- What is the morphology of Alport’s?
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LM – segmental glomerular proliferation or sclerosis, increased mesagngial matrix. Foam cells. Tubular atrophy, interstitial fibrosis.
EM – thin BM, thickens with age. Basket weave appearance. - How can you tell the difference between metabolic and respiratory acid-base disturbances just by looking at H+ and bicarb?
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If they change in same direction, it is RESPIRATORY
If they change in opposite directions, it is METABOLIC -
If this also stained brown on silver stain, what would this be? - Diabetic nephropathy - this is nodular glomerulosclerosis, a Kimmelsteil-Wilson lesion. Notice also hypocellularity.
- What are the ADRs of ACE-inhibitors?
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hyperkalemia
cough
angiedema
teratogenic
be cautious with renal insufficiency (decreases GFR initially) - What are examples of ACE-inhibitors?
- Captopril, lisinopril
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What is this? - Diabetic nephropathy - thick GBM, foot process effacement secondary to hyperfiltration
- When might renal compensation for metabolic alkalosis not be complete?
- If there is accompanying severe volume depletion, because that will result in high also levels, which will result in increased H+ secretion.
- How does autoregulation work?
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1) Myogenic response in afferent arteriole – increased pressure opens stretch-activated Ca2+ channels, Ca enters smooth muscle cell, binds to calmodulin, activates MLCK, stimulates contraction, constricting arteriole
2) Tubuloglomerular feedback – macula densa monitors tubular fluid, signals to afferent and efferent arterioles through renin - What is the mechansim of Angiotensin II Receptor Blockers?
- Blocks AI receptor of AII
- Which amyloidosis is primary? Secondary?
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AA -secondary
AL -primary -
If this is also silver-negative, what is this? - Amyloidosis. This is also paler pink than Diabetic Nephropathy's nodular glomerulosclerosis.
- What are examples of ARBs?
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Losartan
Valsartan - What is the effect of the sympathetic nervous system on the kidney?
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Sympathetic only.
Alpha receptors – stimulate contraction, more of afferent than efferent (more muscle on aff)
Beta receptors – on JGA of afferent arterioles, release renin when stimulated, resulting AII constricts efferent arteriole, mainly. GFR is maintained while RBF is reduced -
? - Amyloidosis w/congo red stain and polarized light.
- In what conditions are beta blockers used?
- Arrhythmias, angina, heart failure, high renin
- What are the effects of angiotensin II?
- Greater constriction of the efferent arteriole than afferent ⬡ increase GFR
- How can you distinguish btw AA and AL amyloidosis?
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AA loses congo red affinity when treated with KMnO4.
Also, secondary immunostains with SAA in mesangium - What is the mechanism of action of beta blockers?
- Decreased renin secretion
- What stimulates the release of renin from the JGA?
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a) Beta-1 receptors
b) Reduction in perfusion pressure (direct effect on JGA)
c) Reduction in Na+ delivery to macula densa (tubuloglomerular feedback) - What are the ADRs of beta blockers?
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Negative dromotrope, inotrope, and chronotrope
Erectile dysfunction
Depression
Claudication - What are the clinical features of adult polycystic disease?
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Normal renal fxn until middle age, when they present with renal insufficiency, hematuria, flank pain, HTN.
Extrarenal: liver cysts, berry aneurysms in circle of Willis, mitral valve disease, colonic diverticula. - What is found in the urine in primary amyloidosis?
- Light chains --> Bence-Jones proteinuria
- What do elevated ANA levels indicate?
- SLE
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What is an example of a non-selective beta blocker?
What are its effects? -
Propranolol
Decreases renin, CO, peripheral resistance (by decreasing SNS activity) - What is the histopathological appearance of the kidney in malignant hypertension?
- Fibrinoid necrosis of arterioles (eosinophilic deposition in vessel walls) If inflammatory cells are present, it is necrotizing arteriolitis.
- How do you distinguish between IgA and Type II SLE (mesangial lupus nephritis)?
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EM looks the same (deposits in mesangium, mesangial proliferation).
IF - SLE stains for everything. IgA only IgA. - What is an example of a beta-1 blocker?
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Metoprolol, atenolol
Less effect on bronchial constriction, vascular dilation - What type of pattern does immunofluorescence reveal in anti-GBM?
- Linear
- What are examples of alpha-1, beta adrenergic blockers?
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Labetalol, carvedilol
Less effect on cardiac output and HR - What are the features of nephritic syndrome?
- Proteinuria, hematuria, RBC casts, varying degrees of renal insufficiency and HTN
- What is the most severe form of SLE?
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Type III - diffuse proliferative GN
Neprhritic + nephrotic - What are the features of nephrotic syndrome?
- Edema, severe proteinuria (>3.5 g/day), hypoalbuminemia, hyperlipidemia
- What are the morphologic characteristics of Type III SLE?
- Hypercellularity, crescents, fibrinoid necrosis. Double contours.
- What is an example of an alpha-1 blocker, and what are its effects?
-
Prazosin, terazosin
Tamulosin (specific for prostate)
Vasodilation w/o reflex tachycardia
Used in BPH -
? - Lupus - this is apparently a wire loop lesion.
- What are examples of alpha-2 agonists? What are their effects?
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Clonidine, alpha methyldopa
Stimulation of presynaptic alpha-2 receptors --> Decreased norepinephrine outflow from CV control centers in brain --> decreased peripheral autonomic tone - What are the most common causes of nephritic syndrome?
- Acute post-strep glomerulonephritis, glomerular diseases (including SLE)
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? - Wire loop lesion --> SLE
- What are the ADRs of alpha 1 blockers?
- First dose orthostasis
- What are the most common causes of nephrotic syndrome?
- Lipoid nephrosis (Minimal change disease) in children and elderly, membranous glomerulonephritis in adults
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? - Wire loops in upper left hand corner --> SLE
- What are the ADRs for alpha 2 agonists?
- Sedation, rebound HTN if stopped, dry mouth
- What are the features of Rapidly Progressive Glomerulonephritis (RPGN, a.k.a. crescentic GN)
- Rapidly deteriorating renal function that accompanies glomerular injury. Nephritic urine sediment, renal failure. Accumulation of crescents (proliferation of parietal epithelial cells and migration of macrophages in Bowman space).
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Oh my god, what is this? -
SLE, Type V: there are deposits everywhere, thick GBM. Hematuria (RBC in urinary space)
SubEPIthelial deposits - What are examples of arterial dilators?
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Hydralazine
Minoxidil
Diazoxide - What are the causes of RPGN?
- Idiopathic, multisystemic disease (vasculitis or Goodpasture), or follow post-strep.
- What are ADRs for arterial dilators?
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Na retention and edema --> use w/furosemide
Reflex tachycardia --> use w/B-blockers
Hydralazine may also lead to headache, N/V, lupus-liks syndrome - What are the clinical features of acute poststreptococcal GN?
- Affects more children. Nephritic syndrome. Elevated antistreptolysin O titers, low serum complement.
- What are the pathological features of acute poststrep GN?
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Diffuse cellular proliferation and leukocytic infiltration--> hypercellularity
Electron microscopy shows subepithelial humps of Ag-Ab complexes
Granular deposits of immunoglobulins - What is the mechanism of CCBs?
- Inhibits voltage-sensitive L-type channel on smooth muscle
- What are examples of CCBs?
-
Dihydropyridine (nifedipine, amlodipine)
Non-dihydropyridine (verapamil, diltiazem) - What are the clinical features of MCD? (lipoid nephrosis)
- Nephrotic syndrome. Caused by food allergy, medications, or hematologic malignancies.
- What are ADRs of CCBs?
-
Dihydropyridines: headache, edema
non: negative inotropic, conduction delay, constipation w/verapamil - What is the proposed pathogenesis of MCD?
-
Lymphokine from T cells
Fusion of epithelial foot processes --> loss of polyanionic filter, leading to proteinuria - What is the mechanism and effect of reserpine?
- Binds to central and peripheral adrenergic neuron storage vesicles --> antagonizes
- What is the treatment of MCD?
- Steroids --> complete recovery
- What are the pathological findings of MCD?
-
Light- normal
Electron – loss of foot processes, but no electron-dense deposits in GBM
No immunofluorescence. - What are the potential side effects of alpha methyldopa?
-
- Hemolytic anemia
- Edema
- Impotence
- Sedation
- Increased prolactin -> lactation - What are the clinical and pathogenesis features of membranous GN?
-
Nephrotic syndrome, insidious onset. Usually idiopathic, but may be cause by infection, drugs, tumors, systemic disease.
Path: subepithelial immune disease deposits in GBMs ⬡ damage capillary walls - What are the indications for nitroprusside?
- Severe hypertensive crisis, aortic dissection
- What are the adverse reactions associated with nitroprusside?
-
cyanide toxicity (lactic acidosis, arrhythmias, hypotension, hypoxia)
thiocyanate toxicity (weakness, disorientation, psychosis, muscle spasms)
Reflex tachycardia - What is the pathological appearance of the kidneys in membranous GN?
-
Swollen and pale grossly. Diffuse thickening of capillary walls.
Subepithelial deposits.
Granular pattern of Ig and complement - What are the clinical features of membranoproliferative GN?
- Nephrotic or mixed nephritic/nephrotic syndrome.
- Which calcium channel blocker is safe in CHF?
- Amlodipine
- What are examples of thiazide diuretics?
- Hydrochlorothiazide (HCTZ), chlorthalidone, metolazone (increasing in potency)
- What is the pathogenesis of MPGN?
-
Type I: immune complex deposition in *subendothelium* and mesangium
Type II: C3 nephritic factor (an antibody against C3) with IgG antibody in serum. Dense deposits along glomerular and tubular BM - How does amiloride induce diuresis?
- K+ sparing, directly inhibits Na+ reabsorption in collecting duct.
- What is the pathological appearance in MPGN?
-
Mesangial proliferation, BM thickening, tram-tracking
EM: Type I subendothelial deposits of C3 and IgG
Type II: deposits of C3 in GBM - What are the clinical features of Focal Segmental Glomerulosclerosis?
- Nephrotic syndrome, often with hematuria, HTN, impaired GFR, and non-selective proteinuria
- What is the pathological appearance of FSGS?
-
Segmental sclerosis, hyalinization of glomeruli
EM: nonsclerotic regions show loss of foot processes. Sclerotic segments show increased mesangial matrix and mesangial deposits.
IgM and C3 deposits in sclerotic segments - What is the pathological appearance of Anti-GBM?
-
Crescents and fibrinoid necrosis
EM: no deposits, but GBM disruption
IF: linear pattern of Ig - What are the clinical features of Focal Proliferative GN?
- May be primary or secondary to SLE, Goodpasture, SBE, or Wegener’s. May be subclinical or present with hematuria/proteinuria, occasionally nephrotic syndrome.
- What are the clinical features of Berger disease (IgA nephropathy)?
- Mild proteinuria. Recurrent hematuria. Occasional nephrotic syndrome. Usually follows a respiratory infection. Common cause of GN. Related to HSP.
- What are the pathological features of Berger disease?
-
Variable. May be normal. Segmental proliferation, mesangial proliferation, or crescent formation.
EM: mesangial deposits
IF: mesangial IgA w/o complement - What are the clinical features of hereditary nephritis (Alport syndrome)?
-
Hereditary abnormality of collagen ⬡ renal disease, deafness, ocular abnormalities (dislocated lens, corneal dystrophy, cataracts)
Hematuria, proteinuria, slowly progress to renal failure