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Cells of the adrenal medulla and its characterisitics?
Chromaffin cells that release catecholamines such as ACTH. Post-ganglionic sympathetic neurons derived from neural crest cells.
What is the bias that classifies investigators having a prior knowledge of the exposure status?
A complication of nephrotic syndrome is renal vein thrombosis. How does it present and what is lost in the urine?
- Left-sided varicocele
- Sudden onset flank pain
- Loss of anticoagulant: anti-thrombin III.
If a patient is using loop diuretics and then is given NSAIDs, why do they get a decreased diuretic response?
Loop diuretics stimulate prostaglandin release which causes dilation of the afferent arteriole, increasing blood flow and GFR. NSAIDs inhibit this.
Renal artery stenosis or decreased systemic BP causes what compensatory mechanism in the kidney?
Stimulation of the RAAS system to increase GFR and maintain BP.
Acyclovir causes what major adverse effect and how can it be prevented?
Crystalline nephropathy (excreted in the urine via glomerular filtration and tubular secretion) and can be prevented by adequate hydration.
What type of antibodies are found in idiopathic membraneous nephropathy?
IgG4 antibodies against PLA2R located on the podocytes.
All types of RPGN have crescent formation but differences too, and examples.
Type 1 RPGN?
Type II RPGN?
Type III RPGN?
Type I: antibodies against glomerular BM antibodies, IgG and C3 deposits found on immunofluorescence and also prevent with hemoptysis
- Type II: Immune-complex mediated and lumpy-bumpy granular appearance on immunofluorescence, subepithelial humps on EM
- Examples: SLE, PSGN (decreased C3 levels), IgA nephropathy, Henock: Schloen purpura.
- Type III: Pauci-immune: no immunoglobulin or complement deposits (no IgG or C3), ANCA +
- Examples: Wegeners.
Side-effects of ACE-inhibitors?
- Nephrotoxicity: dilates the efferent arteriole causing decreased GFR (increased creatine)
In what part of the nephron is the [PAH] the lowest?
When can [PAH] decrease along the nephron instead of increasing?
Bowman's space: PAH is freely filtered and then secreted by the PCT by carrier mediated transporters. No reabsorption occurs.
Can happen when carriers are saturated (i.e. no more secretion occurs). Any further increase in PAH past its Tm will be due to increased filtration.
Post-strep glomerulonephritis is what type of hypersensitivity reaction?
Type III H.S. mediated by immune complexes.
Patient presents with bilateral renal masses composed of fat, smooth muscle, and blood vessels, brain hamartomas, ash-leaf spots on the skin lacking pigment, cardiac rhabdomyomas, and facial angiofibromas. What is the disease and how is it inherited?
Tuberous sclerosis, AD.
Patient presents with neurofibromas, optic gliomas, pigmented nodules on the iris, hyperpigmented macules (cafe-au-lait spots)? Disease and inheritance?
NF type I, AD.
What happens in the urine during metabolic acidosis?
- Increased excretion of H+ ions as more accumulates in the blood. = decreased pH
- Decreased excretion of HCO3-
- Titratable acids are excreted which is H+ bounds to bases so less free H+ not causing a drastic change in free pH (H2PO4 and NH4)
Selective proteinuria (loss of albumin only) in minimal change disease occurs due to what mechanism?
Loss of negative proteins on the GBM
Findings of tubular injury, anion gap metabolic acidosis, and presence of oxalate crystals in the urine are duet to what?
Ethylene glycol (found in anti-freeze)
Anion gap metabolic acidosis, oligouria, brown muddy casts, and tubular injury is due to?
Ischemic tubular necrosis: chronic hypotension or severe infection.
1. Acute salicylate poisoning causes what?
2. Chronic salicylate poisoning (= few hours) causes what?
- 1. Respiratory alkalosis
- 2. Superimposed by metabolic acidosis (pH comes back to normal)
IgA nephropathy associated with extra-renal symtpoms such as rash on extensor surfaces, GI symptoms (bleeding, intussecption) is what disease?
Henock: Schloen purpura.
HIV patient with visual impairement is treated with what drugs and its adverse effects?
- Due to CMV-retinitis:
- 1. gangicylovir - neutropenia
- 2. foscarnet - hypocalcemia and hypomagnesemia
- 3. cidofovir.
Acute tubular necrosis occurs in what 2 parts of the nephron?
- 1. proximal tubules
- 2. thick ascending loop of Henle
Hyperacute rejection is what type of hypersensitivity?
Type II H.S - preformed antibodies within the recipient directed against donor antigens.
In the presence of ADH, what nephron segment contains the most concentrated urine, and which one contains the most dilute urine?
- Concentrated: collecting ducts
- Dilute: ascending limb of loop of Henle and DCT
How is digoxin primarily cleared, and what precautions must be taken in the elderly?
Via the kidneys, and in elderly, they have age-related renal insufficiency hence the dose of digoxin must be decreased.
A multi-drug regimen is started for a patient with congestive heart failure. Which drug is added to benefit the overall survival of the patient?
- Spironolactone: aldosterone antagonist which inhibits aldosterone, hence, decreases ventricular modelling and cardiac fibrosis
- (RAAS stimulated in CHF)
What is the principle site of uric acid precipitation = formation of uric acid crystals?
- Uric acid (pKa = 5.4) is soluble in acidic environments. Lowest pH found along the distal tubules and collecting duct.
- Occurs when a large number of cells are destroyed by chemo and hence precipitates uric acid
A patient undergoes treatment with Ampotericin B, and complains of weakness and palpitations and ECG reveals premature ventricular beats. Why?
Amphotericin B causes hypokalemia and hypomagnesemia - decreases GFR and causes direct toxic effects on the tubular epithelium.
How does acetazolamide treat glaucoma?
CA inhibitor: blocks the production of HCO3- and its reabsorption and aqueous humor production
In a DKA patient, what respiratory problem can occur with metabolic acidosis?
Respiratory acidosis when PCO2 is above the range: PCO2 = 1.5(HCO3-) + 8 +/-2.
A patient undergoes renal transplant, and three weeks later compains of malaise. Lymphocyte infiltrate is seen on microscopy. Dx?
Acute rejection can be antibody mediated or cell mediated immunity. Latter is associated with lymphocytic infiltrate.
Where does the left kidney lie anatomically?
Deep to the tip of the 12th rib (ribs 9,10, 11 overlie the spleen)
Stages of ATN?
- 1. Initiation: ischemic injury to renal tubules precipitated by hemorrhage, acute MI, sepsis, surgery.
- 2. Maintenance: decreased urine output, fluid overload, hyperkalemia, increased BUN/Cr.
- 3. Recovery: Increase in urine output leads to high-volume diuresis. Decreased concentrations of K, Mg, PO4, and Ca. . Patients can become dehydrated.
5 year old child with acute-onset colicky abdominal pain and loose stools develops altered mental status. Has oligouria and red coloured urine, and has pallor. Dx?
Mechanism of nephrotic syndrome?
- 1. increased permeability of the glomerular capillaries leading to albumin loss in the urine.
- 2. decreased colloid osmotic pressure in the blood - fluid moves into the interstitial space and edema occurs.
- 3. fluid decreases intravascularly, reduces renal perfusion pressure. Stimulates RAAS, and ADH is also stimulated and causes Na+ and water retention.
- 4. liver increases synthesis of proteins including LOW-DENSITY lipoproteins
- 5. followed by lipiduria.
Extreme physical activity or trauma to the muscle causing red urine, but no red blood cell casts. Dx?
What drug is contraindicated and why?
Myoglobinuria due to muscle breakdown
K+ sparing diuretics are contraindicated in renal failure. Crushed muscles will increase a lot of K+, PO4-, uric acid, and metabolic acidosis. K+ sparing diuretics will exacerbate the hyperkalemia.
When is renin stimulated?
- 1. increased SNS activation
- 2. decreased blood flow
- 3. decreased Na+ and Cl- sensed by the macula densa
What is seen on microscopy with Wilm's tumor?
Embryonic glomerular structures surrounded by mesenchymal spindle cells.
Patient presents with flank pain, yellow-brown hexagonal staghorn calculi.
- Disease: Cystinuria
- Dx test: Positive cyanide test with nitroprusside
- Tx: alkalinization of the urine
Sickle cell anemia affects what part of the kidney?
Affects the medulla, causing papillary necrosis.
Bladder rupture would cause urine to leak out into the peritoneal cavity. What are the characterisitics of the urine?
Low protein and bilirubin, low amylase, low RBCs, high urea, high ammonia
What two diseases impair the gradient for ADH to work?
- 1. nephrogenic DI
- 2. Diabetes = causes polyuria and reduces ability to maintain the medullary osmotic gradient.
Pathophysiology of minimal change disease?
Cell-mediated immunological response with increased production of lymphokines by T cells reduces the production of polyanions in the glomerular BM, which allows albumin to go through and thus show up in the urine.
At 200mg/dl, what happens to the glucose in the kidney?
It's at threshold: i.e. glucose first starts appearing in the urine.
In a renal biopsy, appearance of amyloidosis is seen. Cause?
- Deposition of altered immunoglobulin light chains due to chronic antigenic inflammation.
- E.g. TB (can also cause sterile pyuria)
n.b. DM has Kimmelstein nodules.
Which renal drugs increase Na and K excretion, with no effect on free water clearance?
Carbonic anhydrase inhibitors.
Patient has urinary urgency and urge incontinence and is Type II diabetic taking glyburide. Treatment?
Muscarinic antagonist such as oxybutynin and tolterodine.
In renal failure when creatinine and urea levels are normal, and plasma sodium is normal, what is going on?
What changes in chronic renal failure with no compensation?
- GFR decreases; therefore, you're not filtering as much Na+ which will lead to hypernatremia. But because the plasma sodium level is normal, you're increasing the excreting the Na+ to keep it balanced.
- Same thing occurs with K+.
GFR decreases; hence you decrease the filtration of Na+ and K+ and cannot compensate for it. Thus, hypernatremia and hyperkalemia.
A patient presents with metabolic alkalosis and is on a drug that inhibits Na+ and Cl- in the ascending limb of loop of Henle. What is going to be low in the plasma?
Loop diuretics; hence, K+ will be low as its reabsorption is prevented as well.
What is the fractional excretion rate of Na+ in prerenal failure and ATN?
<1% and >2%
What is the BUN/Cr in prerenal failure vs ATN?
>15 and normal
What is the urine osmolarity is prerenal failure vs ATN?
>500 and <350
Hypertension can affect the media of the interlobular arteries and the arcuate arteries. Dx and what else can be seen?
Fibroelastic dysplasia: hyaline arteriosclerosis and patchy, ischemic atrophy.
What will be seen on light microscopy in a SLE patient?
Mesangial expansion with cellular proliferation
What is the major adverse effect of cyclosporine?
A patient with a neurogenic bladder (bladder that doesn't empty properly) and a spinal cord injury will have what problem? Tx?
- PNS response is hyper-sensitive so bladder hyper-reflexia.
- Tx: Muscarinic antagonist: Tolterodine/Oxybutynin.
A patient with chronic renal failure must have what dietary modifications?
- 1. Limit amouth of sodium and water
- 2. Low protein
- 3. High carb
- 4. High fat
What is a complication of urinary calcium stones?
- Small stones: renal colic
- Large stones: acute pyelonephritis (microtraumatic changes leading to stasis)
Patient with sharp, radiating pain to the back presents with bilateral flank pain and hematuria. Dx?
- Dissecting aortic aneurysm leading to renal infarction.
- (a-fib can dislodge a thrombus and cause renal infarct too)
Why are the vasa recta affected in sickling patients?
Located in the renal medulla which is an ischemic region and it is hypertonic too.
What are the cysts like in ARPKD?
Smooth cysts made by the medulla
What is the pathophysiology behind RPGN?
Proliferation of the glomerular cells of the Bowman's capsule causing crescent formation. All nephritic syndromes cause RPGN which can cause renal failure.
In IgA nephropathy (Berger's disease), where are the antibodies deposited?
In the mesangium causing mesangial proliferation
Pathophysiology of Type I MPGN?
- Tram-track appearance due to mesangial deposits causing GBM splitting
- Sub-endothelial deposits.
Pathophysiology of Type II MPGN?
- Associated with the C3 nephritic factor (an autoantibody that stabilizes C3 convertase) so it overactivates the alternate complement pathway decreasing C3 levels
- Ribbon-like appearance due to C3 deposits
- Intramembraneous deposits (dense deposits)
Pathophysiology of Alport's syndrome? Nephrotic or nephritic syndrome?
- Type IV collagen due to BM splitting of the lamina densaNephritic.
What are the four main causes of membraneous glomerulonephropathy?
- 1. Drugs.
- 2. Infections (e.g. hepatitis)
- 3. SLE
- 4. tumors
In which disease do you have deposition of all complement factors and all immunoglbulins?
Where are the deposits located?
Type IV SLE, subendothelial (diffuse proliferative glomerulonephritis)
Small and shrunken kidneys are associated with what 2 causes?
- 1. Chronic glomerulonephritis (ESRD)
- 2. Benign nephrosclerosis due to DM or HT causing a decrease in GFR and blood flow leading to atrophy of the kidneys.
Ischemic acute tubular necrosis involves what part of the nephron?
Toxic acute tubular necrosis involves part of the nephron?
- 1. PCT and ascending limb of loop of Henle
- 2. PCT only.
Acute pyelonephritis caused by what three things? Pathophysiology?
- 1. adult females: UTIs
- 2. kids: vesicouteral reflux
- 3. kidney stones causing #2.
Renal papillary necrosis: medulla becomes necrotic and sloughs off causing obstruction in the ureter.
Pathophysiology of chronic pyelonephritis?
Dilated calyces causing thyroidization of the kidneys (tubules dilate and fill with colloid-rich material)
Interstitial nephritis is what type of hypersensitivity reaction? Caused by what drugs?
- 1. Type I (eosinophils) and Type IV H.S. (granulomas)
- 2. Acute = methicillin, Chronic = acetaminophen
- Papillary necrosis.
Where do kidney stones most commonly occur?
Calyces, pelvis, and urinary bladder.
RCC can be associated with what chromosome?
VHL syndrome: chr. 3.
What 4 paraneoplastic syndromes are associated with RCC?
- 1. EPO = polycythemia
- 2. renin = HT
- 3. ACTH = Cushings
- 4. PTHrP = hypercalcemia
If a young child between ages 2-5 presents with an abdominal mass, differentials?
- 1. Wilm's tumor (nephroblastoma)
- 2. Neuroblastoma
- 3. ALL
Wilm's tumor is associated with what chromosome? Presence of more tubules indicate a good or bad prognosis?
Chr 11, good prognosis.
Patients with ESRD suffer from renal osteodystrophy and have to undergo dialysis. What toxicity can they receive?
NH3 toxicity which is used in the dialysylate: NH3 cannot be excreted from the kidneys due to renal failure (not allowing H+ to be excreted) and hence it builds up.
Pathology of benign hypertension?
Pathology of malignant hypertension?
Hyalinization of the arterioles causing ischemia and small, shrunken kidneys.
Flea-bitten kidney (petechial hemorrhages on the kidney) and onion-skinning pattern, along with papilledema and stroke.
How does medullary cystic kidney dz differ from ADPKD?
- Cysts are only present in the medullary collecting ducts.
- Shrunken kidneys instead of enlarged ones.
Acute intrarenal failure such as ATN causes an increase in the BUN:Cr ratio. Why?
- Injury and necrosis of the tubular epithelial cells, hence reabsorption fails to occur. BUN accumulates in the kidneys.
- Consequence: Metabolic acidosis with hyperkalemia.
Causes of nephrotoxic ATN?
- 1. Metals
- 2. Aniline dyes
- 3. Aminoglycosides
- 4. Myoglobinuria
- 5. Ethylene glycol (anti-freeze) causes oxalate crystals
- 6. Tumor lysis syndrome with urate
A patient is treated for leukemia and then develops acute tubular necrosis. How could this have been prevented?
- Leukemia tx kills all cells, releasing uric acid. Uric acid damages the renal tubules causing ATN.
What does it mean when a patient with minimal change dz has a selective loss of albumin?
Cytokines are damaging the foot processes, causing foot process effacement. There is no loss of gamma-globulins and no immune complexes as seen with other nephrotic syndromes.
How does DM cause microalbuminuria?
- DM affects the efferent arteriole more than the afferent, constriction causes an increases in GFR leading to sclerosis of the mesangium (Kimmelstein nodules)
- Hyperfiltration doesn't allow sufficient time for reabsorption of albumin, causing microalbuminuria.
Causes of renal papillary necrosis?
- 1. Acute pyelonephritis
- 2. Sickle cell anemia
- 3. DM
- 4. ATN especially with chronic analgesic abuse.
To measure ECF, what marker is used?
What is the Hendersen-Hasselbach equation?
pH = pKa + log A-/HA
How does an increase in filtration fraction produce an increase in reabsorption at the PCT?
Increase FF will increase the RPF and increase the amount of oncotic proteins being filtered. This will decrease GFR, allowing for more reabsorption.
With PAH, when the  in the renal vein is less than the renal artery, what is happening to PAH?
Hasn't been saturated with all its transporters: PAH is filtered as well as secreted by the kidney in the form of urine.
What values change in a person with water deprivation?
Increase in plasma osmolarity and increase in ADH volumes. This causes an increase in the water absorption at the collecting ducts, causing a decrease in free water clearance.
What distinguishes a person from water deprivation with one who has SIADH?
Plasma osmolarity: Water deprivation patient will have an initial plasma osmolarity, and SIADH has low plasma osmolarity due to constant ADH reabsorption.
What hormone acts on the renal tubule by stimulating adenylate cyclase to generate cAMP?
Chronic renal failure and DKA both produce metabolic acidosis. How do you differentiate them with lab values?
- Chronic renal failure are not able to excrete the fixed acids (NH4+) produced.
- DKA produces fixed acids and can excrete them because renal NH3 production is increased.
When will the tubular fluid inulin concentration be at its lowest?
Bowman's space: inulin concentration increases as water reabsorption increases.
What are some causes that lead to hydronephrosis?
- 1. stones
- 2. endometriosis
- 3. tumors (e.g. SCC of the cervix)
- 4. B/L hydronephrosis = BPH
A patient presents with throbbing headaches and is treated with Methysergide but now develops renal failure. Dx?
Retroperitoneal fibrosis: fibrosis entrapping the ureters (scarred tissue of the retroperitoneum)
n.b. this drug can also affect Reidel's thyroiditis (endocrine)
Adenocarcinoma of the bladder can be caused by?
- 1. Exystrophy of the bladder leading to columnar metaplasia, associated with epispadias (abnormal opening of the dorsal end)
- 2. Urachal remnant (urachus allows bladder to drain urine into the yolk sac) Patent urachus will cause urine to come out of the umbilicus = open communication between bladder and umbilical cord)
BPH constricts the urethra and complicates a urinary tract obstruction. This leads to?
Acquired diverticula (elderly men)
What part of the kidney makes EPO?
Renal peritubular interstitial cells
Which kidney stones are not seen on X-ray?
Calcium stones develop due to what two causes?
Uric acid as radioluscent.
Hypercalciuria and Crohn's disease (small bowel destruction causes an increased absorption of oxalate)
RCC can involve the loss of the VHL supppressor gene on ch3. How does this promote the tumor?
Loss of VHL gene associated with what else?
Loss of VHL gene increases IGF-1 which promotes growth and increases HIF T.F. which increases the VEGF and PDGF (angiogenesis and growth of the tumor).
Loss of VHL gene also associated with hemangioblastomas of the cerebellum.
Which TCC is worse: flat or papillary?
Flat because it starts off as a high grade cancer whereas papillary starts off as a low grade cancer. Flat cancers are also associated with early p53 mutations.