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Designated study period: daily cards > March 18 - Renal > Flashcards

March 18 - Renal Flashcards

1
Q

Anatomy of ureters

A

Pass posterior to gonadal vessels, anterior to common and internal iliac arteries

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2
Q

Acute tubular necrosis: three phases

A
  1. Initiation: ischemic injury to renal tubules
  2. Maintenance: decreased urine output resulting in fluid overload. Increase in Cr/BUN. Hyperkalemia.
  3. Recovery: Increase in urine output with vigorous diuresis. Can decrease electrolyte levels - most serious is hypokalemia. See muddy brown casts
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3
Q

Progression of ATN

A

Severe hyperperfusion plus toxicity lead to ischemia, which leads to infarction and necrosis. Kidney cells slough off yielding muddy brown casts.

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4
Q

Causes of ATN

A
  1. Sepsis and hypoperfusion

2. Drugs - aminoglycosides, cisplatin, amphotericin B

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5
Q

Lbas in ATN: BUN:Cr, urine Osm, FeNa, urine sediment, urine sodium

A

BUN:Cr is 10:1 indicating damage to renal tubules. Initially may be 20:1 because to start the patient is in pre-renal azotemia that then progresses to ATN.

Urine Osm low - very dilute urine, can’t concentrate, less than 350

FeNa is >1% as can’t reabsorb sodium

Urine sediment shows muddy brown casts

Urine sodium high, over 40

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6
Q

Eosinophils in parasitic defense

A

Th2 and mast cells produce IL-5 which stimulates eosinophils.

When parasite invades, gets coated by IgG and IgE. Antibodies bind Fc receptors on eosinophil surface, the eosinophil degranulates and releases major basic protein. Form of antibody-dependent cell-mediated cytotoxicity.

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7
Q

Acute hemolytic transfusion reaction: pathogenesis

A

Antibody mediated hypersensitivey (type II). IgM binds leading to complement-mediated cell lysis

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8
Q

Vasopressin and urea

A

Vasopressin activates urea transporters in medullary collecting duct, increasing urea reabsorption and decreasing urea clearance. Increase in urea reabsorption increases medullary osmotic gradient, further increasing water reabsorption

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9
Q

Creatinine, para-amino hippuric acid, and inulin handling in kidney

A

Creatinine freely filtered by glomerulus. Small amount secreted by proximal tubule.

PAH filtered by glomerulus and then compleletly secreted by the proximal tubules with no significant reabsorption. Amount excreted is greater than amount filtered.

Inulin is filtered with no net secretion or absorption. Thus filtration=excretion and it is good for measuring GFR

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10
Q

Kidney med associated with ototoxicity

A

Loop diuretics

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11
Q

Sodium and potassium concentrationin prox tubule

A

No change in concentration along proximal nephron because reabsorbed euqlally with water

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12
Q

Bicarb handling in nephron

A

Actively reabsorbed in proximal tubule due to carbonic anhydrase. Thus, bicarb concentration decreases as move through nephron.

Bicarb is filtered by glomerulus and present in tubular fluid. H+ is actively secreted by Na+/H+ antiporter and primary active transport. H+ and HCO3- bind in the tubular fluid yielding H2CO3. Carbonic anhydrase in apica membrane converts to H2O and CO2. CO2 freely crosses into tubular epithelial cell where it reforms bicarb and H+. H+ is transported by mechansisms above to tubular fluid. Bicarb reabsorbed into blood across basolateral membrane by Na+-bicarb cotransport and cl- bicarb countertransport

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13
Q

Fetal hydronephrosis: three causes

A

Kinking/narrowing at ureteropelvic junction: most common cause of obstructive unilateral hydronephrosis.

Posterior urethral valves: most common cause of bilateral obstructive hydronephrosis in boys

Vesicoureteral reflux: incomplete closure at VU junction. Causes uni or bilateral non-obstructive hydronephrosis

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14
Q

Tubular fluid osmolarity throughout regions of nephron

A

Proximal tubule: isotonic with plasma (around 300 mOsm) because water reabsorbd along with electrolytes

Descending loop: becomes hypertonic (over 300) because water reabsorbed but impermeable to solutes

Ascending loop: becomes hypotonic (less than 300) because solutes but not water reabsorbed

Distal tubule: stays hypotonic (less than 300) because solutes but not water reabsorbed; where most dilute

Collecting duct: in presence of ADH, highly permeable to water and becomes hypertonic

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15
Q

Description of Bence Jones proteins in multiple myeloma

A

Large glassy casts that stain intensely eosinophilic

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16
Q

Causes of acute interstitial nephritis

A

Most commonly drug induced. Can also be due to infection or autoimmune disease

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17
Q

Crescents in RPGN

A

Proliferated glomeruluar parietal cells + macrophges/monocytes + fibrin

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18
Q

Calculation of clearance

A

CL = urine concentration x urine flow / plasma concentration

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19
Q

Foscarnet: MOA, Use, toxicity

A

MOA: pyrophosphate analog. Viral polymearase inhibitor, HIV RT inhibitor. No activation by viral kinase

Use: gancyclovir-resistant CMV, acyclovir-resistant HSV

Toxicity: nephrotoxicity with electrolyte abnormalities (hypocalcemia and hypomagnesemia) that can lead to seizures

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20
Q

Cidofovir: MOA, use , toxicity

A

MOA: inhibits viral DNA polymerase, no activation by viral kinase required

Use: Resistant CMV retinitis, acyclovir resistant HSV

Toxicity: nephtotoxicity

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21
Q

Calculating RPF and RBP

A

RPF = PAH clearance = urine PAH x urine flow rate / plasma PAH

Divide by 1-HCT to get renal blood flow

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22
Q

Calculating GFR

A

GFR = inulin clearance = urine inulin - urine flow rate / plasma inulin

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23
Q

Uric acid crystals: where forma nd why

A

Precipitate in distal tubules and collecting duct where pH is the lowest

24
Q

Hemolytic uremic syndrome pathogenesis and how to distinguish from henloch shonlein pupora

A

Toxins injure the endothelium leading to platelet activation, microthrombi formation and thrombocyptoneia. Red cells get sheared leading to formation of schistocytes and microangiopathic hemolytic anemia

In HSP platelet count is normal and palpable purpora are present

25
Q

Chlorthalidone

A

Thiazide diuretic. More potent than other thiazides but more associated electrolyte abnormalities (greater risk of hypokalemia and metabolic alkalosis)

26
Q

Severe hypokalemia presentation

A

Muscle weakness, cramps, rhabdo

27
Q

Poor prognostic factors for PSGN

A

Increased age, pre-existing renal disease

28
Q

Phenylephrine

A

Alpha agonist

29
Q

Oxybutynin

A

Antimuscarnic used for urge incontinence

30
Q

Imipramine

A

TCAD

31
Q

Anatomy and function of JG apparatus

A

Consists of macula densa + JG cells

Macula densa: cells in distal tubule that monitor salt content and distal flow rate and transmit info to JG cells and regulate dilation/constriction of afferent arteriole. Increased Na+ delivery to distal tubule signals high filtration and causes macula densa to decrease NO synthase in the afferent, decreasing GFR. Decreased Na+ delivery to distal tubule causes macula densa to increase NO synthase in the afferent, increasing GFR

JG cells: modified smoth muscle cells in wall of afferent arteriole that secrete renin via granules when stimulated by macula densa

32
Q

Effect of long term renal artery stenosis on JG apparatus

A

Causes hypertropha and hyperplasia of JG apparatus

33
Q

Membranous vs membranoproliferative glomerulonephritis

A

Membramous is the most common cause of nephrotic syndrome in adults. Uniform, diffuse thickening of glomerular capillary wall without hypercellularity. On EM irregular dense deposits that resembles spikes on silver staining. On IF, IgG and C3 immune complex deposits

Membranoproliferative: large hypercellular glomeruli - membranous thickening plus hypercellularity

34
Q

Minimal change disease: pathophysiology

A

Cytokine damage to podocyte foot processes. Can be idiopathic or associated with the large amounts of cytokines release in Hodkin lymphoma

35
Q

FSGS: population, pathology

A

Population: Hispanics and african americans. Can be idiopathic or associated with HIV, heroin, sickle cell disease

Pathology: Foot process effacement, segmental collagen deposition in some of glomeruli. No immune complex deposits

36
Q

Membranous nephropathy: population

A

Caucasian adults. Usually idiopathic but can be associated with SLE, cancer, hepatitis B or C

37
Q

Reason for low Ca++ in CKD

A

Decreased active vitamin D results in decreased Ca++ absorption

Phosphate retention results in increased serum phosphate which binds free serum Ca++, exacerbating hypocalcemia

38
Q

Acetazolimide: MOA and adverse effect

A

MOA: carbonic anhydrase inhibitor in proximal tubule

Adverse effect: Metabolic alkalosis due to decreased bicarb reabsorption

39
Q

ENaC blockers

A

Amiloride and triamterene. Can cause metabolic acidosis

40
Q

Clear cell carcinoma

A

Most common form of RCC. Cells contian intracellular glycogen and lipids

41
Q

Renal compensation for metabolic acidosis

A

1) increasing bicarb reabsorption
2) increasing H+ secretion
3) increasing acid buffer secretion: HPO4-2 and NH3. NH3 is the major mechanism as kidney can increase its production in chronic acidosis

42
Q

EFfects of angiotensin II

A

Increases aldosterone

Causes vasoconstriction

43
Q

Selective proteinuria

A

Albumin loss with minimal loss of more bulky proteins. Occurs because albumin small enough to fit through slits and is mostly excluded by charge.

44
Q

Drug-induced AIN: presentation, labs, pathology, mechanism

A

Presentation: fever, rash, acute renal failure after starting new drug

Labs: Can see elevated eosinophils and IgE

Pathology: Edema and mononucleuar infiltrate in interstitium

Mechanism: IgE mediated or type IV depending on drug

45
Q

Horseshoe kidney

A

Inferior poles fail to separate. When kidneys try to ascend, get stuck on IMA.

46
Q

Kidney drug associated with hyperglycemia

A

Thiazides

47
Q

Renal papillary necrosis: causes, pathology, presentation

A

Causes

  • sickle cell trait/disease: sickled cells obstruct small kidney vessels leading to ischemia
  • NSAIDS: constriction of afferent arteriole leads to renal hypoperfusion
  • diabetes: renal vasculopathy leads to hypoperfusion
  • pyelonephritis: edema compresses medullary vasculature leading to ischemia

Pathology

  • macro: gray white or yellow necrosis of distal renal pyramides
  • micro: coagulative necrosis

Presentation

  • dark or bloody urine
  • flank pain
  • urinary obstruction
48
Q

ACE inhibitors and renal failure

A

For patients with renovascular HTN, ACEIs can precipitate renal failure because they need ang II to constrict the efferent to maintain their GFR

49
Q

Potassium citrate

A

Given to prevent kidney stones. Increasing urinary citrate binds free Ca++ and decreases stone formation

50
Q

Nodular glomerulosclerosis: pathophys and pathology

A

Most commonly due to diabetes. GBM thickening and mesangial matrix deposition. Appears as nodules in the peripheral mesangium. Eosinophilic and PAS positive. Causes nephrotic syndrome.

51
Q

ACEIs in pregnancy

A

Contraindicated because can cause renal agenesis

52
Q

Metabolic alkalosis due to vomiting

A

Lose H+ and Cl- in vomit. Metabolic alkalosis with low urine Cl-, corrects with isotnoic saline

53
Q

Metabolic alkalosis due to diuretics

A

Increased distal NaCl delivery + hypovolemia leads to increased aldosterone production and increased Na+ reabsorption in the collecting duct while K+ and H+ keep being lost. Leads to metabolic alkalosis.

Ongling use: high urine Cl-
Stopped: low urine Cl-

Corrects with isotonic saline

54
Q

Metabolic alkalosis due to excess mineralocorticoids

A

Increased Na+ reabsorption with increased K+ and H+ loss leads to metabolic alkalosis. Causes expansion of extracellular fluid and HTN. High urine Cl-. Not corrected with isotonic saline. Aldo still being made

55
Q

Acute tubular necrosis: pathology

A

Proximal tubular cell ballooning and vacuolar degeneration

56
Q

Renal clear cell carcinoma vs renal oncocytoma

A

RCC originates from proximal renal tubules

Oncocytoma: rare tumor arises from collecting duct cells

57
Q

Mannitol: MOA, use, ADRs

A

MOA: osmotic diuretic
Use: Manage cerebral edema and ICP
ADRs: pulmonary edema, volume depletion, hypernatremia

Designated study period: daily cards (32 decks)

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