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Renal/Resp > Diseases of nephron > Flashcards

Diseases of nephron Flashcards

1
Q

What is normal pH?

A

7.4

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2
Q

What is the systemic approach to determining acid base issues?

A 
Look at pH
Determine primary disorder
Calculate expected compensation
calculate anion gap
review change in HCO3- and change in AGAP (delta/delta)
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3
Q

What is the equation for determining compensated pCO2 for metabolic acidosis?

A

pCO2=1.5*[HCO3-]+8

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4
Q

What is the equation for determining compensation for pCO2 in metabolic alkalosis?

A

pCO2=0.9*[HCO3-]+9

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5
Q

What is pCO2 and [HCO3-] at normal pH?

A

40mmHg pCO2

24 mmol/L HCO3-

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6
Q

Urine flow is equal to what?

A

Urine volume/time of collection

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7
Q

What equation is for renal clearance?

A

(Ux*UF)/Px

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8
Q

How do you measure renal excretion

A

X=Ux*UF

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9
Q

What is the presentation of Apparent Mineralcorticoid Excess?

A 
low birth weight
failure to thrive
severe HTN
organ damage
Renal failure
w/ HTN
hypokalemia
metabolic alkalosis
low plasma renin
low plasma aldosterone

similar to primary aldosteronism

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10
Q

How do you diagnose AME?

A

measure urine cortisol to cortisone ratio

gene sequencing of 11Beta-HDS2

AR inheritence

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11
Q

What is the pathogenesis of AME?

A

11-BetaHSD mutation leading to lack of conversionof cortisol to cortisone

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12
Q

What is Liddle syndrome and clinical picture of it?

A

pseudoaldosteronism

Clinical picture:
HTN
hypokalemia
metabolic alkalosis
low plasma renin activity
low plasma aldosterone and urinary aldosterone
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13
Q

What is the diagnosis of liddle syndrome?

A

gene sequencing of SCNN1g and SCNN1B along with clinical picture

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14
Q

What is the pathogenesis?

A

mutation in the renal epithelial sodium channel leading to constituitive expression
gain of function mutation

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15
Q

What is the cellular ultrastructure and tranport characteristics of principal cells of late distal tubule and cortical collecting duct?

A

reabsorbs Na and secretes K
regulated by aldosterone
water permeability regulated by ADH
reabsorption of sodium and secretion of potassium blocked by K sparing diuretics

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16
Q

How do you treat apparent mineralcorticoid excess?

A 
therapy to reduce endogenous cortisol production
-amiloride
-triamterene
block mineral corticoid receptor
-spironolactone
-eplerenone
potassium repletion
dexamethasone for ACTH suppression
poor prognosis
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17
Q

How do you treat LIddle syndrome?

A

agents that decrease sodium channel activity
-amiloride
-triamterene
with treatment prognosis is good

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18
Q

What is Bartter syndrome presentation?

A

early childhood growth and mental retardation
polyuria and polydipsia
hypercalciuria

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19
Q

What is Gitelman syndrome presentation?

A 
adolescence/adulthood
cramping of arms and legs
fatigue
hypomagnesemia
polyuria and nocturia
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20
Q

What is the clinical picture?

A

hypokalemia
hyperreninemia
hyperaldosteronism
metabolic alkalosis

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21
Q

What is bartter syndrome?

A

mutations in genes that encode proteins in ascending part of henle’s loop
tubular defect mimic chronic loop diuretic ingestion
poor prognosis

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22
Q

What is Gitelman syndrome?

A

mutation in SLC12A3 gene

tubular defect mimic chronic thiazide ingestions
prognosis is good with tx

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23
Q

What is nephrotic syndrome?

A 
proteinuria>3.5 g/day
hypoalbuminemia
edema
-loss of plasma oncotic pressure vs. Na/H2O retention
hyperlipidemia
-increased hepatic protien production

lipiduria
hypercoagulability
-loss of proteins C and S

24
Q

What is nephritis?

A 
mild proteinuria
hematuria
-RBCs and RBC casts
HTN
Edema
25
Q

What causes acute glomerulonephritis?

A 
IgA nephropathy
Post-infectious GN
Anti-GBM disease/Goodpasture's
Small vessel vasculitis
Lupus nephritis
membranoproliferative GN
26
Q

What is the most common glomerulonephritis worldwide?

A

IgA Nephropathy

27
Q

What are the clinical features of IgA nephropathy?

A

50-60% episodic gross hematuria
30% presistent microhematuria
proteinuria, if present, is generally mild

Dysuria and loin pain
hematuria occurs in cojunction with URI

28
Q

What are the histologies associated with IgA nephropathy

A

LM: variable mesangial hypercellularity
IF: mesangial IgA deposition
EM: mesangial electron dense deposits

29
Q

How is IgA nephropathy treated?

A

progonosis based on creatinine and proteinuria

fish oil may slow progression
ACE-inhibitor controls BP
corticosteroids, other immunosuppressants also may be used in progressive disease

30
Q

What is henoch-Schonlein purpura?

A

systemic disorder characterized by IgA deposition

  • skin
  • joints
  • GI tract
  • hematuria
31
Q

What is post-strep GN?

A

sudden onset HTN, azotemia, oliguria, edema and tea colored urine
labs:
low C3 complement level
anti-streptolysin O can be elevated
urinalysis: red blood cell castts, mild proteinuria

32
Q

What are the histology features of post-strep GN?

A

LM: enlarged, hypercellular glomeruli. DIffuse mesangial endocapillary proliferation with neutrophils
IF: granular capillary wall and mesangial
EM: mesangial and large subepitheila hump like depoists

33
Q

What causes rapidly progressive GN?

A 
anti-GBM/Goodpastures
Immune complex GN
-lupus nephritis
-post-infectious
-cryoglobulinemia
ANCA associated GN (Pauci immune)
34
Q

What is the syndrome associated with anti-GBM/GOodpastures?

A 
hemoptysis
pulmonary infiltrates
glomerulonephritis
-GN alone in anti-GBM disease
due to circulating anti-GBM antibody
35
Q

What is the diagnosis of anti-GBM/Goodpastures?

A

anti-GBM antibody in blood

linear IgG and C3 on kidney biopsy IF

36
Q

What is the treatment of anti-GBM/Goodpasture?

A

plasmapheresis
prednisone
cytoxan

37
Q

What is the syndrome associated with pauci GN?

A

crescenteric GN with little deposition of immune reactants

idiopathic or associated with antineutrophil cytoplasmic antibody vasculitis

38
Q

What are the three small vessel vasculitis?

A

microscopic polyangiitis
wegners
churg-strauss

39
Q

How do you diagnose wegneners granulomatosis in kidney problems?

A

renal biopsy, c-ANCA

40
Q

What primary renal diseasses cause nephrotic syndrome?

A

membrane nephropathy
focal segmental glomerulosclerosis
minimal change disease

41
Q

What is the primary cause of nephrotic syndrome in children?

A

80% will ahve minimal change disease

42
Q

What are the secondary causes of nephrotic syndrome?

A

systemic diseases-DM, SLE, amyloidosis
infections-HIV, Hep B, Hep C, syphilis
drugs-NSAIDS, gold, penicillamine

43
Q

What is the treatment for all causes of nephrotic syndrome?

A

Ace inhibitor or angiotensin-II blcoker
lipid lowering therapy
diuretics, slat restriciton to improve edema

44
Q

What is minimal change disease associated with in adults?

A

drugs-NSAIDs
neoplasma esp Hodgkins lymphoma
infections-symphilis or HIV

45
Q

What are the histology/morphology of minimal change disease?

A

all but EM normal, EM reveals podocyte foot pocess efacement and fusion

46
Q

What is the treatment for minimal change disease?

A

corticosteroids

47
Q

What is the most common cause of nephrotic syndrome in caucasion adults?

A

membranous nephropathy

48
Q

What are secondary causes of membranous nephropathy?

A

HBV
SLE
neplasms, pretty much all of them
drugs

49
Q

What is the presentation of membranous nephropathy?

A

onset insiduous

present with heavy proteinuria and nephrotic syndrome

50
Q

What is the morphology/histology of membranous nephropathy?

A

diffuse thickening of GBM, GBM spikes on silver stain

51
Q

What is the most common cause of idiopathic nephrotic syndrome in african-americans?

A

focal segmental glomerulosclerosis idiopathic

52
Q

What are common causes of focal segmental glomerulosclerosis?

A 
NSAIDs
HIV**
massive obesity
healed previous glomerular injury
loss of funciton renal mass
53
Q

What is the focal segmental glomerulosclerosis morphology/histology?

A

focal and segmental glomerular sclerosis with capillary collaspe
podocyte foot process effacement

54
Q

What is the clinical syndrome associated with membranoproliferative glomerulonephritis?

A

proteinuria and hematuria
HTN in 1/3
low C3
variable clinical presentation

55
Q

What is the common cause of membranoproliferative glomerulonephritis secondarily?

A

SLE
HCV**
cyroglobulinemia
neoplasms

56
Q

What is the morphology of membranoproliferative glomerulonephritis?

A

hypercellular glomeruli, endocapilary cell proliferation

granular C3 deposition

Renal/Resp (22 decks)

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