Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Renal/Resp > Diseases of nephron > Flashcards

Diseases of nephron Flashcards

(56 cards)

Start Studying
1
Q

What is normal pH?

A

7.4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

pCO2=1.5*[HCO3-]+8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

pCO2=0.9*[HCO3-]+9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A

40mmHg pCO2

24 mmol/L HCO3-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Urine flow is equal to what?

A

Urine volume/time of collection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What equation is for renal clearance?

A

(Ux*UF)/Px

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How do you measure renal excretion

A

X=Ux*UF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How do you diagnose AME?

A

measure urine cortisol to cortisone ratio

gene sequencing of 11Beta-HDS2

AR inheritence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the pathogenesis of AME?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the diagnosis of liddle syndrome?

A

gene sequencing of SCNN1g and SCNN1B along with clinical picture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the pathogenesis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do you treat LIddle syndrome?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is Bartter syndrome presentation?

A

early childhood growth and mental retardation
polyuria and polydipsia
hypercalciuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is Gitelman syndrome presentation?

A 
adolescence/adulthood
cramping of arms and legs
fatigue
hypomagnesemia
polyuria and nocturia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the clinical picture?

A

hypokalemia
hyperreninemia
hyperaldosteronism
metabolic alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is Gitelman syndrome?

A

mutation in SLC12A3 gene

tubular defect mimic chronic thiazide ingestions
prognosis is good with tx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is nephrotic syndrome?

Study These Flashcards
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?

Study These Flashcards
A 
mild proteinuria
hematuria
-RBCs and RBC casts
HTN
Edema
25
What causes acute glomerulonephritis?
``` IgA nephropathy Post-infectious GN Anti-GBM disease/Goodpasture's Small vessel vasculitis Lupus nephritis membranoproliferative GN ```
26
What is the most common glomerulonephritis worldwide?
IgA Nephropathy
27
What are the clinical features of IgA nephropathy?
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
What are the histologies associated with IgA nephropathy
LM: variable mesangial hypercellularity IF: mesangial IgA deposition EM: mesangial electron dense deposits
29
How is IgA nephropathy treated?
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
What is henoch-Schonlein purpura?
systemic disorder characterized by IgA deposition - skin - joints - GI tract - hematuria
31
What is post-strep GN?
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
What are the histology features of post-strep GN?
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
What causes rapidly progressive GN?
``` anti-GBM/Goodpastures Immune complex GN -lupus nephritis -post-infectious -cryoglobulinemia ANCA associated GN (Pauci immune) ```
34
What is the syndrome associated with anti-GBM/GOodpastures?
``` hemoptysis pulmonary infiltrates glomerulonephritis -GN alone in anti-GBM disease due to circulating anti-GBM antibody ```
35
What is the diagnosis of anti-GBM/Goodpastures?
anti-GBM antibody in blood | linear IgG and C3 on kidney biopsy IF
36
What is the treatment of anti-GBM/Goodpasture?
plasmapheresis prednisone cytoxan
37
What is the syndrome associated with pauci GN?
crescenteric GN with little deposition of immune reactants | idiopathic or associated with antineutrophil cytoplasmic antibody vasculitis
38
What are the three small vessel vasculitis?
microscopic polyangiitis wegners churg-strauss
39
How do you diagnose wegneners granulomatosis in kidney problems?
renal biopsy, c-ANCA
40
What primary renal diseasses cause nephrotic syndrome?
membrane nephropathy focal segmental glomerulosclerosis minimal change disease
41
What is the primary cause of nephrotic syndrome in children?
80% will ahve minimal change disease
42
What are the secondary causes of nephrotic syndrome?
systemic diseases-DM, SLE, amyloidosis infections-HIV, Hep B, Hep C, syphilis drugs-NSAIDS, gold, penicillamine
43
What is the treatment for all causes of nephrotic syndrome?
Ace inhibitor or angiotensin-II blcoker lipid lowering therapy diuretics, slat restriciton to improve edema
44
What is minimal change disease associated with in adults?
drugs-NSAIDs neoplasma esp Hodgkins lymphoma infections-symphilis or HIV
45
What are the histology/morphology of minimal change disease?
all but EM normal, EM reveals podocyte foot pocess efacement and fusion
46
What is the treatment for minimal change disease?
corticosteroids
47
What is the most common cause of nephrotic syndrome in caucasion adults?
membranous nephropathy
48
What are secondary causes of membranous nephropathy?
HBV SLE neplasms, pretty much all of them drugs
49
What is the presentation of membranous nephropathy?
onset insiduous | present with heavy proteinuria and nephrotic syndrome
50
What is the morphology/histology of membranous nephropathy?
diffuse thickening of GBM, GBM spikes on silver stain
51
What is the most common cause of idiopathic nephrotic syndrome in african-americans?
focal segmental glomerulosclerosis idiopathic
52
What are common causes of focal segmental glomerulosclerosis?
``` NSAIDs HIV** massive obesity healed previous glomerular injury loss of funciton renal mass ```
53
What is the focal segmental glomerulosclerosis morphology/histology?
focal and segmental glomerular sclerosis with capillary collaspe podocyte foot process effacement
54
What is the clinical syndrome associated with membranoproliferative glomerulonephritis?
proteinuria and hematuria HTN in 1/3 low C3 variable clinical presentation
55
What is the common cause of membranoproliferative glomerulonephritis secondarily?
SLE HCV** cyroglobulinemia neoplasms
56
What is the morphology of membranoproliferative glomerulonephritis?
hypercellular glomeruli, endocapilary cell proliferation | granular C3 deposition

Renal/Resp (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions