Pathology
1. What are the general findings of Nephritis?
2. Where would you expect to find the following circulating complexes and do they have an
distinctive appearance
a. Cationic
b. Anionic
c. Neutral
d. Anti-Glomerular Basement Membrane
e. Heyman
3. What are the outcomes of attack by the following antibodies
a. Glomerular cell antibodies
b. Mesangial
c. Endothelial
d. Visceral/Epithelial
4. What are some of the mediators of damage in nephritic syndrome and what do they do
5. How would you describe and what would the findings be of Focal Segmental Glomerular
Nephritis
6. How would you describe and what would the findings be of Tubulointerstitial Fibrosis
7. How would you describe and what would the findings be of Acute Postinfectious
Glomerulonephritis
8. How would you describe and what would the findings be of Rapdily Progressive GN
(cresentric)
9. How would you describe and what would the findings be of Anti-GMB GN
10.How would you describe and what would the findings be of IgA Nephropathy (Bergers)
11.How would you describe and what would the findings be of Henoch Schonlein
12.How are Bergers and HS similar and different
13.What is the general population of SLE and what are the general findings
a. How do you treat it
14.How would you describe and what would the findings be of SLE Class 1
15.How would you describe and what would the findings be of SLE Class 2
16.How would you describe and what would the findings be of SLE Class 3
17.How would you describe and what would the findings be of SLE Class 4
18.How would you describe and what would the findings be of SLE Class 5
19.What are the SLE classes with the best and worse outcomes
20.How would you describe and what would the findings be of Alports Syndrome
21.What are the major differences between Nephritic and Nephrotic syndromes
22.What are the similarities between them
23.What are the primary and secondary examples of Nephritic syndrome
24.What are the examples of nephrotic syndrome
25.How would you describe and what would the findings be of Membranous GN
26.How would you describe and what would the findings be of Minimal Change Disease
27.How would you describe and what would the findings be of Focal Segmental
Glomerulosclerosis
28.How would you describe and what would the findings be of membranoproliferative GN
29.What differentiates Type 1 and Type 2 membranoprolfierative GN
30.How would you describe and what would the findings be of Diabetic nephropathy
31.How would you describe and what would the findings be of Diabetic glomerulosclerosis
32.What are the two types of Acute Tubular Injury and what is their associated morphology
a. What is ATI characterized by
b. What is ATI the most common cause of
c. What are the changes associated with ATI
d. What is the clinical course of ATI
33.What is Tubular Interstitial Nephritis
of
of
of
of
of
Benign Nephrosclerosis
Malignant Nephrosclerosis
Simple Cysts
Adult PKD
Childhood PKD
Clinical
1.
2.
3.
4.
5.
6.
7.
8.
9.
c.
d.
19.What
a.
b.
c.
d.
20.What
a.
b.
c.
d.
16)
How do genetics play a role (ie. what major gene is important and what is its inheritance
pattern)
a) What are the risks associated with the this gene
i) FSGS association = what risk increase
ii) HTN association = what risk increase
iii) What progression of End stage kidney disease is seen with this gene
17)
What is increase in risk for ESRD associated with
a) Acute kidney injury
b) Acute kidney injury + pre-exisiting kidney disease
18)
What are the manifestations by stage of CKD
a) 1
b) 2
c) 3
d) 4
e) 5
19)
What are the major symptoms to look for that signal impending failure (ie. need to do
something now)
20)
What is the workup for CKD like
a) What pt population is estimating GFR a problem for and what is the solution (why is this
hard)
b) What other things, aside from GFR, do you have to look at
21)
What are the complications of CKD
a) What is the major cause of death
b) Why are most CKD patients at stage 3, rather than at later stages
22)
What is renal osteodystrophy
23)
What is the goal of treatment for CKD
a) BP goal and how to get there
b) What drugs are used for non black pts
c) What drugs are used for black pts; why
24)
What did the following trials demonstrate
a) Sprint
b) Nephron d
c) Simplicity
d) Coral
25)
What are diabetic pts. Predisposed to, in relation to kidney function
a) What are the goals for tx. For diabetics
i) What if there is proteinuria
26)
How are CKD associated disorders managed and what are the associated disorders
27)
What are some things that signal that renal replacement therapy should be started soon
28)
In regards for transplantation
a) What is the outcome for ESRD pts
b) What about donors
29)
30)
31)
32)
33)
34)
35)
36)
a)
b)
c)
d)
e)
f)
37)
38)
a)
b)
39)
40)
a)
41)
a)
b)
42)
a)
b)
43)
44)
a)
45)
a)
46)
a)
47)
a)
b)
48)
49)
a)
>18 + CKD tx
what did KDIGO highlight
what percentage of htn is primary/essential
what is the typical onset
what are the risk factors
i) race
ii) kidney status
what is correlation between BP and CV risk
what are the labs and studies that you generally order to investigate htn
kidney one
How are minority populations different in regards to htn
Women?
Elderly?
What is secondary htn
Etiology
What drugs may be involved
How do you evaluate a pt for htn
What is the PE for a htn patient like
What are the different ways in which BP can be measured
i) What the benefits of each
Tx for htn
When does systolic BP become more important
What is the difference between htn emergency and htn urgency
How is each treated
What is autoregulation of BP
How is it changed by chronic htn
Why is this a problem
i) How do you deal with this in regards to tx
How much of a problem is non adherence
What is the treatment for resistant htn
Etiologies
i) Renal
ii) Endocrine
iii) Sleep
(1) 2 conditions
Pharm
1. Where are glucocorticoids produced
a. What signals their release
b. What regulates this
2. What are the equiv doses and effect on anti-inflammatory and salt retention of the
following
a. Hydrocortisone
b. Prednisosne
c. Methyl prednisone
d. Triamcinolone
e. Dexamethasone
f.
3. What
a.
b.
4. What
a.
b.
c.
d.
e.
f.
g.
5. What
a.
b.
c.
d.
e.
f.
g.
h.
6. What
a.
7. What
8. What
a.
9. What
a.
Betamethasone
are the effects of glucocorticoids
Metabolic
Anti inflammatory
are the therapeutic usages of GCs
General
Replacement
Adjuavant
Endocrine
Allegies
Neoplastic states
GI
are the ADRs of GCs
MSK
Metabolic
Fluid/electrolyte
GI
Derm
Psych
Immune
Endocrine
are the effects of chronic GCS
How long can it take and how long can recovery take
are the drug interactions for GCs
is Mifepristone
What is it used for
is Mitotate/lysodren
What is it used for
1. What
a.
b.
c.
2. What
a.
are mineralcorticoids
What is signaling pathway
How is this regulated
What is their effect on the kidney, metabolic profile, volume and BP
is aldosterone and how does is compare to corticosteroids
What is its pharm action
i. Feedback effect
ii. Metabolic
Usages
is fludrocortisone
What are its effects
What are its actions
i. What are the side effects of these
What are its uses
What are its ADRs
i. Fluid
ii. MSK
iii. Gi
iv. Derm
v. Endocrine
vi. Metabolic
is spirolactone and eplerenoen
What are they used for
i. What conditions
What are their side effects
i. How is eplerenone different
ii. What other drugs must you watch out for if you give a pt these drugs
b.
3. What
a.
b.
c.
d.
4. What
a.
b.