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Nephrology Questions

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

34.What is Acute Pyelonephritis and how does it present


a. What are the common etiologies
b. What population is it most commonly seen in
c. What is the morphology
35.What is chronic pyolnephritis and how does it present
a. What are the two main etiologies
b. What is the clinical course
36.What is acute drug induced interstitial nephritis
a. Etiology
b. Presentation
c. Prognosis and treatment
37.How would you describe and what would the findings be
38.How would you describe and what would the findings be
39.How would you describe and what would the findings be
40.How would you describe and what would the findings be
41.How would you describe and what would the findings be
42.What differentiates APKD and CPKD

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.

What do the eyes of a pt with htn nephropathy look like


What is BUN and how is its production affected
What is Creatinine and how is its production affected
What does normal urine look like and what are its chemical features
What is relationship of GFR between Males and Females
a. When can it be increased naturally
b. Where is GFR most sensitive
What findings in urinalysis are associated with increased risk
If found in the urine, what are the following associated with
a. RBC
b. WBC
c. RBC Cast
d. WBC Cast
e. Granular/Muddy Cast
f. Broad Cast
What is a renal arteriogram used for
What is a renal ultrasound used for

10.How is the RAAS regulated


a. What five things does ANGII affect
b. What does ANP do and where is it from
c. What does Aldosterone do and where is it from
d. What other effect does ACE have aside from coverting ANGI ANGII
e. What arteriole does ANGII preferentially constrict and what does this cause
11.What do prostaglandins do
12.What does high dose ANGII, NE, Endothelin, ADH do
13.What are the pros of ANGII
a. What are the cons (ie. chronic presence)
14.What system maintains osmolality
a. Where are its receptors located
b. What is its effector
15.What system maintains volume
a. Where are its sensors located

b. What are its effectors


16.What are the effects of clipping a kidney on BP, Renin, and Volume
17.What are the effects of clipping a kidney and removing the other on BP, Renin, and Volume
18.In essential htn,
a. What group generally has increased renin and what is the incidence
b. How common is it to have normal range renin (should be lowered to decrease bp)
c. What group generally has decreased or absent renin and what is the incidence
19.What are the effects of ACE-I
a. What arteriole is mostly effected
b. What was the first drug
20.What are the effects of an ARB
a. Why would a pt. get this drug
b. Can you use both ACEI + ARB drugs
21.Sodium and Potassium balance
a. What does increasing sodium/decreasing aldosterone do
b. What does decreasing sodium/increasing aldosterone do
c. What does increasing potassium/increasing aldosterone do
d. What does decreasing potassium/decreasing aldosterone do
22.What are the effects of renal artery stenosis
23.What are the effects of primary aldosteronism (aldosterone producing adenoma)
a. How do you treat it
b. What is the history of a patient presenting with it like
24.What are the effects of an acute MI on kidneys and their function
25.What are the effects of diabetes on the kidneys
a. What drugs do you use to help
26.How does CHF effect kidneys
a. What other problem can it cause
i. What are the signs of this problem and what can it lead to
1. What
a.
b.
2. What
a.
b.
c.
d.
e.
3. What
4. What
5. What
a.
b.
6. What
a.
b.
7. What
a.
8. What
a.
9. What
a.
10.What
a.
b.

is Acute Interstitial Nephritis (AIN)


What percent of Acute Renal Failure is caused by AIN
What does the morphology look like
is the etiology of AIN
What drugs
What kinds of infections
What kind of disorders
What kind of toxins
What kind of nephopathy
is the presentation of AIN
is the therapy
is Chronic Interstitial Nephritis (CIN)
How is it different than AIN
What major transformation is seen
is the presentation
What other disease can it present like
What is treatment for it
is chronic pyelonephritis
What are the three types
is sarcoidosis and what is its hallmark feature
How do you treat it
is analgesic nephropathy
What was it caused by
is nephrocalcinosis
What is its etiology
Pathology

1. What does CKD do to Phosphate levels


a. How does that affect Calcium and Vitamin D
i. How do these changes affect bones and vasculature
b. What are PTH levels like
2. What are the clinical consequences of Secondary Hyperparathyroidism
a. What is therapy for it
b. How does vitamin D therapy work for it and what are the potential negatives
c. What are the aggravating factors of it
d. What is the progression, in terms of physical changes to the PT gland
3. Why are vascular calcifications bad
4. How do low bone turnover and high bone turnover lead to the same problem (ossification
of vasculature)
5. What are the therapeutic strategies for
a. Low calcium
b. High calcium
c. High PTH
i. Unresponsive therapy
6. What are the general recommendations for pts with Secondary Hyperparathyroidism
7. Where is the majority of potassium in the body
a. Where does it leak constantly
8. Where is it excreted and what percentage
9. What causes K to shift intracellularly
10.What causes K to shift extracellularly
11.Where is K reabsorbed and how much
12.Where is K secreted
a. What channel mediates this
i. What increases the activity of this channel
b. What happens when K is secreted
13.What are the etiologies of Hypokalemia
a. What is Pseudohypokalemia
b. What is redistribution hypokalemia and what causes it
c. What is hypokalemic periodic paralysis
i. What is it associated with
ii. What are the genetics
iii. What groups are associated with it
iv. How is it treated
d. What is extra renal loss defined as
i. What are some examples
e. What is ogilvies syndrome
i. What is activated to cause K secretion
ii. What k channels are upregulated
f. What is renal losses defined as
i. What drugs are associated with it
ii. What do you find in urine
iii. What kind of damage is seen
iv. What deficiency is seen and how does it affect K
g. What is Liddles syndrome
i. Genetics
ii. How is the kidney affected
1. What channel
iii. What are the symptoms
iv. What is the treatment
h. What is barters syndrome
i. Genetics

ii. Effects on thick descending limb


1. Type 1
2. Type 2/3
3. Type 4
4. Type 5
iii. What are the symptoms
iv. What is the treatment
i. What is gitlemans syndrome
i. Genetics
ii. What part of the kidney is effected
iii. What are the symptoms
iv. What is the treatment
j. What is primary hyperaldosteronism
i. Genetics
ii. Effect
iii. What are the symptoms
iv. Treatment
k. What is syndrome of apparent mineralcorticoid excess
i. Genetics
ii. Effect
iii. Symptoms
iv. Treatment
l. What is the treatment for general hypokalemia
m. What is the consequences of hypokalemia
i. Renal
ii. Cardiac
iii. Msk
iv. What do you get predisposed to
n. What hyperkalemia
i. Etiology
ii. What foods are highest in potassium
iii. What causes extracellular shifts
1. General
2. Drugs
iv. How does low renin and low aldosterone affect electrolytes
1. What are the general affects
v. What is familial pseudohyperkalemia
1. Genetics
2. Affects
vi. What are the consequences for hyperkalemia
1. Cardiac
2. Msk
3. Kidney
vii. How do you prevent arrhythmis
viii. How do you treat hyperkalemia
1. Enhance shift intracellularly
2. Eliminate excess K
14.How do you calculate plasma osmolarity
15.What is the normal range for sodium in the body
16.What are the symptoms of dehydration
17.What are the symptoms of sodium and water overload
18.What is hypovolemic hyponatremia
a. How would one get this
b. What are the effects to TBW and TBS

c.
d.
19.What
a.
b.
c.
d.
20.What
a.
b.
c.
d.

What are the symptoms


What is the treatment
is euvolemic hyponatremia
How would one get this
What are the symptoms
What is the effect to TBW and TBS
What is the treatment
is hypervolemic hyponatremia
Etiology
Effect on TBW and TBS
Symptoms
Treatment

1) What is metabolic acidosis


a) Etiology
b) Outcomes on physiology
2) What is normal HCO3
a) When should it be lowered/increased
3) What is normal PCO2
a) When should it be lowered/increased
4) How do you calculate anion gap
a) What is the normal range
b) What signals metabolic acidosis (ie. gapped metabolic acidosis)
c) What can falsely decrease the anion gap (ie. mask it) and how do you account for this
5) How do you calculate appropriate resp compensation
a) What does a greater number mean
b) What does a lesser number mean
6) What is delta/delta a ratio of
a) What does a ratio >1 =
b) What does a ratio <1 =
7) What is an osmolar gap
a) What is the normal range
b) What does an elevated osmolar gap mean
8) What is the mnemonic for a Gapped Acidosis
a) what is the common association of factors that precipitate a gapped acidosis
b) how do toxic alchols cause both an anion gap and osmolar gap
i) how does this change with time
9) What is a non gapped acidosis; what is another name for it
a) What has happened to create this (ie. what changes have happened to solutes)
b) What is the mnemonic for non gapped acidosis
c) What is an urine anion gap
i) What does a positive value mean
ii) What does a negative value mean
d) When should you suspect a non gapped acidosis, or what conditions should you be wary of
one
10)
What is the definition of CKD
11)
What are the stages of CKD
a) What are the respective GFRs for each
12)
What other thing, aside from GRF do you have to watch out for
13)
What test is more valuable than a 24 hour urine collection
14)
For the albumin:creatine, what are the 3 categories and what ratios are associated with
each
15)
What are the major etiologies for CKD

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)

What is primary/essential hypertension


What is pre htn
What is white coat htn
What is masked htn
What is resistant htn
What is pseudo-resistant htn
What is malignant htn
What are the criteria for JNC 8
>60 old
<60
>18 + DM
Non black tx
Black tx

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.

c. What are they used for (ie. indications)

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