Renal and Anemia Test memorization Flashcards
1
Q
Estimate GFR using the Cockroft-Gault formula. (give the formula).
What if it’s a woman?
A
GFR = (140-age) x weight (kg) / 72 x serum [Cr]
Multiply by 0.85 if female
2
Q
Define AKI (3).
A
W/in 48 hrs: ↑ in serum creatinine of > 0.3mg/dL OR Percentage ↑ in serum creatinine of 50% OR Oliguria of < 0.5mL/kg/hr for > 6 hours
3
Q
How many months must GFR decline for (at least) for it to be considered CKD?
A
3 months
4
Q
What are the 3 hematuria imposters?
A
Free Hemoglobin
Myoglobin
Menstrual contamination
5
Q
3 characteristics of nephritic syndrome?
A
Acute onset:
- hematuria with dysmorphic cells and RBCs/casts in the urine,
- some degree of oliguria and azotemia and
- hypertension.
6
Q
What is proteinuria defined as, in terms of loss (mg/day) of protein?
What is “massive proteinuria” defined as?
A
> 30 mg/day
> 3.5g/day
7
Q
What is considered hypoalbuminemia? (< ___ g/dL)
A
< 3 g/dL
8
Q
What is the characteristic clinical syndrome a/w diabetic nephropathy?
A
- proteinuria,
- progressive decline in GFR
- hypertension
9
Q
Why do a kidney bx in SLE?
A
- to determine the severity of kidney involvement
- to determine potential for reversibility of lesions
- to determine treatment options
10
Q
What 3 drugs can cause acute drug-induced interstitial nephritis?
A
- PCN derivatives
- Diuretics
- NSAIDs
(also PPIs, rifampin)
11
Q
What specific kidney pathology can NSAIDs cause?
A
Acute hypersensitivity interstitial nephritis
Clinical: *nephrotic syndrome + *renal failure
12
Q
What does each of these become?
Pronephros
Mesonephros
Metanephros
A
- Pronephros is redimentary, doesn’t fcn
- Mesonephros fcns a short time
- So mesonephros forms ureter (ureteric bud) and part of kidney that connects to it
Ureteric bud derivatives: become renal pelvis, major calyx, minor calyx - Metanephros forms kidney
Mesenchymal derivatives: become collecting duct system
Metanephric blastema: nephrons
13
Q
Genes a/w childhood polycystic kidney disease?
Adult?
A
Child (AR): PKHD1 gene, 6p, fibrocystin
Adult (AD):
- APKD1 – polycystin 1, cell-cell, cell-matrix interaction (85%, earlier onset of renal failure, more severe)
- APKD2 – polycystin 2, regulation of intercellular Ca2+ levels (later onset of renal failure)
14
Q
What two clinical findings is APKD a/w?
A
Mitral prolapse, berry aneurysms
15
Q
Genes a/w angiomyolipoma?
A
Tuberous Sclerosis:
TSC1 - Hamartin 9q34
TSC2 - Tuberin 16p13
16
Q
Gene mutated in RCC?
What ts factor then accumulates? Leading to what cellular effect?
A
VHL gene (tumor suppressor gene, nlly ubiquitinates HIF)
- Loss of VHL gene results in accumulation of the ts factor HIF-1α, facilitating adaptation to tissue hypoxia
- Origin from proximal tubular epithelium
(VHL = von Hippel Lindau, also a syndrome; earlier onset vs RCC, a/w CNS hemangioblastoma)
17
Q
What drug is a risk factor for urothelial carcinoma?
A
Analgesics (smoking also big risk factor, I believe.
Strong association w/hematuria, esp. gross
18
Q
What genes are a/w Wilm’s tumor?
A
WT1, WT2
WAGR: WT1 deletion, DDS: WT1 mutation, BWS: WT2 gene cluster mutation
19
Q
RPF = \_\_\_\_\_\_\_\_\_\_\_ clearance RBF = \_\_\_\_\_\_\_\_\_\_\_ (equation)
A
PAH
= RPF/(1-Hct)
20
Q
Filtration fraction (FF) = _____/_____
A
GFR/RPF
21
Q
“The typical _________ decline in GFR will be evident when GFR is plotted vs. time” in CKD.
How would Cr change in chronic?
Acute?
A
linear
- Exponential increase
- Linear increase
22
Q
What is the fractional excretion formula.
A
Fractional excretion = Amount excreted / Amount filtered
FENa = (UNa/PNa) / (UCr/PCr)
23
Q
How is FeNa+ affected by changes in GFR?
A
Assuming no change in dietary sodium intake, the FENa will double for every halving of GFR.
24
Q
Casts seen in prerenal AKI?
A
hyaline
25
Why is FENa lower in prerenal AKI?
| also higher U specific gravity, higher U osmolality
FENa is based on the fact that sodium reabsorption is enhanced in the setting of volume depletion.
(in renal AKI, FENa is higher because it can't reabsorb)
26
How do prostaglandins affect RPF?
| How about NSAIDs, then?
Dilate afferent arteriole (Increase)
| - Block this
27
What is the specific gravity in ATI?
Isosthenuria
28
Prerenal azotemia commonly progresses to what condition?
ATN
29
What are the 2 main categories of ATN?
| What are the 2 main categories of AIN?
AIN: Drug-associated and non-drug-associated
ATN: Ischemic and nephrotoxic
30
How does the urine appear in ATN?
Gross: “Dirty” or “Muddy brown”
- Granular "muddy brown" casts
(recall, oliguric followed by polyuric)
31
Vascular causes of AKI?
```
Vasculitis
Thromboembolic disease
HUS/TTP
Malignant HTN
Scleroderma renal crisis
```
32
Classic triad seen in AIN?
Fever, eosinophilia, rash
| usually only 1 sx present
33
What are the general indications for hemodialysis (RRT) in AKI?
```
AEIOU
A- acidosis
E - electrolyte derangement (^K+)
I - intoxication syndrome
O - overload (volume)
U - Uremia
```
34
Define CKD.
Progressive decline in GFR
Duration least 3 months
+/- Albuminuria
DM, HTN make up 72% of cases
35
Most important SLE kidney subtype to know?
Diffuse proliferative nephritis (IV)
V has the nephrotic syndrome
36
What pathopneumonic finding is seen in each of the 3 RPGNs?
Crescents
37
What's 1 symptom to associate w/cholesterol atheroembolic disease?
Livedo reticularis
38
What label should we a/w CKD: Stage II/III Management?
Conservative Renoprotection
| lifestyle, drug adjustments, drugs for risk factors
39
What is step 1 in CKD Stage IV management? What else need be addressed?
1. Nephrology referral
- HTN control (diet, drugs, *ACEIs)
- Proteinuria reduction (ACEIs, diet) (want < 300-500mg/day loss)
- Hyperparathyroidism (restrict PO43-, meds)
- Hypocalcemia (eat more, meds)
- Anemia (EPO, Fe) (goal Hgb 10-12 mg/dL)
40
Describe hemodialysis mechanism.
What are 3 determinants of solute diffuse rates?
Diffusion of molecules in solution across a semipermeable membrane along an electrochemical concentration gradient.
1. Solute concentration
2. Molecular weight
3. Protein binding status
41
What is ultrafiltration? How does it work?
| What is the overall goal of the procedure?
Passage of solutes through pores in dialysis membrane via convective process
Hydrostatic/osmotic pressure gradients drive the process. No overall change in solute concentrations.
*Overall goal: remove excess total body H2O
42
List the sequelae of chronic ESRD (4)
Uremic cardiovascular disease
- Medial vascular calcification
- Arterial stiffness
- LV hypertrophy
- Higher risk of cardiac arrest and CHF
43
Most common glomerular hematuria?
Upper urinary tract hematuria?
Lower urinary tract hematuria?
Uncertain etiology hematuria?
IgA
Stone
Infection
Exercise
44
Compare and contrast clinical indications to treat kidney stones medically vs. interventionally.
Medical therapy reasonable
- Small stones (< 5mm)
- Distal ureteral location
- Adequate pain control with analgesics
- No associated UTI or localized obstruction
Interventional therapy reasonable
- Larger stones (>6mm), especially proximal
- Not passing after 4 weeks of medical therapy
- Intractable pain
- Associated UTI or localized obstruction
45
Foods high in purine content that should be restricted when dealing w/ a urate stone?
- Meats: Offal, Seafood, Shellfish
| - Alcohol
46
Foods high in oxalate that should be restricted when dealing w/ a Ca2+ stone?
- Black tea
- Chocolate
- Soymilk
- Nuts
- Berries
- Beans, spinach (but high Ca2+), okra
- Beets, rhubarb
- Carrots
- Celery, Swiss chard
- Sweet potatoes
47
Causes of monogenic (single gene) HTN? In other words, what genetic diseases cause HTN besides polygenic.
- Glucocorticoid remedial aldosteronism (GRM)
- Syndrome of apparent mineralocorticoid excess (AME)
- Mineralocorticoid receptor mutation, (increases Na Ca activity)
- Liddle Syndrome: gain of function ENac
- T594M mutation African-American subtype salt sensitive (increases ENac activity)
48
_____________ is the most common form of secondary hypertension.
CKD
| HTN seen in most nephritic syndromes; due to salt retention
49
```
In CKD, what med combo tx would be best?
If this doesn’t work, what med class could you consider adding?
```
ACEI + diuretics
Consider BBs
Lastly CCBs (due to risk)
50
In what pt demographic may low number urine cultures (10^2-4) be significant?
- Young women w/ cystitis
- Males
- Pts w/ indwelling catheters
51
In what urinary infections will blood cultures be positive as well?
- Acute pyelonephritis
| - Prostatitis
52
Difference b/w Type & Screen vs. Type & Crossmatch (Major + Minor)?
Type & Screen: ABO Rh and AB screen
Type & Crossmatch: ABO Rh and...
- Major crossmatch: recipient plasma with donor cells
- Minor crossmatch: donor plasma with recipient cells
(last 2 are analogous to forward and reverse TYPING, i think. Screen is DAT/IAT)
*72 hour hold for the unit once crossmatched
53
What ABO type combo b/w mother and fetus can produce HDN?
Group O mom with an A fetus (mild, if any HDN)
| - ABO HDN: 15% of pregnancies. Common!
54
What are 2 ways to assess for presence of fetal Hgb?
- Amniocentesis
| - PUBS, (percutaneous umbilical blood sampling) or cordocentesis
55
Observation within _________ (time) of start of transfusion is critical for detection of an acute reaction.
15 min
56
What are the intraluminal causes of obstruction?
What are the intramural (intrinsic) causes of obstruction?
What are the extramural causes of obstruction?
Intraluminal: renal calculi, blood clots, sloughed renal papillae, urothelial tumors, Fungal ball
Intramural (intrinsic): UPJ obstruction, structural lesions
Extramural: prostatic disease; gynecologic, colorectal or retroperitoneal malignancy; crossing vessel to lower pole of the kidney, idiopathic retroperitoneal fibrosis
57
Most common site for kidney stone obstruction?
Uretero-vesicular junction
58
What are 3 diseases and 1 drug a/w sloughed renal papilla?
Diabetes
Sickle Cell
Pyelonephritis
Phenacetin abuse
59
Define hydronephrosis.
Dilatation of the pelvis and calyces.
60
Define obstructive uropathy.
Structural impedance to the flow of urine along the tract.
61
Define obstructive nephropathy.
Functional (GFR) and/or anatomic damage to the renal parenchyma that results from obstructed urine flow.
62
What are the sx in ACR Lupus classification?
```
SOAP BRAIN MD
Malar Rash
Discoid Rash
Serositis
Oral ulcers
Arthritis
Photosensitivity
Blood disorder
Renal disorder
ANA
Immunologic abnormalities (Smith/dsDNA/pho'lipid ABs)
Neurologic symptoms
```
63
2 important tests to monitor SLE disease activity?
C3, C4
| dsDNA
64
Drugs to treat SLE? (4)
NSAIDs
Anti-malarials
Corticosteroids
Immunosuppressive medications
65
What 2 AB tests are useful in Sjogren's?
| What abnormality is seen in the kidney?
+ Anti-SSA and/or anti-SSB antibody
+ Rheumatoid factor
Renal tubular acidosis (RTA)
66
Having Sjogren's syndrome increases risk of what disease by 40x?
Lymphoma (esp. mucosa-associated lymphoid tissue (MALT)
67
What type of AB is positive w/diffuse scleroderma?
| - Describe the main sx
Anti-topoisomerase (Scl70)
- Extensive skin involvement w/early visceral involvement
- *Interstitial lung disease (--> pulm HTN; HIGH MORTALITY)
- Kidney --> scleroderma renal crisis
(- GI)
68
What type of AB is positive w/limited scleroderma?
| - Describe the 2 main sx
```
Anti-centromere
CREST:
C: calcinosis (anti-Centromere)
R: reynaud phenomena
E: esophageal dysmotility
S: sclerodactyly
T: telangiectasia
```
69
What AB is a/w scleroderma renal crisis (and malignancy)?
Anti-RNA-polymerase III
70
Name the Anti-phospholipid antibodies, and what test they can give a false positive for.
- Anticardiolipin antibodies (aCL)
- Anti-beta2-Glycoprotein I antibodies
- Lupus anticoagulant (LAC)
PS: Can cause false positive VDRL/RPR test (syphilis).
LAC can prolong PTT. (even tho these are a/w increased clotting)
71
Test for dx of CVID?
Serum protein electrophoresis (SPEP)
72
What 3 sx characterize Wiskott-Aldrich syndrome?
- Thrombocytopenia
- Eczema
- Recurrent infections
(bleeding is a major cause of death)
73
What is the tx for acute hereditary angioedema? (just read thru a few times, too much to learn)
- Treatment of Acute event: C1-inhibitor concentrate, kallikrein inhibitor - ecallantide, or icatibant -bradykinin receptor antagonist
- Prophylactic Rx: attenuated androgens (stanozolol, danazol- increase C1-inhibitor via increased hepatic synthesis), fibrinolytic agents (tranexamic acid, aminocarpoic acid- help in fibrinolysis and spare C1-inhibitor this work)
74
What is the mutation in ataxia-telangiectasia?
Mutation in ATM gene which is responsible for DNA repair
- Therefore higher risk of cancer
- Sx are in the name
75
What is the mechanism behind chronic granulomatous disease?
What tests are used to dx it?
NADPH oxidase deficiency results in a reduction in leukocyte oxidative burst (in neutrophils) that is responsible for killing bacteria and fungi after phagocytosis
Diagnosis - abnormal nitroblue tetrazolium test (respiratory burst assay) or flow cytometry DHR (dihydrorhodamine-1, 2, 3) assay
76
List some physical signs of primary immunodeficiencies (if you can; probably ok to just read thru)
Recurrent infections (key)
Dysmorphic facies: look for midline defects, listen for heart murmur
Failure to thrive
Head: microcephaly
Mouth: oral thrush, teeth, oral sores, gingival disease
Oropharynx: absence of tonsils tissue
Skin: atypical atopic dermatitis/erythroderma
Lymphatics: - absence of palpable lymph nodes, Lymphadenopathy/organomegaly
Telangiectasias
77
At what serum bilirubin level can you typically begin to detect scleral icterus?
Some people can detect scleral icterus at as little as 2.5mg/dL of bilirubin, but typically it becomes more evident around 4mg/dL.
78
How is MCH calculated?
| How is MCHC calculated?
```
MCH = (Hemoglobin x 10) / RBC
MCHC = Hemoglobin / Hematocrit
```
79
In macrocytic anemias, what is the MCHC? (high, low, or nl)?
Nl
80
What are acanthocytes or spur cells?
| What dz are they seen in?
(acantho = "spiny")
Have multiple tiny projections seen all over their surface.
Seen in liver disease.
81
What are echinocyte or burr cells?
| What dz are they seen in?
These cells are often confused with spur cells. The projections on burr cells are smaller and more evenly spaced than spur cells. They also show a small area of central pallor as compared to spur cells.
These cells are often present in chronic kidney disease.
82
What are dacrocyte or teardrop cells?
| What dz are they seen in?
These cells are typically seen in myleofibrosis (bone marrow fibrosis) or infiltration of the bone marrow by a proess like metastatic cancer. These cells take on a teardrop shape because they are forced to squeeze themselves in narrow spaces in a fibrosed bone marrow or marrow crowded with cancer cells.
83
What's another name for target cell?
| What diseases can they be seen in?
Codocyte
| Liver dz or thalassemia (I believe there is more)
84
Sickle cell pts are at risk for what type of infections?
Encapsulated bacteria
85
What are the causes of non-AG metabolic acidosis?
```
HARDASS
Hyperalimentation
Addison's disease
RTA
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
```
86
What are the causes of AG-metabolic acidosis?
```
MUDPILES
Methanol (formic acid)
Uremia
DKA
Propylene glycol
Iron tabs or INH
Lactic acidosis
Ethylene glycol (--> --> oxalic acid)
Salicylates (late)
```
87
Nephritic syndrome is due to ___________ disruption, while nephrotic syndrome is due to __________ disruption.
Nephritic: GBM
Nephrotic: podocyte
88
What can cause papillary necrosis?
```
SAAD pap
Sickle cell dz/trait
Acute pyelonephritis
Analgesics (NSAIDs)
DM
```
89
Classic triad of RCC?
Palpable mass
Flank pain
Hematuria
90
Formula for serum osmolality?
2xNa + glucose/18 + BUN/2.8
