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MHD > Renal and Anemia Test memorization > Flashcards

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

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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
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3
Q

How many months must GFR decline for (at least) for it to be considered CKD?

A

3 months

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4
Q

What are the 3 hematuria imposters?

A

Free Hemoglobin
Myoglobin
Menstrual contamination

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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.
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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

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7
Q

What is considered hypoalbuminemia? (< ___ g/dL)

A

< 3 g/dL

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8
Q

What is the characteristic clinical syndrome a/w diabetic nephropathy?

A
  • proteinuria,
  • progressive decline in GFR
  • hypertension
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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
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10
Q

What 3 drugs can cause acute drug-induced interstitial nephritis?

A
  • PCN derivatives
  • Diuretics
  • NSAIDs

(also PPIs, rifampin)

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11
Q

What specific kidney pathology can NSAIDs cause?

A

Acute hypersensitivity interstitial nephritis

Clinical: *nephrotic syndrome + *renal failure

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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
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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)
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14
Q

What two clinical findings is APKD a/w?

A

Mitral prolapse, berry aneurysms

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15
Q

Genes a/w angiomyolipoma?

A

Tuberous Sclerosis:
TSC1 - Hamartin 9q34
TSC2 - Tuberin 16p13

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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)

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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

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18
Q

What genes are a/w Wilm’s tumor?

A

WT1, WT2

WAGR: WT1 deletion, DDS: WT1 mutation, BWS: WT2 gene cluster mutation

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19
Q 
RPF = \_\_\_\_\_\_\_\_\_\_\_ clearance
RBF = \_\_\_\_\_\_\_\_\_\_\_ (equation)
A

PAH

= RPF/(1-Hct)

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20
Q

Filtration fraction (FF) = _____/_____

A

GFR/RPF

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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
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22
Q

What is the fractional excretion formula.

A

Fractional excretion = Amount excreted / Amount filtered

FENa = (UNa/PNa) / (UCr/PCr)

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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.

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24
Q

Casts seen in prerenal AKI?

A

hyaline

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25
Q

Why is FENa lower in prerenal AKI?

also higher U specific gravity, higher U osmolality

A

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)

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26
Q

How do prostaglandins affect RPF?

How about NSAIDs, then?

A

Dilate afferent arteriole (Increase)

- Block this

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27
Q

What is the specific gravity in ATI?

A

Isosthenuria

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28
Q

Prerenal azotemia commonly progresses to what condition?

A

ATN

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29
Q

What are the 2 main categories of ATN?

What are the 2 main categories of AIN?

A

AIN: Drug-associated and non-drug-associated
ATN: Ischemic and nephrotoxic

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30
Q

How does the urine appear in ATN?

A

Gross: “Dirty” or “Muddy brown”
- Granular “muddy brown” casts

(recall, oliguric followed by polyuric)

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31
Q

Vascular causes of AKI?

A 
Vasculitis
Thromboembolic disease
HUS/TTP
Malignant HTN
Scleroderma renal crisis
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32
Q

Classic triad seen in AIN?

A

Fever, eosinophilia, rash

usually only 1 sx present

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33
Q

What are the general indications for hemodialysis (RRT) in AKI?

A 
AEIOU
A- acidosis
E - electrolyte derangement (^K+)
I - intoxication syndrome
O - overload (volume)
U - Uremia
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34
Q

Define CKD.

A

Progressive decline in GFR
Duration least 3 months
+/- Albuminuria

DM, HTN make up 72% of cases

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35
Q

Most important SLE kidney subtype to know?

A

Diffuse proliferative nephritis (IV)

V has the nephrotic syndrome

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36
Q

What pathopneumonic finding is seen in each of the 3 RPGNs?

A

Crescents

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37
Q

What’s 1 symptom to associate w/cholesterol atheroembolic disease?

A

Livedo reticularis

38
Q

What label should we a/w CKD: Stage II/III Management?

A

Conservative Renoprotection

lifestyle, drug adjustments, drugs for risk factors

39
Q

What is step 1 in CKD Stage IV management? What else need be addressed?

A
  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
Q

Describe hemodialysis mechanism.

What are 3 determinants of solute diffuse rates?

A

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
Q

What is ultrafiltration? How does it work?

What is the overall goal of the procedure?

A

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
Q

List the sequelae of chronic ESRD (4)

A

Uremic cardiovascular disease

  • Medial vascular calcification
  • Arterial stiffness
  • LV hypertrophy
  • Higher risk of cardiac arrest and CHF
43
Q

Most common glomerular hematuria?
Upper urinary tract hematuria?
Lower urinary tract hematuria?
Uncertain etiology hematuria?

A

IgA
Stone
Infection
Exercise

44
Q

Compare and contrast clinical indications to treat kidney stones medically vs. interventionally.

A

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
Q

Foods high in purine content that should be restricted when dealing w/ a urate stone?

A
  • Meats: Offal, Seafood, Shellfish

- Alcohol

46
Q

Foods high in oxalate that should be restricted when dealing w/ a Ca2+ stone?

A
  • Black tea
  • Chocolate
  • Soymilk
  • Nuts
  • Berries
  • Beans, spinach (but high Ca2+), okra
  • Beets, rhubarb
  • Carrots
  • Celery, Swiss chard
  • Sweet potatoes
47
Q

Causes of monogenic (single gene) HTN? In other words, what genetic diseases cause HTN besides polygenic.

A
  • 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
Q

_____________ is the most common form of secondary hypertension.

A

CKD

HTN seen in most nephritic syndromes; due to salt retention

49
Q 
In CKD, what med combo tx would be best?
If this doesn’t work, what med class could you consider adding?
A

ACEI + diuretics
Consider BBs
Lastly CCBs (due to risk)

50
Q

In what pt demographic may low number urine cultures (10^2-4) be significant?

A
  • Young women w/ cystitis
  • Males
  • Pts w/ indwelling catheters
51
Q

In what urinary infections will blood cultures be positive as well?

A
  • Acute pyelonephritis

- Prostatitis

52
Q

Difference b/w Type & Screen vs. Type & Crossmatch (Major + Minor)?

A

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
Q

What ABO type combo b/w mother and fetus can produce HDN?

A

Group O mom with an A fetus (mild, if any HDN)

- ABO HDN: 15% of pregnancies. Common!

54
Q

What are 2 ways to assess for presence of fetal Hgb?

A
  • Amniocentesis

- PUBS, (percutaneous umbilical blood sampling) or cordocentesis

55
Q

Observation within _________ (time) of start of transfusion is critical for detection of an acute reaction.

A

15 min

56
Q

What are the intraluminal causes of obstruction?
What are the intramural (intrinsic) causes of obstruction?
What are the extramural causes of obstruction?

A

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
Q

Most common site for kidney stone obstruction?

A

Uretero-vesicular junction

58
Q

What are 3 diseases and 1 drug a/w sloughed renal papilla?

A

Diabetes
Sickle Cell
Pyelonephritis
Phenacetin abuse

59
Q

Define hydronephrosis.

A

Dilatation of the pelvis and calyces.

60
Q

Define obstructive uropathy.

A

Structural impedance to the flow of urine along the tract.

61
Q

Define obstructive nephropathy.

A

Functional (GFR) and/or anatomic damage to the renal parenchyma that results from obstructed urine flow.

62
Q

What are the sx in ACR Lupus classification?

A 
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
Q

2 important tests to monitor SLE disease activity?

A

C3, C4

dsDNA

64
Q

Drugs to treat SLE? (4)

A

NSAIDs
Anti-malarials
Corticosteroids
Immunosuppressive medications

65
Q

What 2 AB tests are useful in Sjogren’s?

What abnormality is seen in the kidney?

A

+ Anti-SSA and/or anti-SSB antibody
+ Rheumatoid factor
Renal tubular acidosis (RTA)

66
Q

Having Sjogren’s syndrome increases risk of what disease by 40x?

A

Lymphoma (esp. mucosa-associated lymphoid tissue (MALT)

67
Q

What type of AB is positive w/diffuse scleroderma?

- Describe the main sx

A

Anti-topoisomerase (Scl70)
- Extensive skin involvement w/early visceral involvement
- *Interstitial lung disease (–> pulm HTN; HIGH MORTALITY)
- Kidney –> scleroderma renal crisis
(- GI)

68
Q

What type of AB is positive w/limited scleroderma?

- Describe the 2 main sx

A 
Anti-centromere
CREST:
C: calcinosis (anti-Centromere)
R: reynaud phenomena
E: esophageal dysmotility
S: sclerodactyly
T: telangiectasia
69
Q

What AB is a/w scleroderma renal crisis (and malignancy)?

A

Anti-RNA-polymerase III

70
Q

Name the Anti-phospholipid antibodies, and what test they can give a false positive for.

A
  • 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
Q

Test for dx of CVID?

A

Serum protein electrophoresis (SPEP)

72
Q

What 3 sx characterize Wiskott-Aldrich syndrome?

A
  • Thrombocytopenia
  • Eczema
  • Recurrent infections
    (bleeding is a major cause of death)
73
Q

What is the tx for acute hereditary angioedema? (just read thru a few times, too much to learn)

A
  • 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
Q

What is the mutation in ataxia-telangiectasia?

A

Mutation in ATM gene which is responsible for DNA repair

  • Therefore higher risk of cancer
  • Sx are in the name
75
Q

What is the mechanism behind chronic granulomatous disease?

What tests are used to dx it?

A

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
Q

List some physical signs of primary immunodeficiencies (if you can; probably ok to just read thru)

A

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
Q

At what serum bilirubin level can you typically begin to detect scleral icterus?

A

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
Q

How is MCH calculated?

How is MCHC calculated?

A 
MCH = (Hemoglobin x 10) / RBC
MCHC = Hemoglobin / Hematocrit
79
Q

In macrocytic anemias, what is the MCHC? (high, low, or nl)?

A

Nl

80
Q

What are acanthocytes or spur cells?

What dz are they seen in?

A

(acantho = “spiny”)
Have multiple tiny projections seen all over their surface.
Seen in liver disease.

81
Q

What are echinocyte or burr cells?

What dz are they seen in?

A

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
Q

What are dacrocyte or teardrop cells?

What dz are they seen in?

A

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
Q

What’s another name for target cell?

What diseases can they be seen in?

A

Codocyte

Liver dz or thalassemia (I believe there is more)

84
Q

Sickle cell pts are at risk for what type of infections?

A

Encapsulated bacteria

85
Q

What are the causes of non-AG metabolic acidosis?

A 
HARDASS
Hyperalimentation
Addison's disease
RTA
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
86
Q

What are the causes of AG-metabolic acidosis?

A 
MUDPILES
Methanol (formic acid)
Uremia
DKA
Propylene glycol
Iron tabs or INH
Lactic acidosis
Ethylene glycol (--> --> oxalic acid)
Salicylates (late)
87
Q

Nephritic syndrome is due to ___________ disruption, while nephrotic syndrome is due to __________ disruption.

A

Nephritic: GBM
Nephrotic: podocyte

88
Q

What can cause papillary necrosis?

A 
SAAD pap
Sickle cell dz/trait
Acute pyelonephritis
Analgesics (NSAIDs)
DM
89
Q

Classic triad of RCC?

A

Palpable mass
Flank pain
Hematuria

90
Q

Formula for serum osmolality?

A

2xNa + glucose/18 + BUN/2.8

MHD (20 decks)

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