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B4W1 Flashcards

1
Q

What does AKI stand for and what does it mean

A

Acute Kidney Injury - damage to kidney function measured by GFR due to a rapid decline (within days or hours)

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2
Q

Anuria (define it)

A

(failure to produce urine) < 50 mL of urine in 24 hours due to acute obstruction, cortical necrosis or vascular catastrophe

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3
Q

CKD - what is it what does it mean

A

Chronic kidney disease with a GFR of <60 mL/min per 1.73 m^3 that is present for more than 3 months

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4
Q

Oliguria (what is it)

A

<400 mL of urine output in 24 hours (the lowest amount of urine produced by a person on a healthy diet)

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5
Q

Uremia (what is it)

A

non specific symptoms of fatigue, weakness, nausea, confusion, pericarditis and coma due to waste product retention in kidney disease (seen with elevated BUN)

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6
Q

Azotemia (what is it)

A

pt having a elevated BUN and creatinine without uremia symptoms)

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7
Q

What are the components of the GFB

A
  1. glycocalyx via mesangial cells
  2. basement membrane
  3. endothelial cells with fenestrations
  4. podocytes with slit diaphragm

has negative charge which repels larger molecules

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8
Q

Serum creatinine is a ________ indicator of GFR

A

poor (because it is freely filtered and secreted which can lead to incorrect readings)

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9
Q

MDRD equation (what is it and what does it require)

A

It is a creatinine eq to estimate GFR with requiring serum creatinine levels, age and sex of pt

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10
Q

When assessing AKI v CKD what would you use to evaluating GFR

A

AKI - because there is no steady state, we would use serum creatinine levels
CKD - because there is a steady state of function, we would use eGFR to asses renal function

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11
Q

SCr levels of an AKI patient would be expected to be around

A

Have an increased SCr (>0.3 mg/dl over 48 period, or an overall increase of 50% within 48 hour)

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12
Q

What is the leading cause of AKI

A

sx

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13
Q

Most common tests to determine AKI

A

serum creatinine, and BUN

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14
Q

Mortality for AKI

A

30%

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15
Q

Following AKI what are the pathways that a patient could experience

A
  1. full recovery
  2. development of progressive CKD
  3. Acute onset CKD
  4. ESRD
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16
Q

What are the three (general) causes of AKI?

A
  1. pre renal (hypovolemia, decreased CO, renal regulation impairment)
  2. intrinsic (glomerulus, tubules or vascular complication)
  3. post renal (bladder)
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17
Q

Pre renal causes of AKI include:

A

Hypovolemia (gastritis, diarrhea, vomiting) decreased CO, CHF, Liver failure, NSAID use, ACE-i use, renal vasoconstriction

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18
Q

Intrinsic causes of AKI include:

A

Glomerular: Acute glomerulonephritis
Tubular: ischemia, sepsis, nephrotoxins, ATN (acute tubular necrosis) AIN (acute interstitial nephritis), allergic reactions, auto immune diseases
Vascular: vasculitis, hypertension

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19
Q

Post Renal Causes of AKI include:

A

Bladder obstruction, kidney stone, Tumor, BPH (benign prostatic hyperplasia), prostate cancer, neurogenic bladder

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20
Q

How to determine the cause of AKI:

A
  1. Fractional excretion of Na (FENa)
  2. Renal ultrasound
  3. Patient medical hx
  4. Intrinsic AKI (sloughing off of cells due to ischemia would show up in the urine)
  5. albuminuria/hematuria (not really helpful in differentiation)
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21
Q

ATN

A

Acute tubular necrosis

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22
Q

AIN

A

Acute interstitial nephritis

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23
Q

RBC casts - what do they mean and what are they associated with

A

indicate glomerular disease (there is blood in the urine)

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24
Q

Fatty cases - what do they mean and what are they associated with

A

indicate nephrotic syndrome (too much protein in the urine) (glomerulonephritis)

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25
Hyaline casts - what do they mean and what are they associated with
devoid of any contents and are seen with pre renal AKI
26
granular casts - what do they mean and what are they associated wtih
muddy brown casts that indicate sloughing off of cells in the lumen and necrosis (ATN)
27
WBC casts - what do they mean and what are they associated with
indicate inflammation in renal parenchymal (AIN) (they are the presence of eosinophils which could be consistent with an allergic rxn)
28
Differentiation of AKI Dx via FENa and BUN (PreRenal AKI and ATN)
Prerenal AKI: FENa < 1%, BUN > 20:1 ATN: FENa > 2%, BUN < 20:1
29
What would non dysmorphic RBC in urine signify?
This would be consistent with a post renal AKI dx because there is no problem with the glomerulus and rather a problem with a downstream target which is in the late tubule, or the urinary tract
30
Kidney size in AKI
AKI: normal sized or hydronephrotic kidney (normal sized in AKI due to hypovolemia and acute tubular necrosis)
31
Tx for AKI
-Dependent on severity of symptoms -Dialysis -Drug therapy -Avoidant therapy (no NSAIDS, no contract dye) -treat systemic problem (ACEi, volume correction, furosemide, remove obstruction)
32
How do you determine dialysis for a patient
AEIOU A-Acidosis E- electrolytes I- Intoxications O- Overload of volume U- Uremia
33
What are the two types of dialysis
1. peritoneal dialysis = through the abdomen 2. hemodialysis = cath through subclavian or jugular vein (although preferably via fistula in the arm)
34
What is the defining lab result for CKD
eGFR < 60 mL/min per 1.73 m^3, or albuminuria and abnormal findings on kidney for 3+ months
35
GFR is proportional to ________
the number of functioning nephrons
36
Risk factors for CKD include:
Primary: DM, HTN Secondary: Family hx, age, systemic infection, loss of kidney mass, Autoimmune disease
37
GFR levels for stages of CKD
Stage 1: > 90 2: 60-90 3: 30-60 4: 15-30 5: < 15 (kidney failure)
38
Kidney size on US in CKD
CKD: reduces in size with an irregular surface due to renal atrophy , loss of nephrons, and loss of blood supply to the kidneys
39
What are the normal size dimensions of a kidney and cortex?
normal size: 10-12 cm Normal cortex: 2.5 cm
40
Progression of a CKD diagnosis via DM
Onset of DM leads to DM dx. DM dx leads to microalbuminuria, which progresses to ESRD
41
How does systemic dx lead to kidney disease: (think of the cycle diagrpham)
systemic dx leads to reduced # of nephrons, leading to structural changes, leading to hyperfiltration, leading to increase P(gc), leading to sclerosis of nephrons which leads to reduced # of nephrons (never ending cycle)
42
How does ANG II and ACEi work into CKD (general affect)
They will aid in decreasing P(gc) to allow for more use of functioning nephrons
43
How does ANGII work on CKD
increases GFR by increasing P(gc) by constricting efferent arteriole more than the AA -allows short term preservation of eGFR however is a bad long term outcome due to sclerosis of nephron
44
How does ACEi work on CKD
ACEi dilate the efferent arterioles to lower P(gc) allowing for a short term decrease in GFR but long term decrease in sclerosis of nephons, which aid in preservation of renal function
45
How does renal insufficiency progress via the pathological clinical feature starting with HTN
HTN leads to increases in PTH, leading to anemia, leading to phosphorus increases, leading to acidosis, leading to uremic syndrome
46
What is the best treatment for ESKD
transplant
47
What are the clinical indications for transplant qualification
1. ESKD on dialysis 2. eGFR < 20 mL/min 3. CKD with eGFR < 30 mL/min and in need of another organ transplant
48
Avg wait for a kidney
5 years
49
How long does it take for survival benefit from transplant
3-6 months
50
Trends of people on the kidney transplant wait list
There has been a steady increase of people until 2014 where it has begun to decrease slightly
51
How do we get consent for living donation
1. drivers license 2. family approval
52
Contradictions for transplant include
cancer an active untreatable infection active drug use significant vascular compromise non adherence to medical therapy lack of family/social support
53
Post transplant management includes:
drug interaction tracking tx of chronic disease contraception treatment and prophylaxis for opportunistic infection
54
What do we treat a pt with that is waiting for a transplant
dialysis (peritoneal and hemodialysis)
55
If dialysis is needed 1 week post transplant this is called...
delayed graft function
56
What is the immunology surrounding rejection in transplantation (hint: APC, T and B)
APC originate from the donor/recipient organ and innate immune system can travel to lymph nodes to present the new organ. This can lead to activation of B and T cells to destroy the organ
57
What are the three defenses against rejection?
HLA matching Detection of HLA natibodies Cross matching
58
What is HLA matching
HLA are human leukocyte antigens which are markers on cells to recognize self. matching to lower risk of rejection
59
What is HLA antibody detection
screening for any HLA antibodies to show prior exposure to HLA antibodies (from pregnancy, blood transfusions, previous transplant, immunosuppression)
60
What is cross match
tests whether a donor has antibodies specific for the donor. If there is a positive cross match, no transplant
61
Hyperacute rejection
hours to days post transplant - not responsive to tx
62
accelerated rejection
1-2 weeks post transplant, T cell mediated rejection, tx response depends on antibody levels
63
acute rejection
weeks to months post transplant, T cell mediated, responsive to anti rejection therapy
64
chronic rejection
months to years post transplant, pathogenesis is unresponsive to transplant, and not influenced anti rejection therapy
65
rank rejections from shortest time to longest
hyperacute, accelerated, acute, chronic
66
What are the 4 types of immunosuppressive agents
induction agents desensitization agents primary immunosuppressants adjuvant agents
67
What are the types of immunosuppressive agents: induction agents
monoclonal antibodies (muromonab, thymoglobulin)
68
What are the types of immunosuppressive agents: desensitization agents
desensitize to HLA (IVI, rituximab)
69
What are the types of immunosuppressive agents: primary immunosuppressants
calcineurin inhibitors (CNI)
70
What are the types of immunosuppressive agents: adjuvant agents
CNI + (corticosteroids, MMF, AZA, SRL)
71
What are CNIs
calcineruin inhibitors -- more used immunosuppressive therapy (most potent) inhibts the T cell pathway
72
What are the known side effects of CNIs
HTN, toxicity, malignancies
73
Metabolic interactions that can increase CNI
Ca channel blockers (amlodipine, verapamil) antifungal agents (ketoconazole, fluconazole) immunosuppressants antibiotics (azithromycin) protease inhibitors (saquinavir, nelfinavir) foods (grapefruit)
74
metabolic interactions that can decrease CNI
these drugs activate p450 enzyme in the liver that decreases CNI antituberculosis drugs (rifampin, rifabutin, isoniazid) anticonvulsants (barbiturates, phenytoin, carbamazepine) herbal preparations (st. johns wort) antibiotics (nafcillin, cipro, cephalosporins) other (ticlopidine, octreotide)
75
What is acute cellular rejection
T cell mediated rejection in the 1st 6 months post transplant that is not accompanied by symptoms, but has an increased SrCreatnine
76
How do you treat acute cellular rejection
high dose corticosteroids, monoclonal/polyclonal immunosuppressants
77
What is antibody mediated rejection
form of rejection that is not amenable to standard immuno therapy
78
How do you treat antibody mediated rejection
high does IVIg, rituximab, plasmapheresis, anti-CMV-IgG therapy

Translational Physiology (8 decks)

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