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CDM 1 Exam 2 > Renal: Lecture 1 > Flashcards

Renal: Lecture 1 Flashcards

1
Q

Clearance in healthy individual?

A

100-120ml

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2
Q

Afferent arteriole

A

Brings blood in, slightly thicker

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3
Q

Efferent arteriole

A

Brings blood out, but more constricted to increase pressure and push filtrate through Glomerulus

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4
Q

Kidney functions

A

Regulatory Function
Excretory Function
Hormone Function
Metabolic Function

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5
Q

Regulatory Function of Kidney

A

Control composition and volume of blood volume

Maintain acid-base balance

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6
Q

Excretory Function of Kidney

A

Produce urine

Remove metabolic waste

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7
Q

Hormone Function of Kidney

A

Produce renin for BP control
Produce erythropoietin which stimulates RBC production
Activate Vitamin D

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8
Q

Metabolic Function of Kidney

A

Gluconeogenesis

Metabolize drugs and endogenous substances

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9
Q

Kidneys role in Regulation of BP

A

Decreased blood coming through afferent stimulates renin from juxtaglomerular cells of kidney

Renin turns A-> A1, A1 -> A2 by ACE, A2 = vasoconstriction, stimulates Na retention, release of ADH to increase Na

Prostaglandin will decrease efferent in HTN

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10
Q

Primary function of kidneys are….

A

Filtration (Glomerulus)

Reabsorption and Secretion (Tubule)

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11
Q

Pre-renal event

A

Any injury to Arterioles/vasculature

change in volume/tone of either afferent or efferent

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12
Q

Where can kidney injury occur

A

Arterioles
PCT
DCT
Collecting duct

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13
Q

Injury in PCT will lead to sodium….

A

waste

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14
Q

What to look for in Afferent Arteriole that influence perfusion pressure

A

Volume and tone

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15
Q

What aspect of Efferent Arteriole influences perfusion pressure

A

Tone

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16
Q

Meds/conditions that impact Volume/tone of afferent arteriole

A

Anything affecting diameter of afferent arteriole (DM,HTN)

Disease that limit perfusion pressure to kidney (HF,Cirrhosis)

Meds that alter volume or tone (Diuretics + meds w/ constrictive properties)

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17
Q

Meds/Conditions that impact tone of Efferent arteriole?

A

ACE/ARB = dilate

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18
Q

RBC or protein in urine is. sign of

A

renal damage in glomerulus or the tubule

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19
Q

If tubular cells are damaged then….

A

Na and other electrolytes will be wasted and increased urine sodium

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20
Q

FeNA

A

Fraction of excreted Sodium

want 1% or less

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21
Q

BUN

A

Often high in dehydration

Extent of rise in BUN is a marker of a change in perfusion pressure (rapid rise in pre renal injury)

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22
Q

Creatine Clearance

A

Tendency to over estimate GFR, ~10 points

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23
Q

What is AKI

A

acute increase in creatinine with or without decrease in urine output over a short period of time

over ~24-48hrs

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24
Q

AKI 3 categories of Kidney Injury

A

Prerenal = decreased renal blood flow

Intrinsic/intrarenal = structural damage within Glomerulus,tubule, interstitium

Postrenal - obstruction within urine collection system

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25
Q

RIFLE Classification of AKI is….

A

Doubling Cr

26
Q

AKIN Stage 2 classification is….

A

increased Cr X 2

27
Q

KDIGO Classification of AKI is….

A

Doubling Cr

28
Q

Nonoliguria

A

Urine output > 500ml per day

29
Q

Oliguria

A

Urine output 100-500ml per day

30
Q

Anuria

A

Urine output <100ml per day

31
Q

Markers of AKI

A

2 X increase in Cr
Posible Change in Urine Output
Time frame, short period of time

32
Q

What to NOT use to measure AKI

A

Cockcrof and Gault eq = CrCL
MDRD and MDRD4 eq = GFR
CKD-EPI eq = GFR

33
Q

Who develops AKI?

A

Pt on high meds = increase risk
Community generally <1% risk

Inpatient setting = risk ~10%

Critically ill = ~25%, survival rate 10-30%

34
Q

% of AKI cases thought to develop in hospital?

A

50%

increase risk of death, length of stay, move to ICU

35
Q

AKI Risk Factors

A 
Non-modifiable:
CKD
Diabetes
Older age
Cirrhosis
CHF
Renal artery stenosis
PVD
Modifiable:
Major surgery/anesthesia
Sepsis/shock
Volume depletion
Hyper/Hypotension
Nephrotoxic meds
36
Q

Tenting of skin suggests….

A

Prerenal

37
Q

Dark “Tea colored” Urine suggests….

A

Prerenal

38
Q

Fever and High WBC count suggests….

A

AIN and Glomerulonephritis

39
Q

Fever and rash Suggests….

A

AIN and Glomerulonephritis

40
Q

Blood in Urine suggests…

A

Post renal or Glomerulonephritis

41
Q

Causes of pre renal AKI

A

Hypovolemia
Decrease Cardiac output
Decreased circulatory volume

NSAIDs = Vasoconstriction of AA
ACEi/ARBs = vasodilation of EA
42
Q

Prerenal AKI risk factors

A 
Advanced Age
Diuretic Use
Poor oral intake
GI Fluid Loss
CHF
Renal Artery Stenosis
ACEi/ARBs
NSAIDs
43
Q

Prerenal AKI treatment

A

Fluid replacement with NaCl

44
Q

Counseling and prevention of pre renal AKI

A 
Avoid NSAIDs (ASA 81 OK)
Maintain adequate hydration

Look for darkening urine, “tea” color and less urine output

45
Q

Intrarenal AKI Diagnostics

A 
BUN/Scr: 16/1 ratio
Urine output: Down
**Urine Sediment: (ATN = muddy brown casts)(AIN = WBC casts +/- eosinophil cast)(Glom = RBC casts)**
Urine RBC: 2-4 (in Glomerulonephritis)
Urine WBC: 2-4 (in AIN)
Urine Na: >40 mEq/L
Urine protein: none
FeNA % = >2%
46
Q

Markers of intrinsic/intrarenal AKI

A

KEY: damage inside glomerulus, tubule or interstitium

Leads to cell death, and debris (cell casts) which cause obstruction

present as a wasting order of sodium (FeNA >2%)

47
Q

ATN (acute tubular necrosis) causes

A

Tubular Disease

prolonged ischemia from pre renal AKI, infection, nephrotoxins

48
Q

AIN (Acute interstitial nephritis) causes

A

Injury to interstitial space but can also affect tubules

Ischemia, infection, connective tissue damage, nephrotoxins

49
Q

Glomerulonephritis

A

inflammation of glomerulus

Form RBC casts

50
Q

AIN causes….

A

infection or drug-induced

51
Q

Glomeruloneophritis causes…

A

Immune reaction or Drug induced

52
Q

Prerenal Diagnosis parameters

A 
BUN/Scr: 20/1 ratio
Urine output: Down
Urine Sediment: none
Urine RBC: none
Urine WBC: none
Urine Na: < 20 mEq/L
Urine protein: Variable
FeNA % = <1%
53
Q

Postrenal Diagnosis parameters

A 
BUN/Scr: 16/1 ratio
Urine output: Down
Urine Sediment: Possible
Urine RBC: Variable
Urine WBC: 1+
Urine Na: >40 mEq/L
Urine protein: Variable
FeNA % = >2%
54
Q

AIN Findings

A 
Sediment: WBC + Eosinophils
Cells: WBCs 2-4, + Eosinophils
Crystals: None
Protein: Mild, <0.5/day
Timing: Slower develop, 7-10 days after "insult" event
55
Q

Glomerulonephritis Findings

A

Sediment: RBC Casts
Cells: RBC
Crystals: Urate and or calcium crystals maybe present
Protein: Mod - Large proteinuria
Timing: Slower develop, 7-10 days after “insult” event

56
Q

Treatment for ATN

A

Restoring Volume/BP

57
Q

Treating for AIN

A

Discontinue cause of infection, need corticosteroids

58
Q

Postrenal Kidney injury also known as….

A

post-obstructive AKI or obstructive uropathy

Physical obstruction along urinary tract

59
Q

Common drug induced Postrenal AKI

A

acyclovir, indinavir, sulfadiazine

drugs can cause crystals

60
Q

Kidney Stones

A

might cause Postrenal AKI

Largely impacted by diabetes

Prevention: hydration and low oxalate/urate foods

CDM 1 Exam 2 (16 decks)

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