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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
RIFLE Classification of AKI is....
Doubling Cr
26
AKIN Stage 2 classification is....
increased Cr X 2
27
KDIGO Classification of AKI is....
Doubling Cr
28
Nonoliguria
Urine output > 500ml per day
29
Oliguria
Urine output 100-500ml per day
30
Anuria
Urine output <100ml per day
31
Markers of AKI
2 X increase in Cr Posible Change in Urine Output Time frame, short period of time
32
What to NOT use to measure AKI
Cockcrof and Gault eq = CrCL MDRD and MDRD4 eq = GFR CKD-EPI eq = GFR
33
Who develops AKI?
Pt on high meds = increase risk Community generally <1% risk Inpatient setting = risk ~10% Critically ill = ~25%, survival rate 10-30%
34
% of AKI cases thought to develop in hospital?
50% | increase risk of death, length of stay, move to ICU
35
AKI Risk Factors
``` 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
Tenting of skin suggests....
Prerenal
37
Dark "Tea colored" Urine suggests....
Prerenal
38
Fever and High WBC count suggests....
AIN and Glomerulonephritis
39
Fever and rash Suggests....
AIN and Glomerulonephritis
40
Blood in Urine suggests...
Post renal or Glomerulonephritis
41
Causes of pre renal AKI
Hypovolemia Decrease Cardiac output Decreased circulatory volume ``` NSAIDs = Vasoconstriction of AA ACEi/ARBs = vasodilation of EA ```
42
Prerenal AKI risk factors
``` Advanced Age Diuretic Use Poor oral intake GI Fluid Loss CHF Renal Artery Stenosis ACEi/ARBs NSAIDs ```
43
Prerenal AKI treatment
Fluid replacement with NaCl
44
Counseling and prevention of pre renal AKI
``` Avoid NSAIDs (ASA 81 OK) Maintain adequate hydration ``` Look for darkening urine, "tea" color and less urine output
45
Intrarenal AKI Diagnostics
``` 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
Markers of intrinsic/intrarenal AKI
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
ATN (acute tubular necrosis) causes
Tubular Disease prolonged ischemia from pre renal AKI, infection, nephrotoxins
48
AIN (Acute interstitial nephritis) causes
Injury to interstitial space but can also affect tubules Ischemia, infection, connective tissue damage, nephrotoxins
49
Glomerulonephritis
inflammation of glomerulus Form RBC casts
50
AIN causes....
infection or drug-induced
51
Glomeruloneophritis causes...
Immune reaction or Drug induced
52
Prerenal Diagnosis parameters
``` 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
Postrenal Diagnosis parameters
``` 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
AIN Findings
``` 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
Glomerulonephritis Findings
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
Treatment for ATN
Restoring Volume/BP
57
Treating for AIN
Discontinue cause of infection, need corticosteroids
58
Postrenal Kidney injury also known as....
post-obstructive AKI or obstructive uropathy Physical obstruction along urinary tract
59
Common drug induced Postrenal AKI
acyclovir, indinavir, sulfadiazine drugs can cause crystals
60
Kidney Stones
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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