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Year 1: Patho/Pharm > Kidney Patho > Flashcards

Kidney Patho Flashcards

1
Q

Definition
Acute Kidney Injury (AKI)

A

Acute onset (hours to days)

3 types
1. pre-renal
2. intra-renal
3. post-renal

Increase in serum creatinine
Decrease urinary output
OR
BOTH

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2
Q

Definition
Oligouria

A

urinary output < / = 30cc/hour

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3
Q

Definition
Azotemia

A

Increased serum creatinine
Increase serum blood urea nitrogen (BUN)
BUN:Cr ratio > 20:1

*inability kidney to filter waste products (nitrogenous waste)

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4
Q

Definition
Uremia

A

Systemic signs and symptoms resulting from loss of kidney function (inability filter waste)

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5
Q

3 categories of acute kidney injury

A
  1. pre-renal
    - before the kidney
    - blood volume
    - cardiac output
    - obstruction blood flow
  2. intra-renal
    - inside the kidney
  3. post-renal
    - after the kidney
    - obstruction of urine flow
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6
Q

Pre-renal AKI
Definition

A

Trigger –> decrease renal blood flow –> decrease glomerular perfusion, filtration

Triggers include
1. obstruction
2. decrease blood volume - hemorrhage, dehydration, third spacing
3. decrease cardiac output
4. decrease renal blood flow

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7
Q

Urinalysis and serum indicators
Pre-renal AKI

A

Decrease renal blood flow sensed by juxtaglomerular cells

Release renin and activation RAAS compensation
Reabsorption sodium, water, urea
- BUN:Cr > 20:1

Oliguria (< 30ml/hour)

High urine osmolality > 500mOsm/kg
- aldosterone promotes water reabsorption

Decreased excreted sodium
- FEna = Na excreted / Na filtered < 1%

Decrease glomerular filtration
increase creatinine, increase BUN

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8
Q

Most common cause of pre-renal AKI

A

sepsis

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9
Q

Compensatory systems
Decreased renal blood flow

A
  1. SNS
    - NE and E released
    - vasoconstriction
  2. HPA axis
    - Cortisol release
    - vasoconstriction
  3. ADH
    - anti-diuretic hormone release
    - reabsorption water
  4. RAAS pathway
    - vasoconstriction
    - retention sodium and water
    - reabsorption urea
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10
Q

Drugs that potentiate pre-renal AKI

A

Vasoactive medications
- dopamine
- ACE inhibitors
- ARBs

NSAIDS & Radioactive contrast dyes
- decrease blood flow to kidney

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11
Q

Definition
Intra-renal AKI

A

INtra-renal AKI
- intrinsic
- direct damage to the renal parenchyma
- results in nephron dysfunction

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12
Q

Causes of Intra-renal AKI

A
  1. Glomerulus: Glomerulonephritis
  2. Tubules: acute tubular necrosis
  3. Vasculature: infarct, thrombosis (pre-renal progresses to intra-renal)
  4. interstitial disease: infection, tumors (acute nephritis)
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13
Q

Most common cause of intra-renal AKI

A

Acute tubular necrosis (ATN)

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14
Q

Glomerulonephritis
Definition

A

Injury to the glomerulus

Leads to inflammation of the glomerular capillaries and destruction of the glomerular membrane

Acute or chronic

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15
Q

Nephrotic Syndrome
Definition

A

Results from injury to the glomerulus

Unable to prevent filtration of proteins

Results in >/= 3.5g / day of protein in urine

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16
Q

Pathophysiology
Acute Tubular Necrosis

A
  1. Injury: nephrotoxins
  2. Ischemia

Nephrotoxins
- direct damage to tubular epithelial cells

Ischemia
- Lack of blood supply

Tubular epithelial cell dysfunction

  1. Cannot reabsorb
    - High urine sodium (> 30mmol/L)
    - High FEna (Na excreted / Na filtered) > 1 %
    - Low urine osmolality (<400mOsM/L)
    - Low urine specific gravity (1.010-1.012)
    - Low BUN:Cr ratio < 15:1
  2. Cannot secrete
    - hyperkalemia
    - metabolic acidosis (cannot secrete H+ ions)
  3. Increase Tubular pressure = decrease GFR
  • necrotic cells slough off
  • plug the tubule
  • formation brown casts in urine
  • tubule opposes filtration pressure in artery
  • decrease GFR
  • increase serum creatinine, increase serum urea (azotemia)
  • decrease urinary output (oliguria)
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17
Q

Factors required for reversible intra-renal AKI

A
  1. ischemia is not prolonged
  2. basement membrane is present
  3. tubular epithelial cells regenerate
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18
Q

Definition
Post-Renal AKI

A

Obstruction of urinary flow
Backs up into the renal pelvis
increase intra-tubular pressure
Decreases filtration

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19
Q

Causes of Post-Renal AKI

A

tumour
stones
trauma
strictures
prostate
neurogenic bladder

*< 5% of AKI

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20
Q

4 stages to the clinical course of AKI

A
  1. Initiation (onset)
    - oligouria
    - increase Cr
    - increase BUN
    -*reversible before damage at this stage
  2. Extension
    - ischemia
    - inflammation
  3. maintenance phase (oliguric phase)
    - initiation event resolved
    - injury established by extension phase (ischemia, inflammation)
    - 10-14 days (healing inflammation)
    - longer duration is poor prognosis
  4. recovery phase (polyuria)
    - most recovery within 3 weeks, can take up to 1 year for full recovery of function
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21
Q

Clinical Signs and Symptoms
Oliguric phase (maintenance phase) AKI

A

Oligouria
- decrease U/O
- normal SG (cannot reabsorb water)
- high urine sodium (cannot reabsorb sodium)
- low urine osmolality (cannot reabsorb water)
- BUN:Cr < 15:1
- FEna > 1%

Urinalysis
- RBC, protein (damage glomerular membrane)
- brown casts (tubular necrosis)
- WBC (inflammation)

FVO
- decrease GF = fluid retention
- edema, hypertension, heart failure
- pulmonary edema, crackles
- bounding pulses, jugular venous distention

metabolic acidosis
- tubules cannot excrete H+
- tubules cannot reabsorb HCO3-
- decrease pH

hyponatremia
- tubules cannot reabsorb sodium
- sodium excrete in urine
- hyponatremia serum

hyperkalemia
- tubules cannot excrete potassium
- hyperkalemia in serum
- cardiac dyrhythmias

hypocalcemia, hyperphosphatemia
- kidney cannot activate vitamin D
- cannot absorb calcium in GI
- PTH released increase bone reabsorption - increase phosphate in blood

Azotemia and neurological symptoms
- increase waste, creatinine, BUN
- fatigue, stupor, coma, confusion

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22
Q

Clinical Signs and Symptoms
Recovery (polyuric) phase

A

Kidney able to excrete waste (unable to concentrate urine)

result is polyuria > / = 3-5 L / day urine

Recovery function 1-3 weeks , up to 1 year

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23
Q

Risk in Recovery phase

A

dehydration
hypovolemia
electrolyte imbalances

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24
Q

Management of AKI

A

Hospital admission

  1. electrolytes
    - monitor and manage sodium, potassium, calcium, phosphate
  2. fluid
    - monitor fluid volume overload / dehydration
    - replacement / diuretics / dialysis
  3. blood pressure and cardiac output = kidney perfusion
  4. dietary changes
    - fluid volume restrictions
    - sodium or potassium restrictions or supplements
    - increase protein
  5. dialysis
    - acidosis, FVO, hyperkalemia
  6. medication renal dose adjustments
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25
Prevention of AKI
Renal dose adjustments for medications and age Fluid to wash out nephrotoxic medications Maintaining renal perfusion - treating infections (sepsis) - hydration and prevention dehydration - monitoring fluids post operatively, trauma, burns - maintaining healthy blood pressure and cardiac output - maintaining normoglycemia - maintaining healthy liver Immediate treatment of urinary obstructions - BPH, tumours, stones
26
Definition Chronic Kidney Disease
Also known as - renal insufficiency - chronic renal failure chronic, irreversible loss of kidney function - nephron destruction change in structure or function present for > 3 months
27
Classification Chronic Kidney disease
1. GFR 2. Albuminuria GFR Stage 1, normal, > 90ml/min stage 2, mild, 60-89ml/min stage 3, moderate, 30-59ml/min stage 4, severe, 15-29ml/min stage 5, end stage renal disease < 15ml/min albuminuria stage 1, mild, < 3mg/mmol stage 2, moderate, 3-30mg/mmol stage 3, severe, > 30mg/mmol
28
Definition Glomerular filtration rate
Amount of blood filtered in mL per minute by the glomerular membrane = number functioning nephrons = kidney function
29
Factors that affect GFR
Age sex height weight *serum creatinine
30
Over-estimation GFR
kidney actively secretes creatinine in addition to creatinine that is filtered at the glomerulus
31
Clinical ways to assess albuminuria
Urinalysis - albumin - creatinine 24 hour urinalysis - albumin - creatinine POCT - albumin dipstick
32
Who should be screened for CKD?
Anyone who has risk factors for CKD - smoking - diabetes - hypertension - hyperglycaemia - physically inactive Screen 1. GFR 2. albuminuria earlier diagnosis = slow progression
33
Nephropathy secondary to Diabetes Mellitus Pathophysiology Clinical signs
1. Hyperglycemia 2. Inflammation -> scaring -> dysfunction glomerular filtration membrane/tubular dysfunction hyperglycaemia --> oxidative radicals --> microvascular damage, glomerular filtration membrane damage, epithelial cell damage glucose -> free radicals -> inflammation -> scaring/fibrosis -> decreased filtration, decreased tubular reabsorption, proteinuria, waste/FVO
34
Nephropathy secondary to hypertension
1. HTN 2. renal artery stenosis 2. ischemia -> inflammation -> scarring/dysfunction (glomerular filtration membrane, tubular epithelium) Hypertension --> microvascular damage --> renal artery stenosis --> decreased renal blood flow --> ischemia --> inflammation --> scarring/fibrosis --> damage and reduce glomerular filtration --> ischemia tubular epithelium --> dysfunction
35
What percentage of kidney function do you see clinical signs and symptoms of CKD manifest?
25% kidney function
36
Clinical manifestations all body systems Chronic Kidney Disease (CKD)
Neuro - confusion, fatigue, HA, sleep disturbances, encephalopathy Eyes - retinopathy Cardiac - dysrhythmias (hiperkalemia) - HF - HTN - uremic pericarditis - CAD (dyslipidemia) Pumonary - edema (FVO) - uremic pleurites GI - uremic gastritis - ulcers, hemorrhages - N/V/anorexia Integumentary - urochromes (yellow skin, brown/white nails) - pruitis uremia - ecchymosis (loss of clotting factors) - pale (loss of EPO, RBC, anemia) MSK - weakness, numbness, tingling - fractures - electrolyte disturbances (hyponatremia, hyperkalemia, hypocalcemia, hyperphsophatemia) Metabolic - hyperglycemia - dyslipidemia Haematological - bleeding (loss of platelets, clotting factors) - infection (loss of blood cells, immunoglobulins) - decreased response to vaccination - anemia Endocrine - dysmenorrhea, infertility - loss of libido
37
Diagnosis CKD
1. history 2. clinical signs and symptoms 3. GFR and albuminuria (stage of kidney disease) 4. urinalysis (casts, RBC, WBC, protein) 5. imaging (US, CT, etc.)
38
Pharmacological Management Supportive management CKD
Management: HTN - ACEi (IPRIL) and ARBs (SARTAN) - renal protective - slow eGFR decline, slow microalbuminuria *not effective for end stage Management: Dyslipidemia Management: Glucose Dietary modifications - plant based proteins - weight loss (not end stage) - protein restriction ( not old people ) Vaccinations - infection risk Blood products - anemia Dialysis - acidosis - hyperkalemia - FVO - waste products
39
3 functions of the kidney
1. water and electrolyte balance 2. acid-base balance 3. remove waste 4. hormones (EPO, activation vitamin D)
40
pre-renal AKI Absolute loss of fluid examples
blood loss trauma surgery diarrhea vomiting diabetes mellitus uncontrolled burns diuretics
41
pre-renal AKI relative fluid loss examples
Hypotension decreased cardiac output heart failure DIstributive shock sepsis ascites
42
pre-renal AKI renal artery hypo perfusion examples
Emboli tumour stenosis Vasoactive medications - dopamine - epinephrine - NSAIDS - ARBs - ACE inhibitors
43
Pre-Renal AKI BUN:Cr Ratio
Normal BUN: Cr ratio 20:1 pre-renal AKI > 20:1 - decrease waste filtration - urea follows sodium
44
Example nephrotoxins that cause intra-renal AKI
aminoglycosides NSAIDS heavy metals - lead ethylene glycol - antifreeze radiocontrast dyes myoglobulin uric acid waste (tumour lysis syndrome)
45
Glomerular filtration membrane anatomy
3 layers of cells 1. endothelial layer (fenestrations) 2. basement membrane (selectively permeable, negative charge, pores) 3. epithelial layer (podocytes, filtration slits)
46
Clinical Signs and Symptoms Early post-renal AKI
Intra tubular pressure decreases glomerular filtration - increase serum creatinine, BUN - oligouria - increase absorption sodium, water, urea - FEna < 1% - urine osmolality > 500mOsM/L
47
Clinical Signs and sympotms Late post-renal AKI
Back pressure destroys the tubular epithelial cells mimics intra-renal AKI - high urine sodium - low urine osmolality - FENa > 1% - BUN:Cr < 15:1 - high urine sodium concentration > 30mmol/L
48
End of recovery phase AKI
marked by normalization acid-base balance, electrolytes, fluids
49
Goal of treatment AKI
1. Remove mechanism of injury Supportive care to keep patient alive during recovery and correct imbalances 3. correct fluid volume 4. correct electrolyte imbalances 5. correct acid-base imbalances 6. monitor and correct HTN, dyslipidemia, hyperglycaemia 7. monitor and correct infection, immunosuppression, anemia 8. diet changes and supplementation 9. renal replacement therapy / dialysis
50
Goal Treatment CKI
Correct fluid volume, acid-base, electrolyte imbalances Correct HTN, dyslipidemia, hyperglycemia Correct anemia, infection, immunocompromised protein restriction (exception old, end stage) weight loss (exception old, end stage) Dialysis (end stage) Avoid nephrotoxins
51
Nephrotic syndrome Clinical manifestations
1. Proteinuria > 3.5 g per day - loss of albumin (hypoalbuminuria), edema; loss of immunoglobulins (infection); loss of WBC (infection); loss of clotting factors (bleeding) and anti-thrombin (clots) 2. lipiduria - fat floating on urine "foamy" 3. hematuria - RBC found in urine - dark brown, tea coloured 4. Edema - third spacing, decreased oncotic pressure - increase RAAS and ADH 5. Dyslipidemia - increase TG, LDL, cholesterol
52
Nephritic syndrome Clinical manifestations
Proteinuria < 3.5g per day *most common cause is post-infectious glomerulonephritis
53
Types of Glomerulonephritis
1. acute vs. chronic 2. immune vs. non immune 3. primary vs. secondary primary - direct injury to the glomerulus - trauma, infection, type II-IV hypersensitivity reactions, clots secondary - diabetes mellitus, hypertension etc.
54
Pathophysiology Glomerulonephritis
1. Immune mediated OR 2. non-immune mediated --> injury to the glomerulus --> inflammation - deposition inflammatory mediators, auto-immune complexes, complement - proliferation mesangial cells and endothelial cells --> decrease renal blood flow --> decrease GFR - inflammation damages epithelial cells (filtration slits) and basement membrane (negative charge) --> loss of selective filtration --> proteinuria, hematuria - inflammation --> fibrosis --> scaring --> decrease GFR Result: oligouria azotemia (increase creatinine, increase urea)
55
Post-infectious glomerulonephritis Clinical symptoms
Prior infection that has since cleared - staphylococcus - streptococcus - HBV/HCV - varicella virus Type III hypersensivity reaction (IgM/IgG) deposit in the glomerular membrane --> mesangial proliferation --> decrease RBF --> decrease GFR Most common cause of nephritic syndrome proteinuria < 3.5g per day
56
Explain how creatinine and eGFR are related
estimated GFR = 24 urine creatinine clearance (calculation compared to plasma creatinine) Creatinine - filtered = excreted in urine (not reabsorbed) - slightly overestimated (some secreted) - reflect kidney function (functional nephrons) - muscles produce at stable rate (false rhabdomyolysis, malnutrition) - calculation affected by (age, height, weight, gender)
57
Intact nephron hypothesis What is it What stage of CKD
Stage 2 CKD Mild GFR 60-89mL/min surviving nephrons compensate for loss of nephrons - hyperfunction, hypertrophy - maintain normal fluid balance, electrolytes, acid-base balance
58
Uremic Syndrome What is it What stage of CKD or % kidney function
Systemic signs occur at 25% kidney function Normal eGFR 90mL/min Moderate eGFR 30mL/min (stage 3) clinical signs and symptoms appear Uremic syndrome (stage 5)
59
Anatomy Nephron
Renal corpuscle - bowman's capsule - glomerulus - mesangial cells (macrophages, vasoconstriction afferent arteriole) Renal tubules - proximal convoluted tubule - loop of henle - distal tubule
60
Renal tubules Cells and Function
Proximal tubule - brush boarder cells - microvilli increase SA for reabsorption - high mitochondria for active transport Distal tubule - Intercalated cells - H+ excretion, HCO3- absorption (acid base balance) - Principle cells - sodium and potassium balance, (influenced by macula densa - sodium sensing cells, and aldosterone)
61
Glomerulus Cells and function
Mesangial cells - vasoconstriction of glomerulus capillaries (smooth muscle cell function) - phagocytosis and release of inflammatory cytokines (monocyte function) Juxtaglomerular cells - located around afferent arteriole - sense decrease in renal blood flow - release renin in response to beta 1 adrenergic stimulation Macula densa cells - located between the afferent and efferent arteriole - sodium sensing cells of the distal convoluted tubule
62
Natriuretic peptides Function
ANP - atrial natiuretic peptide BNP release from overstretch of cardiomyocytes prevention sodium/water reabsorption by kidney increase diuresis CNP released by vascular endothelium from stretch increase vasodilation afferent arteriole icnrease GFR increase diuresis Renal natriuretic peptide released by collecting duct stretch increase vasodilation afferent arteriole increase diuresis
63
Hormones produced by the kidney
EPO - erythropoetin - juxtaglomerular complex - sensation hypoxia --> stimulation RBC production RNP - renal natriuretic peptide - released by collecting duct - increase diuresis Vitamin D3 activation - 1,25 dihydroxyvitamin D - allows for calcium reabsorption Renin - release day juxtaglomerular cells in response to low blood flow - angiotensinogen -> angiotensin I - angiotensin I --> angiotensin II (ACE) - Aldosterone - vasoconstriction - vascular/cardiac remodeling - sodium and water reabsorption
64
5 functions of the kidneys
1. Fluid balance, blood pressure 2. acid-base balance 3. hormones, aldosterone, renin (RAAS), vitamin D (active), urodilantin (diuretic) 4. excretion waste (urine)
65
Anatomy: Location of the Kidney
T12-L3 retroperitoneal cavity R kidney lower than L kidney (liver displaces)
66
Definition Nephron Measurement of nephron function
Nephron - functional unit of the kidney Glomerular filtration rate = number of functioning nephrons 1. Creatinine (muscle waste product) 2. Cystatin C (early kidney damage marker) 3. BUN (blood urea nitrogen)
67
Components of the Renal Corpuscle
Bowman's Capsule Glomerular capillaries Mesangial Cells (release cytokines, vasoconstriction to maintain RBF, phagocytosis)
68
3 Layers of the glomerular filtration membrane
1. Endothelial cells 2. Basement membrane (anionic charge, repels protein) 3. Epithelial cells (filtration slits) Selectively permeable 1. size 2. charge 3. hydrostatic pressure, oncotic pressure
69
Components of the Juxtaglomerular apparatus
1. Juxtaglomerular cells (produce renin, afferent arteriole) 2. Macula densa (sodium sensing cells, between afferent/efferent arteriole)
70
Components of the Nephron
1. Proximal convoluted tubule 2. Descending loop of henle (thick, thin) 3. Ascending loop of henle (thin, thick) 4. distal convoluted tubule 5. collecting duct
71
Function and cells Proximal convoluted tubule
Function - production of primary urine - reabsorption of solutes Brush boarder cells - microvilli, increase SA, reabsorption - Active reabsorption sodium, secretion hydrogen (Na/H pump) - water and urea passively reabsorbed (follow sodium) - cuboidal epithelial cells
72
FUnction and cells Descending loop of henle
Function - concentration and dilution of urine Cuboidal epithelial cells (THICK) - active reabsorption sodium - water passively follows Squamous epithelial cells (THIN) - no transport
73
Function and cells Ascending loop of henle
Impermeable to water Active transport sodium reabsorption
74
Function and cells Distal convoluted tubule
Function - Acid base balance - blood pressure Principle cells - production aldosterone - Na/K pump - reabsorption sodium, excretion potassium Intercalated cells - excretion hydrogen - reabsorption potassium (H/K pump) - reabsorption bicarbonate
75
Function Collecting duct
Function - reabsorption / excretion water - Aquaporins insert via ADH signal
76
Ureter Anatomy, cell type Function Referred pain location
Cell: smooth muscle, involuntary Function: connection renal pelvis to bladder, drain urine ; peristaltic contractions Referred pain: umbilicus (upper ureter), vulva/penis (lower ureter)
77
Bladder Anatomy Function
Anatomy 1. detrusor 2. trigone 3. internal spincter (all smooth muscle, involuntary) and external spincters (voluntary, SNS, skeletal muscle) Function 1. Micturition reflex (involuntary, PNS, mechanoreceptors stretch 300cc)
78
Regulation of renal blood flow (RBF)
1. Autoregulation 2. Hormones 3. Nervous system Autoregulation - mesangial cells - maintain GFR regardless of fluctuation blood pressure (normal range) Hormones 1. RAAS 2. natriuretic peptides 3. sympathetic nervous system (SNS) RAAS - renin released by juxtaglomerular cells (low BP, SNS) - angiotensin II (vasoconstriction systemic, vasoconstriction efferent arteriole, release ADH posterior pituitary) - aldosterone (reabsorption sodium, water) Natriuretic peptides 1. urodilantin - collecting ducts, release in response to stretch 2. ANP (aortic/carotid), BNP (ventricles), CNP (vascular endothelium) - released in response to stretch - vasodilation afferent arteriole - increase GFR and urination SNS - Release NE and E - bind to beta adrenergic receptors on juxtaglomerular cells, release renin - activation of the RAAS pathway
79
Stimuli that increases renin release
1. hypovolemia (detected at afferent arteriole, low RBF) 2. activation SNS and release of NE / E binding beta adrenergic receptors 3. prostaglandins (decrease renal blood flow) 4. low sodium at collecting duct
80
Define Net filtration pressure
1. hydrostatic pressure 2. oncotic pressure inside and outside the bowman capsule determines direction of filtrate
81
Diseases which decrease GFR
Increased Bowman capsule hydrostatic pressure - tumours - strictures - stones Increased plasma oncotic pressure - dehydration - vomitting - diarrhea - loss of water, blood becomes high concentration Loss of glomerular membrane - diabetes - sepsis
82
Renal hormones
1. Vitamin D - activates vitamin D (1, 25 dihydroxyvitamin D) - absorption calcium, excertion phsophate (GI and kidney) - bone health - CKD osteoporosis 2. erythropoetin (EPO) - bone marrow formation RBC - CKD anemia
83
Function plasma creatinine concentration
serial measurments differentiate chronic vs. acute kidney injury
84
Cystatin C function
early detection of decreased GFR
85
Urine chemistry
Bilirubin = dark orange urobilinogen = RBC hemolysis ketones = fat metabolism glucose = hyperglycemia sodium - increase or decrease with disease potassium - increase or decrease with disease protein - glomerular dysfunction, should be negative
86
Microscopic urine
1. bacteria 2. RBC 3. WBC 4. crystals (stones) 5. Fat (nephrosis) 6. casts
87

Year 1: Patho/Pharm (45 decks)

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