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ARCHIVED: Pathophysiology > Exam 3: Renal Pathophysiology > Flashcards

Exam 3: Renal Pathophysiology Flashcards

1
Q

Top two causes of renal failure:

A

Diabetes

HTN

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2
Q

Endocrine functions of kidneys:

A

EPO secretion

Vitamin D activation

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3
Q

Role of Vitamin D:

A

Cofactor for intestinal calcium absorption

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4
Q

Severe renal impairment occurs at this % of nephrone damage:

A

75-90%

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5
Q

Substances not reabsorbed from the tubules:

A

Urea

Creatinine

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6
Q

Substances partially secreted into the tubules according to body’s needs:

A

K+
Cl-
Na+

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7
Q

Substances completely reabsorbed in the proximal tubule:

A

Glucose
Proteins
Amino acids

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8
Q

HCO3- concentration in the filtrate drops at the ______ due to:

A

Distal tubule; switch to phosphate/ammonia buffers

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9
Q

Three aspects of tubuloglomerular feedback:

A
  1. Baroreceptors in the afferent arteriole inhibits renin when pressure is ↑
  2. Stimulation of β1 receptors causes renin release
  3. Macula densa sensing ↑ NaCl inhibits renin release
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10
Q

Glucose transporter on apical side of renal epithelium:

A

SGLT2

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11
Q

The point at which the tubule cannot reabsorb any further glucose is called:

A

Renal threshold

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12
Q

HCO3- is reabsorbed via this process:

A

Combines with H+ in the tubule to form H2CO3, which dissociates to CO2 and water, which can cross the membrane

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13
Q

Renal compensation for acidosis:

A

More H+ excretion

Forming HCO3- via glutamine metabolism

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14
Q

Renal compensation for alkalosis:

A

Excretion of filtered HCO3-

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15
Q

Electrolyte sequelae of renal compensation for acidosis and mechanism:

A

Hyperkalemia due to inhibition of the K+ out/H+ in pump on the apical membrane

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16
Q

Effects of ADH on the nephron:

A

Binds to V2 receptor on basolateral membrane; ↑cAMP activates aquaporin 2 which allows 3 H2O across the apical membrane

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17
Q

Diabetes insipidus is caused by:

A

Insufficient ADH

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18
Q

S/s of DI:

A

Large volumes of dilute fluid excreted into urine; severe fluid imbalanes

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19
Q

Nephrogenic diabetes insipidus is:

A

When collecting tubules are unresponsive to ADH

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20
Q

Three conditions that cause renin release:

A

↓ renal blood flow
↓ serum sodium
Activation of β1-adrenergic nerves

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21
Q

Condition for aldosterone and angiotensin II release:

A

Renin release

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22
Q

Condition for natriuretic peptide release:

A

Overstretch of atrial cells due to excess blood volume

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23
Q

Actions of natriuretic peptides:

A

Inhibits actions of angiotensin II

Loss of Na+ and water in urine

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24
Q

Condition for urodilatin release:

A

Distal/collecting tubule identify increased circulating volume

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25
Q

Actions of urodilatin:

A

Similar to natriuretic peptides; inhibit Na+/H2O reabsorption

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26
Q

How do ACE inhibitors act as diuretics?

A

Inhibit formation of angiotensin II and aldosterone, which work to retain water

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27
Q

How do loop diuretics work?

A

Block the Na+/K+/2Cl- pumps in the aloH

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28
Q

How do thiazide diuretics work?

A

Block Na+ reabsorption

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29
Q

Types of potassium-wasting diuretics:

A

Osmotic
Loop
Thiazide

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30
Q

Types of potassium-sparing diuretics:

A

Aldosterone-blocking agents

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31
Q

Most useful lab studies to evaluate kidney function:

A

Urinalysis
Serum creatinine
BUN
GFR tests

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32
Q

24-hour urine sample good for:

A

Evaluating substances that are secreted in varying amounts throughout day

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33
Q

Abnormal urine odor:

A

Ammonia smell (due to bacteria)

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34
Q

Normal color in urine is due to:

A

Urochrome pigments

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35
Q

Brown or bright red urine is due to:

A

RBCs (hematuria)

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36
Q

Cloudy urine is due to:

A

WBCs (infection)

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37
Q

Dark yellow or orange urine is due to:

A

Concentration

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38
Q

Excess epithelial cells in the urine indicate:

A

Inflammation/injury in the nephron (cells sloughing off lining of tubule)

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39
Q

WBC casts in the urine are associated with:

A

Renal infections (pyelonephritis)

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40
Q

RBC casts in the urine are associated with:

A

Inflammation of the glomerulus (glomerulonephritis)

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41
Q

Epithelial casts in the urine are associated with:

A

Sloughing of tubular cells (acute tubular necrosis)

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42
Q

Normal creatinine level:

A

0.7 to 1.5 mg/dl

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43
Q

Elevated creatinine indicates:

A

Increased rate of muscle breakdown or decrease in renal function

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44
Q

Urea is:

A

An end product of protein metabolism that’s excreted primarily by the kidney

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45
Q

Normal urea level:

A

10-20 mg/dl

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46
Q

Elevated urea level indicates:

A

Decrease in renal function or fluid volume

Increased catabolism/dietary protein intake

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47
Q

Most accurate way to measure GFR:

A

Inulin clearance test

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48
Q

Define azotemia:

A

Elevation of BUN/Cr levels, related to decrease in GFR

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49
Q

Define uremia:

A

Elevation of urea in blood

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50
Q

Define pyuria:

A

Presence of leukocytes in urine

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51
Q

Five categories of intra-renal disorders:

A 
Congenital
Neoplastic
Infectious
Obstructive
Glomerular
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52
Q

Describe pain caused by intrarenal d/o:

A

Felt at CVA
Dull, constant character
May be felt through out T10-L1 dermatomes

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53
Q

Agenesis is:

A

Lack of kidney development in fetus

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54
Q

Bilateral vs. unilateral agenesis:

A

Bilateral: not compatible with life
Unilateral: functional kidney hypertrophies to compensate

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55
Q

Hypoplasia can lead to:

A

Pediatric ESRD if severe enough

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56
Q

Two types of cystic kidney disease and the population they present in:

A

Autosomal recessive: kids
Autosomal dominant: adults

ADults

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57
Q

Genes involved in autosomal dominant cystic kidney diseases:

A

Chromosome 16 –> PKD1 (85%!)

Chromosome 4 –> PKD2

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58
Q

Role of PKD1:

A

Supports Ca2+ channel in renal epithelium

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59
Q

Role of PKD2:

A

Codes for the Ca2+ channel involved

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60
Q

Pathogenesis of cystic kidney disease:

A

↓ Ca2+ in cell and ↑ cAMP leads to cysts and reduction of kidney function

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61
Q

Extra-renal impacts of cystic kidney disease:

A

Other organs (esp. liver) can have cysts

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62
Q

S/s of cystic kidney disease:

A

↓ GFR
Inability to concentrate urine
HTN
Pain (most common)

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63
Q

Dx of cystic kidney disease:

A

Genetic hx and ultrasonography

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64
Q

Tx of cystic kidney disease:

A

Supportive; BP control and managing renal failure

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65
Q

Parts of the kidney affected by renal cell carcinoma:

A

Cortex

PCT

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66
Q

Risk factors for renal cell carcinoma:

A

Smoking
Obesity
HTN
Family hx

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67
Q

S/s of renal cell carcinoma:

A

Asymptomatic until advanced
CVA tenderness
Hematuria
Palpable mass

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68
Q

Tx of renal cell carcinoma:

A

Nephrectomy

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69
Q

Metastases of renal cell carcinoma are:

A

Resistant to radiation, immunotherapy, chemotherapy

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70
Q

Physiological protective measures against renal infection:

A

Acidic pH
Urea present in urine
Secretions (men: prostatic, women: urethral)
Unidirectional urine flow

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71
Q

Most common cause of acute pyelonephritis:

A

Ascending infection from lower urinary tract

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72
Q

Dx of acute pyelonephritis:

A

WBC casts in urine

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73
Q

Tx of acute pyelonephritis:

A

Prompt abx

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74
Q

Pathogenesis of chronic pyelonephritis:

A

Reflux or obstructive process –> urine stasis

Chronic inflammation causing scarring/nephron damage

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75
Q

S/s of chronic pyelonephritis:

A

Abdominal/flank pain
Fever
Malaise
Anorexia

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76
Q

Dx of chronic pyelonephritis:

A

Renal imaging

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77
Q

Tx of chronic pyelonephritis:

A

Correct the underlying process

Extended abx tx

78
Q

Common causes of obstructive renal disease:

A

Stones (most common)
Tumors
Prostatic hypertrophy
Strictures of ureters/urethra

79
Q

Sequelae of complete obstruction:

A 
Hydronephrosis
↓ GFR
Ischemic kidney damage d/t ↑ intraluminal pressure
Acute tubular necrosis
Chronic kidney disease
80
Q

Most renal calculi are composed of:

A

Calcium crystals

81
Q

Non-calcium stones made of:

A

Uric acid
Struvite
Cystine

82
Q

S/s of renal calculi:

A

Intense, abrupt, radiating renal colic pain
N/V
Diaphoresis
Hematuria

83
Q

Dx of renal calculi:

A

CT scan

84
Q

Tx of renal calculi:

A 
Fluids (> 2L/day)
Lithotripsy/endoscopy
Ureteral stenting
Ureteroscopy
Pain medication!!
Dietary changes depending on type of stone
85
Q

Three types of glomerular cells:

A

Endothelial
Mesangial
Podocytes

86
Q

Primary vs. secondary glomerular disorders:

A

Primary: only the kidney involved
Secondary: results from other diseases, conditions, meds

87
Q

Secondary glomerular disorders:

A

Goodpasture syndrome
Systemic lupus erythematosus
Diabetic nephropathy

88
Q

Goodpasture syndrome in the kidney:

A

Antibodies vs. the glomerular basement membrane (also affects lungs)

89
Q

Systemic lupus erythematosus in the kidney:

A

Antibody complexes settle into the mesangial region of the glomerulus

90
Q

Diabetic nephropathy pathogenesis:

A

Glucose binds to protein and complex sticks to endothelial cells, causes damage

91
Q

Three ways to classify glomerular disorders:

A

Diffuse vs. focal (all vs. some glomeruli)
Global vs. segmental (all vs. some parts of glomeruli)
Membranous vs. sclerotic (thickening of capillaries vs. scarring)

92
Q

Three sites of deposition in glomerular disorders:

A

Mesangial (SLE)
Subendothelial
Subepithlial (Goodpasture)

93
Q

S/s of glomerular disorders:

A 
Hematuria
Proteinuria** (classical)
Abnormal casts
↓ GFR
Edema
HTN
94
Q

Nephrotic syndrome characterized by:

A

Protein loss in urine: 3 - 3.5gm in 24 hrs

95
Q

Nephritic syndrome characterized by:

A

Mild to moderate proteinuria, hematuria, RBC casts (nephrotic syndrome + inflammation)

96
Q

Glomerulonephritis is:

A

An immune response to a variety of triggers that produces inflammation in the glomeruli

97
Q

Glomerulonephritis is more common in:

A

Men

98
Q

Pathogenesis of acute glomerulonephritis:

A

Immune cells are attracted to inflammation in glomeruli, resulting in lysosomal degradation of the basement membrane

99
Q

GFR falls in acute glomerulonephritis due to:

A

Contraction of the mesangial cells –> decreased area for filtration

100
Q

S/s of acute glomerulonephritis:

A 
Proteinuria
Oliguria
Azotemia
Edema
HTN
101
Q

Tx for acute glomerulonephritis:

A

Steroids
Plasmapheresis
Dietary, fluid mgmt
HTN mgmt

102
Q

Pathogenesis of postinfectious acute glomerulonephritis:

A

Infectious agent causes antibody-antigen deposition (IgG) in the glomerulus –> proliferation of mesangial cells –> lesions

103
Q

Infections that lead to postinfectious acute glomerulonephritis:

A

Impetigo and throat infections with group A β-hemolytic strep

104
Q

Group in which postinfectious acute glomerulonephritis typically is found:

A

Children in developing countries

105
Q

S/s of postinfectious acute glomerulonephritis:

A

Smoky or coffee-colored urine

106
Q

Pathogenesis of IgA nephropathy (Berger disease):

A

Post-URI or GI viral infection, IgA complex deposition in mesangial cells –> mesangial injury

107
Q

S/s of IgA nephropathy (Berger disease):

A

Proteinuria

Hematuria in 1-2 days

108
Q

Typically IgA nephropathy (Berger disease) is seen in:

A

Adults

109
Q

Difference between post-infectious and IgA nephropathy (Berger disease) glomerulonephritis:

A

Post-infectious: IgG, will see edema and HTN

Berger: IgA, NO edema/HTN

110
Q

Pathogenesis of chronic glomerulonephritis:

A

Progressive course of proliferative, membranous lesions (glomeruli replaced with collagen)
Sclerosis/fibrosis of kidney

111
Q

S/s of chronic glomerulonephritis:

A

Proteinuria
-/+ hematuria
Slowly declining renal fxn

112
Q

Tx of chronic glomerulonephritis:

A

Supportive interventions (fluid mgmt, etc) until dialysis/transplant necessary

113
Q

Pathogenesis of nephrotic syndrome:

A

Increased glomerular permeability to proteins; proteinuria leads to hypoalbuminemia; edema occurs d/t ↓ osmotic pressure in blood

114
Q

Causes of nephrotic syndrome:

A

Minimal change disease
SLE
DM

115
Q

S/s of nephrotic syndrome:

A

Proteinuria
Edema** (most common)
HLD, hypercoag d/t ↑ liver fxn (due to ↓ albumin)

116
Q

Tx of nephrotic syndrome:

A

Diuretics
Lipid-lowering agents
AntiHTNs
Immunosuppression/modulation

117
Q

Pathogenesis of minimal change disease:

A

Triggered by allergic or immune condition

Foot processes of glomerular podocytes fuse together; decreased production of basement membrane anions

118
Q

S/s of minimal change disease:

A

Edema
Nephrotic levels of proteinuria
Hypoalbuminemia

119
Q

Tx of minimal change disease:

A

Corticosteroids

120
Q

Acute renal failure is:

A

Sudden reduction in kidney function

121
Q

ARF causes:

A

Fluid/lyte/acid-base imbalances
Retention of waste products
↑ serum Cr
↓ GFR

122
Q

Causes of pre- vs. intra- vs. post-renal:

A

Pre: ↓ renal perfusion
Intra: parenchymal renal disease
Post: obstruction

123
Q

How can BUN/Cr be used to dx cause of ARF?

A

Only if BUN is elevated - ratio will determine location of cause

124
Q

Normal BUN/Cr ratio:

A

10-20

125
Q

Normal BUN:

A

8-10 mg/dl

126
Q

Normal Cr:

A

0.6 - 1.2 mg/dl

127
Q

BUN/Cr ratio > 20 indicates:

A

Pre-renal ARF; urea has more time to be reabsorbed

128
Q

Bun/Cr ratio < 10 indicates:

A

Intra-renal ARF; tubules failing, reabsorbing less urea

129
Q

Bun/Cr ratio 10-20 indicates:

A

Post-renal ARF

130
Q

BUN and creatinine are each handled in the nephron in this fashion:

A

BUN: filtered in glomerulus, reabsorbed by tubule
Cr: filtered in glomerulus, secreted in filtrate

131
Q

Causes of prerenal ARF:

A

Any sudden/severe drop in BP or interruption of blood flow

Hypovolemia, HoTN, heart failure
Renal artery obstruction
Fever/vomiting/diarrhea
Burns
Diuretics, edema, ascites
132
Q

Drugs that can cause prerenal ARF:

A

ACE inhibitors, angiotensin II blockers, NSAIDs

133
Q

Low GFR in prerenal ARF leads to:

A

Oliguria
High urine SG/osmolarity
Low urine Na+
Azotemia

134
Q

Prolonged prerenal ARF leads to:

A

Acute tubular necrosis

135
Q

Tx of prerenal ARF:

A

Improve renal perfusion via fluid replacement or dialysis

136
Q

Pathogenesis of post-renal ARF:

A

Obstruction distal to the kidney causes elevated pressure all the way back to the Bowman capsule which impairs glomerular filtration

137
Q

Prolonged post-renal ARF leads to:

A

Acute tubular necrosis and irreversible kidney damage

138
Q

Early phase of post-renal ARF:

A

Reflex adaptation to maintain GFR: afferent arteriole dilation
Lasts 12-24 hours

139
Q

Late phase of post-renal ARF:

A

Afferent arteriole dilation ceases after 12-24 hours
Renal perfusion, glomerular blood flow, and GFR drop
Oliguria/anuria
Ischemia/nephron loss

140
Q

Recovery phase of post-renal ARF:

A

Pre-renal vessels relax
Perfusion restored
GFR increases in surviving nephrons
Dilation may be permanent!

141
Q

Causes of acute tubular necrosis:

A 
Nephrotoxic insults (contrast media)
Ischemic insults (sepsis)
142
Q

Vascular pathogenesis of intrarenal ARF:

A

Renal blood flow decreases –> hypoxia, vasoconstriction

143
Q

Tubular pathogenesis of intrarenal ARF:

A

Inflammation/reperfusion injury –> casts, obstruction of flow, tubular backleak

144
Q

Three phases of ATN:

A

Prodromal phase
Oliguric phase
Post-oliguric phase

145
Q

Prodromal phase of ATN:

A

Insult to the kidney has occured

146
Q

Oliguric phase of ATN:

A

~1-2 weeks (up to 8 weeks)
UOP 50-400 ml/day
Progressive uremia
Decreased GFR/hypervolemia

147
Q

Post-oliguric phase of ATN:

A 
Diuresis
Impaired tubular function
Azotemia
Fluid volume deficit until recovery
2-10 days, up to 1 year
148
Q

Prognosis for acute renal failure:

A

Good in otherwise healthy patients if underlying issue is corrected

149
Q

Predictors of mortality from ARF:

A

Oliguria, severe illness, MI, stroke, seizure, immunosuppression, mechanical ventilation

150
Q

Progression of chronic renal failure:

A

Chronic kidney disease –> chronic renal failure –> end-stage renal disease

151
Q

CRF stage which requires dialysis:

A

ESRD

152
Q

Comorbidities linked to CRF:

A

HTN, DM

153
Q

Definition of CRF:

A

Kidney damage/impairment of 3 months or more

GFR < 60 for 3+ months

154
Q

Kidneys compensate until this % of damage:

A

75-80%

155
Q

Stage 1/2 CRF:

A

Minimizing risk factors

156
Q

Stage 3 CRF:

A

Symptoms appear, tx may be needed

157
Q

Stage 4 CRF:

A

Plan for dialysis/transplant

158
Q

Stage 5 CRF:

A

Renal replacement tx needed for survival

159
Q

Role of angiotensin II in renal injury:

A

Vasoconstriction increases GFR

160
Q

Pathogenesis of CRF:

A

Renal injury –> loss of nephrons, vasoconstriction from angiotensin II

Glomerular capillary hypertension, over time, leads to increased permeability/filtration

Proteinuria, increased protein reabsorption

Tubular/interstitial inflammation, fibrosis, scarring

Creates systemic HTN which worsens glomerular capillary HTN

161
Q

Risk factors for CRF:

A 
DM
HTN
Pyelonephritis (recurrent)
Glomerulonephritis
Polycystic kidney disease
Family hx
Toxin exposure
Age > 65
162
Q

Management of CRF:

A

BG control
ACEIs or ARBs to reduce proteinuria
Management of HTN

163
Q

Management of metabolic acidosis:

A

Mild (7.3 to 7.35) no tx

< 7.3 may take NaHCO3

164
Q

CV effects of CRF:

A

Hypervolemia/HTN
Atherosclerosis
Heightened RAAS/SNS activity

165
Q

Metabolic effects of CRF:

A

Uremic syndrome/impaired healing
Hyperkalemia
Metabolic acidosis

166
Q

Electrolyte imbalances in CRF:

A

Hyperkalemia
Hypermagnesemia
Hyperphosphatemia

167
Q

Bone/mineral disorders from CRF:

A

Elevated phos/PTH causes altered bone metabolism

Kidneys unable to reabsorb calcium

168
Q

Hematological effects of CRF:

A

Lack of EPO –> anemia
Uremia shortens RBC lifespan
Blunted immune response

169
Q

Primary reason to initiate dialysis in CRF:

A

Uremia or hyperkalemia unresponsive to other txs

170
Q

Pathogenesis of renal-related HTN:

A

Renin release by injured kidney -or- hypervolemia due to renal mishandling of sodium

171
Q

Pulmonary impacts of CRF:

A

Chronic pulmonary edema

172
Q

Micturition mediated by:

A

Pons
Gravity/pressure
Peristalsis
CNS

173
Q

Pons’ role in micturition:

A

Relaxation of internal sphincter

Contraction of bladder

174
Q

Cerebral cortex’s role in micturition:

A

Inhibition via conscious control of external sphincter

175
Q

ANS role in micturition:

A

SNS: L1-2 allow relaxation and filling
PSNS: S2-4 cause bladder contraction, relaxation of internal sphincter

176
Q

Incontinence is normal when:

A

Never!

177
Q

Urge incontinence is:

A

Involuntary leakage along with/after feeling the need to void

178
Q

Causes of urge incontinence:

A 
Bladder infection
Radiation tx
Tumors
Stones
CNS dmg
Idiopathic
179
Q

Causes of stress incontinence:

A

Weakening of pelvic muscles or urethral sphincter deficiency

180
Q

Causes of overflow incontinence:

A

Obstruction of urethra

Under/inactive detrusor

181
Q

Types of enuresis:

A

Primary nocturnal enuresis
Secondary enuresis: after 6 mo dry
Monosymptomatic nocturnal enuresis: no other signs of lower UTI malfunction
Nonmonosymptomatic nocturnal enuresis: urgency/frequency/daytime incontinence as well

182
Q

Pathogenesis of enuresis:

A

ADH deficiency
Overactivity of destrusor
Immature arousal mechanisms

183
Q

Manifestations of vesicoureteral reflux:

A

Recurrent UTI
Voiding dysfunction
Renal insufficiency
Hypertension in children

184
Q

Ureterocele is:

A

Cystic dilation at distal end of ureter

185
Q

Manifestations of ureteroceles:

A 
Hydronephrosis
UTIs
Voiding dysfunction
Hematuria
Urosepsis
Failure to thrive
186
Q

Tx of ureterocele:

A

Surgical intervention

187
Q

Most cases of cystitis are from:

A

Infection originating in urethra

188
Q

Common minerals that make urinary tract stones:

A

Calcium
Oxalate
Phosphate
Uric acid

189
Q

Effect of dietary calcium on kidney stones:

A

Prevents them via binding of oxalate

190
Q

Endocrine dysfunction associated with kidney stones:

A

Hyperparathyroidism

191
Q

Effect of hydronephrosis on kidney structure:

A

Dilation of pelvis/calyces

Thinning of renal parenchyma

ARCHIVED: Pathophysiology (18 decks)

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