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Patho > Renal > Flashcards

Renal Flashcards

1
Q

What happens to TBW percentage through life

A

Highest in infancy, decreases with age

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2
Q

How osmotic diuretics work

A

Increase osmolality of filtrate, cause more water to remain in tubule which is excreted

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3
Q

How loop diuretics work

A

Block na k 2 cl pumps in ascending loop of henle

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4
Q

How thiazide diuretics work

A

Block na reabsorption, can act on na k atpase pump

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5
Q

How potassium diuretics work. Examples

A

K excreted in urine. Na reabsorption through na pump on na k atpase. Osmotic, ace inhib, loop, and thiazide like

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6
Q

How potassium sparing diuretics work And example

A

Aldosterone blocking. Na pump on apical side DCT.

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7
Q

Infants: why they are renal impaired. Predisposed to what.

A

GFR low postnatal period. Kidney reduced ability to make concentrated urine, predisposed to volume depletion in fluid losses.

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8
Q

When kidney function declines in adults, what happens

A

Diminish in size and function starting 40s, then significantly by mid 60s

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9
Q

What happens to geriatric kidneys. 4. More susceptible to what

A

Loss of nephrons, diminished renal BF, decreased GFR, dec ability to conserve salt and h20. Susceptible to fluid and electrolyte imbalances and renal damage

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10
Q

What normal odor in urine caused by vs abdnormal

A

Normal: slight d/t breakdown of urea to ammonia. Diff foods.
Abn: bacteria and standing for long periods of time

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11
Q

Osmolality and specific gravity. What should and should not happen throughout the day

A

They SHOULD vary. Fixed= possible renal impairment

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12
Q

WBC casts associated with what

A

Renal infections, pyelonephritis

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13
Q

RBC casts associated with what

A

Inflammation of glomerulus, glomerulonephritis

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14
Q

Epithelial casts indicate what

A

Sloughing of tubular cells, acute tubular necrosis

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15
Q

Is bun or creatinine more reliable

A

Serum Creatinine

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16
Q

What is creatinine

A

End product of muscle metabolism excreted by kidney

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17
Q

What 2 factors is creatinine affected by

A

Rate created by muscle (constant in absence of muscle breakdown).
Rate excreted by kidney, determined by GFR

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18
Q

Relationship between GFR and plasma creatinine

A

Inversely related

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19
Q

What is urea. Elevated level indicated what

A

End product of protein metabolism excreted mainly by kidney

Decrease in renal func/fluid volume, inc in catabolism and dietary protein intake

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20
Q

What are 2 ways of measuring GFR

A 
Creatinine clearance (not completely accurate)
Inulin clearance (more accurate)
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21
Q

Azotemia

A

Elevation of BUN and creat. R/t decrease in GFR. Associated with many renal diseases.

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22
Q

Uremia

A

Elevated urea in blood. Sign of failing excretory system and other metabolic and endocrine abn

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23
Q

Proteinuria/albuminuria

A

Inc protein in urine. D/t leaky glomerular filtration barrier and/or nephron abn

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24
Q

Pyruria

A

Leakocytes in urine

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25
Q

Asymptomatic hematuria or proteinuria sign of what

A

Mild glomerular abnormalities

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26
Q

UTI charac by what

A

Bacteriuria and pyuria. May be symptomatic or not, affects kidneys or bladder

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27
Q

Nephrolithiasis. Manifested by what

A

Renal stones. Renal colic, hematuria, recurrent stone formation

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28
Q

Nephralgia. Felt where

A

Kidney and renal pain

Costovertebral angle, recorded as CVA tenderness or flank pain

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29
Q

Nephralgia d/t what

A

Distension and inflammation of renal capsule. Dull and constant.

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30
Q

Pain transmitted where and by what in nephralgia

A

T10 and L1 by sympathetic afferrent neurons. May be felt throughout dermatomes.

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31
Q

What dark, strong smelling urine indicates

A

Decreased renal function

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32
Q

What cloudy pungent urine indicates

A

Infectious process

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33
Q

Agenesis: 2 types and implications

A

Congenital disorder, kidneys dont develop as fetus
Bilateral: not compatible w life
Unilateral: compensatory hypertrophy of 1 kidney

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34
Q

Hypoplasia

What it is. Can lead to what.

A

Some fetal kidney development. Pediatric ESRD

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35
Q

Hypoplasia
Single normal kidney can what
Requires what

A

Maintain normal renal function. Lifelong kidney monitoring

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36
Q

Dont tend to see kidney symptoms in failure until what

A

1 million nephrons per kidney roughly. Symptoms when down to 40% nephrons left

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37
Q

Cystic kidney diseases

How you get them, 2 types

A

Genetic. Autosomal recessive and autosomal dominant forms

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38
Q

Cystic kidney diseases

What can happen in them. Can lead to what

A

Cysts Expand and disrupt urine formation/flow. 1 or both kidneys. Can lead to renal failure, dialysis, or transplant need

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39
Q

Autosomal dominant types of cystic KD

Chromosome, which is most common

A

Chromosome 16 PKD1 (85%), Chromosome 4 PKD2

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40
Q

Cystic kidney disease
What happens on cellular level
What happens to other organs

A

Reduced intracellular calcium and increased intracellular cAMP
Can also develop cysts, esp liver

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41
Q

Manifestations of cystic KD: 3, most common

A

Htn, pain most common, cystic liver involvement

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42
Q

Dx and tx cystic KD

A

DX: genetic hx and ultrasound
Tx: control BP, manage assoc pathologies, dialysis in ESRD

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43
Q

Process of what cystic KD does to body

A

Inability to form urine leads to fluid buildup in systemic vasculature which leads to htn and pain

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44
Q

Renal cell carcinoma
Where it hits
RFs

A

Clear cells, cortex or PCT

Familial, smoking, obesity, htn

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45
Q

Renal cell carcinoma

Symptoms

A

Asymptomatic until advanced. And then CVA tenderness, hematuria, palpable mass

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46
Q

Renal cell carcinoma
Tx
Mets are what

A

Nephectomy. Mets may be resistant to radiation, immunotherapy, and chemo d/t location

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47
Q

Common areas of kidney mets 4

A

Lung, heart, liver, bone

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48
Q

Stage 1-4 renal cell carcinoma involvement

A

1- tumor in capsule. 2- tumor in perirenal fat. 3-tumor extends to renal vein or regional lymphatics

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49
Q

Protective mechanisms against infection 4 main

A

Acidic pH. Urea in urine. Micturition washes pathogens out. Unidirectional flow prevents reflux

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50
Q

Men vs women protective mechanisms

A

M- bacteriostatic prostatic secretions

W- glands in distal urethra secrete mucous

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51
Q

Most common form of pyelonephritis

A

Ascending infection from lower urinary tract (e coli, proteus, enterobacter)

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52
Q

Descending pyelonephritis cause

A

Staph or E. coli. Blood infection that hits kidney from aorta

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53
Q

Acute pyelonephritis
Where it hits and how
Low risk when

A

Renal pelvis and parenchyma. Ascending UTI. Low risk if decreased function

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54
Q

Urosepsis

A

Organisms in blood that originate from a UTI

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55
Q

Acute pyelonephritis
Dx
Tx

A

WBC casts indicative of upper UTI

Abx to avoid decreased renal func

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56
Q

Predisposing factors acute pyelonephritis

A

Calculus, anomalies of kidney or ureter, obstruction in any level, DM, pregnancy, neurogenic bladder, instrumentation

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57
Q

Chronic pyelonephritis
Can result in
Usually assoc with what
Process

A

CKD.
Reflux or obstruction leads to urine stasis.
Chronic inflammation causes scarring and nephron loss

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58
Q

Chronic pyelonephritis
CM
Dx
Tx

A

Abd/flank pain, fever, malaise, anorexia
Renal imaging
Correct underlying process, extend abx

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59
Q

Obstruction causes what to renal tract

A

Urine stasis- infection and structural damage

Dilation of proximal tract

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60
Q

Common causes of obstruction 4. Most common

A

Stones most common. Also tumors, prostatic hypertrophy, and strictures of ureters or urethra

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61
Q

Complete obstruction results in what: 5

A

Hydronephrosis, decreased GFR, ischemic kidney damage d/t inc intraluminal pressure, acute tubular necrosis, CKD

62
Q

Stone formation d/t what, what is required

A

Solute supersaturation required. Low urine volume, abnormal urine pH

63
Q

Stone composition, mostly what

A

Mostly calcium. Also uric acid, struvite, cystine, assoc w meds

64
Q

Symptoms w kidney stones

A

Stationary- usually none. Mobile causes abrupt renal colic that radiates, N/V diaphoresis, hematuria

65
Q

Renal calculi
Tx
Stones tend to what

A

> 2L/day fluids, lithotripsy or endoscopic approaches, stunting, ureteroscopy. Pain meds.
Recur, fluid intake helps and diet changes

66
Q

Factors in glomerulopathies: 6

A

Hereditary or environmental. Metabolic, infectious, hemodynamics, toxic, genetic, injuries

67
Q

Primary glomerolopathy

A

Only kidney involved

68
Q

Secondary glomerulopathy causes: 3

A

Results from other conditions. Goodpasture syndrome, SLE, diabetic nephropathy

69
Q

Classifications of glomerulopathies based on glomeruli/cells
Diffuse v focal
Global v segmental
Membranous, sclerotic

A

Diffuse (all glomeruli) focal (some glomeruli)
Global (all pts of glomerulus, cells) segmental (thickening of glomerular capillary walls) membranous (thickening of capillary walls) sclerotic (scarring)

70
Q

Glomerular disorders
Sites of deposition: 3
Classical CM

A

Mesangial, subendothelial, subepithelial

Proteinuria

71
Q

Glomerular disorders

Result in some combo of: 6 issues

A

Hematuria, proteinuria, abn casts, decreased GFR, edema, htn

72
Q

Nephrotic syndrome

A

Glomerular disorders, extreme loss of protein per 24h

73
Q

Nephritic syndrome

What it is and what shows in urine

A

Glomerular disorder, reflection of inflammation in glomerulus. Mild-moderate proteinuria, hematuria and rbc casts present in sediment

74
Q

What you do not see in nephrotic syndrome vs nephritic

A

Blood/rbc casts in urine. Nephrotic is worse d/t necrosis.

75
Q

Nephrotic system
Due to what
Proteinuria leads to what 3 things

A

Increased glomerular permeability to proteins

Hypoalbuminemia, generalized edema, decreased blood colloid osmotic pressure

76
Q

Nephrotic syndrome
3 things that cause it
Most common finding

A

Minimal change disease, SLE, DM

Edema

77
Q

Nephrotic syndrome

Can inc activity of which organ and leads to what 2 things if so

A

Liver. Hyperlipidemia and hypercoagulability

78
Q

Nephrotic syndrome
Tx 4
Leads to what

A

Diuretics, lipid lowering agents, antihypertensives, immunosuppresion/modulation
ESRD or resolves spontaneously

79
Q

In glomerular disorders stimulation of which system worsens condition

A

RAA stim (from decrease BV from less albumin pulling blood in vessels) leads to worsening edema

80
Q

Minimal change disease
What happens
Occurs in who

A

Lipoid nephrosis. Alt of glomerular podocytes that fuse together. Dec production of anions of GBM
Children

81
Q

Minimal change disease
Initiated by what
Onset of 3
Tx

A

Allergic or immune condition that decreases glom filt
Edema, protein loss, hypoalbuminemia
Corticosteroids

82
Q

Glomerulonephritis
More common in who
Acute caused by what

A

Men
Attraction of immune cells to inflammation, lysosomal degradation of basement membrane. GFR may fall from mesangial cell contraction

83
Q

Glomerulonephritis
CM: 5
TX: 3

A

Proteinuria, oliguria, azotemia, edema, htn

Steroids, plasmapheresis, diet/fluid/htn management

84
Q

What causes membraneous nephropathy

A

Idiopathic, we dont know

85
Q

Difference between granular and linear glomerular disorders

A

Granular- immune complex deposition, wall attacked. Antigen not related to glomerulus
Linear- antibodies interacting spec w antigens on glomerulus, in bm of nephron, directly attacks it

86
Q

Acute glomerulonephritis
Process
Follows which 2 infections

A

Infectious agent= antigen, antigen-antibody deposition, IgG, prolif of mesangial cells
Impetigo and throat infections

87
Q

Acute glomerulonephritis
What kind of disease
Usually in who, urine color

A

POSTINFECTIOUS*

Children, smoky/coffee colored urine

88
Q 
Acute glomerulonephritis 
Berger disease
-how its diff from postinfectious 
-common in who 
-causes 2
A

IgA nephropathy (IgG) in other
Adults
URI or GI viral infections

89
Q

Berger disease
Symptoms, what isn’t evident
Prognosis

A

Hematuria, proteinuria. Edema and HTN= NOT evident

Variable, could be ESRD

90
Q

Chronic glomerulonephritis
What happens to kidney
What fixes it

A

Sclerosis and fibrosis. Proteinuria +/- hematuria.

Dialysis or transplant

91
Q

What happens overall in ARF 4

A

Fluid, electrolyte, and acid base disruption. Retain nitrogen waste, increased serum creat, and decreased GFR

92
Q

ARF isn’t what, is what

A

Not a disease, final pathway of other processes

93
Q

Causes of pre renal ARF

A

Sudden drop in BP (shock) or BF interruption to kidneys from injury or illness

94
Q

Causes of intrarenal ARF

A

Direct damage to kidneys from inflammation, toxins, drugs, infection, or reduced blood supply

95
Q

Causes of postrenal ARF

A

Obstruction of urine flow d/t enlarged prostate, kidney stones, bladder tumor, or injury

96
Q

In ARF if what is elevated, it is diagnostic of the cause

A

BUN : Creatinine

97
Q

Urea and creatinine are filtered in glomerulus but ___ reabsorbed and ___ secreted

A

Urea, creatinine

98
Q

In ARF
bun: creat >20=
Bun:creat <10=
10-20=

A

Pre-renal. Both decreased filtration, urea >time to be reabsorbed
Intra-renal, tubules failing and absorb less urea
Post renal. Both equally affected

99
Q

Causes of pre renal ARF

A

Hypovolemia, hypotension, HF, renal artery obstruction, fever, vomiting, diarrhea, burns, overuse diuretics, edema, ascites
Drugs: ACEIs, ang II blockers, NSAIDS

100
Q

Pre renal ARF
Low GFR leads to what in urine
Prolonged, this leads to what

A

Oliguria, high spec gravity and osmolality, low urine Na, azotemia
Acute tubular necrosis

101
Q

Pre renal ARF tx

A

Volume replacement and dialysis

102
Q

Post renal ARF early phase

A

Reflex adaptation to maintain GFR. Afferrent arteriole dilation enhances perfusion. 12-24h

103
Q

Post renal ARF late phase

A

After 12-24h. Vasodilation stops. Fall in GFR and glomerulus BF. May have anuria. Leads to ischemia and nephron loss

104
Q

Post renal ARF recovery phase

A

After relief of obstruction. Pre renal vessels relax, perfusion restored, GFR restored in surviving nephrons. Dilation of calyces and collecting system may remain forever.

105
Q

Intra renal ARF

Causes

A

Dysfunc nephrons themselves. Results in ATN from nephrotoxic insult (contrast) or ischemia (sepsis). Renal bf decreased leading to hypoxia and vasoconstriction. Tubular: inflam and reperfusion injury, casts, obstructs flow, backleak in tubules.

106
Q

2 causes ATN

A

Tubular (cast obstruction, tubular backleak, etc) or vascular (vasoconstriction, RAA)

107
Q

Lab tests finding pre renal AKI

A

FENa <1. No protein. Spec gravity and osmolality high. BUN/Creat high. Low urine Na, low sediments

108
Q

Lab tests intrarenal AKI

A

High FENa. May have proteinuria. Normal spec gravity and osmolality and bun/cr. Urine na conc high, casts in urine.

109
Q

ATN first phase

A

Prodromal. Insult to kidney occurs

110
Q

ATN second phase

A

Oliguric. Up to 8 weeks, 50-400 UOP/day. Progressive uremia and decreased GFR, hypervolemia. S/s fluid excess, hyperkalemia, uremic syndrome. May need dialysis

111
Q

ATN last phase

A

Post oliguric. Diuresis, tubular func impaired, azotemia continues. Fluid vol deficit until kidneys recover. 2-10 days, full recovery 1 yr when bun and creat normal

112
Q

ATN
Prognosis
When creat normal
Better prognosis for who

A

Good if otherwise healthy and insult corrected.
1-3 weeks
Non icu

113
Q

ATN predictors of mortality

A

Oliguria, severely ill, MI, stroke, seizure, immunosuppresion, need for mechanical ventilation

114
Q

CKD
Linked w which diseases
Definition

A

DM and HTN.
Kidney damage of 3 months based of tests. GFR <60 ml/min/1.73 m2 for 3 months w/o indication of damage to kidney (dont need to mem number)

115
Q

CKD

Overall what happens

A

Progressive and irreversible. Kidneys compensate until 75% nephron loss.

116
Q

CKD stage 1, stage 5

A

1- minimizing RF

5- renal replacement therapy needed or will die

117
Q

RF CKD

A

DM, HTN, recurrent pyelonrephritis, glomerulonephritis, polycystic kidney disease, fam hx CKD, history of exposure to toxins, >65 y/o, ethnicity

118
Q

CKD

Focus on what for tx

A

Manage ATN, BG control in DM, ACEIs or ang 2 blockers to reduce proteinuria, manage HTN

119
Q

CKD w/htn or cv disease

Treatment focus

A

ACEI and ANGII blocker

120
Q

CKD when bicarb admin

A

PH <7.3 chronically

121
Q

CKD

Electrolyte imbalances

A

Retain K, Na, phos, mg

122
Q

CKD

Bone and mineral issues

A

Elevated phos and PTH alters Ca, kidneys unable to reabsorb Ca.

123
Q

CKD

Anemia process

A

Lack EPO, uremia shortens RBC lifespan. HF exac issues

124
Q

Extra renal manifestation of CKD

A

Htn (renin release- inc risk stroke mi and CHF), chronic pulm edema, blunts immune response, NV, anorexia, anemia

125
Q

Role of pons in micturition

A

Relaxes internal sphincter and contracts bladder to allow urination

126
Q

Cerebral cortex role urination

A

Inhibits via conscious control of external sphincter

127
Q

Bladder SNS innervation

A

L1-L2, allows relaxation and filling

128
Q

Bladder PNS innervation

A

S2-S4, bladder contraction and relaxation of internal sphincter to allow bladder emptying

129
Q

Internal sphincter

A

Bladder prevented from emptying until pressure in bladder rises above threshold

130
Q

External sphincter

A

Allows voluntary emptying of bladder or prevention of urination

131
Q

Voiding muscular mechanics

Systems involved

A

Detrusor muscle contracts and sphincters relax

Central, ANS, PNS

132
Q

Urinary dysfunc secondary to

A

Disorders of lower urinary tract, central/ANS/PNS disorder, meds, etc

133
Q

Incontinence is not what

A

Never normal, not even w aging

134
Q

Urge incontinence

A

Sudden leak followed by urgency. Overactive detrusor. Idiopathic, bladder infec, radiation, tumor, stones, or CNS damage

135
Q

Stress incontinence

A

Urine involuntarily lost, inc in intra-abd pressure. Precipitation by effort or exertion, d/t weakening of pelvic muscles or intrinsic urethral sphincter deficiency

136
Q

OAB

A

Inc daytime freq and nocturia, not necessarily incontinence

137
Q

Neurogenic bladder

A

Disrup NS communic governing micturition

138
Q

Overflow incontinence

A

Bladder becomes so full that it leaks urine or overflows. Caused by urethra obstruc, underactive detrusor

139
Q

Functional incont

A

Physical or enviro limitations resulting in inability to access a toilet in time

140
Q

Enuresis

Defn and types

A

Incont when asleep. Primary, secondary (after 6 months of dryness), monosymptomatic nocturnal (no other lower urinary tract malfunction), nonmonosymotinatic (urgency, freq, daytime incont w night incont)

141
Q

Enuresis

Pathogenesis

A

Deficiency of ADH, nocturnal overactivity of detrusor, abn arousal mechanisms, familial

142
Q

Vesicoureteral reflux

Can lead to

A

Reflux of urine from ureter to bladder. Can lead to UTI, void dysfunc, renal ins, htn in kids

143
Q

Vesicoureteral reflux

Grade 1, grade 3, grade 5

A

Reflux into ureter, no dilation
Begin to see dilation of ureter and renal pelvis
Gross dilation of ureter, pelvis, and calyces

144
Q

Ureteral ectopy
What it is
Risks

A

Single ureter implanted in abn location or a duplicate ureter. Inc infection risk and reduce renal func.

145
Q

Ureterocele
What it is
Results in

A

Cystic dilation of distal end of ureter. Inside or outside of bladder. Results in ureteral and renal calyx dilation, reflux and infection

146
Q

Ureterocele

CMs

A

Hydronephrosis, UTIs, voiding dysfunction, hematuria, urosepsis, failure to thrive

147
Q

Ureterocele goals

A

Control infection, preserve UT function, maintain continence, and remove obstruction (malformation)

148
Q

Cystitis

A

Inflam of bladder lining from infec, chemical irritants, stones, or trauma

149
Q

Lower urinary tract urolithiasis

A

Stones anywhere in urinary tract, most often from kidney. May come from bladder or ureters. Tissue irrit and obstruction

150
Q

Kidney stones

Dietary calcium does what

A

Prevents kidney stones by binding oxalate and preventing absorption

151
Q

Hydronephrosis

A

Distention of kidney w urine. Acute: partial obstruc and oliguria. Chronic: oliguria, anuria, may damage kidney leading to ARF, assoc w intestinal symp such as NV and pain

152
Q

Hydronephrosis

What happens on tissue level

A

Dilation of pelvis and calyces and thinning of renal parenchyma

Patho (11 decks)

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