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Patho > Renal > Flashcards

Renal Flashcards

1
Q

Apical membrane

A

Faces the lumen

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2
Q

Basolateral membrane

A

Side facing the capillary

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3
Q

Top two causes of kidney failure

A

DM (due to glycosylation of the glomerulus) and HTN

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4
Q

Functions of the kidney

A

Activate vitamin D, secrete EPO, remove wastes, maintain fluid/electrolyte/pH balance

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5
Q

The kidney can produce glucose from

A

amino acids

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6
Q

Do we generate nephrons?

A

Nah, fool.

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7
Q

Serious renal impairment doesn’t occur until ____-____% of nephrons have been damaged

A

75-90%

This means that clinical findings may not be evident until late in the disease course

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8
Q

What is contained in the cortex?

A

The glomerulus and portions of the tubules

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9
Q

What is contained in the medulla?

A

Loop of Henle and collecting ducts.

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10
Q

The kidneys receive __% of the CO

A

25%

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11
Q

What is a basement membrane?

A

A sheet of fibers beneath any epithelium

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12
Q

Blood and protein in the urine are signs of

A

glomerular injury

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13
Q

What are mesangial cells?

A

Specialized SM cells in the glomerulus. Their function is to provide structural support to the glomerular capillaries, regulate blood flow of the glomerular capillaries by their contractile activity (regulate GFR), and are involved in phagocytosis .

Remember that SM cells can change their phenotype when they are injured, causing them to multiple and begin secreting extracellular matrix (collagen). Secretion can start clogging up our filtration system.

When we have glomerular injury, either the glomerulus will clog up and not filter enough, or it will open up and allow too much stuff to pass through (RBCs and protein).

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14
Q

Normal GFR is about

A

125

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15
Q

These things are totally reabsorbed from the proximal tubule

A

Glucose, amino acids, and proteins.

Most of the bicarb is reabsorbed in the proximal tubule as well.

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16
Q

What does the macula densa do?

A

It senses the concentration of filtrate in the thick ascending limb. Based on the concentration, it will constrict or dilate the afferent arteriole and increase or decrease the release of renin.

Low concentration causes afferent vasodilation and increased renin release.

High concentration causes afferent constriction and decreased renin release.

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17
Q

What do the JG cells do?

A

These are specialized SM cells in the afferent arteriole. They secrete renin in response to a drop in pressure.

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18
Q

Angiotensin II causes constriction mostly in this vessel

A

Efferent arteriole.

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19
Q

Symporter responsible for reabsorbing filtered glucose

A

SGLT2
Glucose travels with a sodium
Symporter can be saturated at a BG of 180, resulting in glucosuria.

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20
Q

How do we reabsorb bicarb?

A

Remember we don’t have a transporter for bicarb, so it combines with H+ in the lumen to form H2CO3, and then dissociates into H20 and CO2 in the presence of CA. This gets absorbed across the membrane.

Once inside the cell, the same process happens in reverse in the presence of CA. At the end, bicarb is reabsorbed, and another H+ is kicked into the lumen to combine with another bicarb.

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21
Q

Where do we get the ammonia used to buffer acid?

A

The amino acid glutamine. This is good for buffering acid because it provides an ammonia group to bind with H+ in the lumen, and also creates a new bicarb that enters the bloodstream, further treating the acidosis.

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22
Q

Kidney response to alkalosis

A

Excreting some of the filtered bicarb

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23
Q

How does aldosterone result in potassium excretion?

A

It increases the activity of the basolateral Na/K pump. More sodium ends up being reabsorbed, and potassium ends up getting excreted.

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24
Q

Effect of ADH

A

ADH (vasopressin) binds to the V2 receptor on the basolateral side, causing the placement of aquaporins in the lumen of the collecting tubule.

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25
Q

Two potential problems with ADH

A

1) Diabetes insipidus
- Damage to pituitary causes insufficient ADH release
2) Nephrogenic diabetes insipidus
- The collecting tubules are unresponsive to ADH

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26
Q

Renin is released in response to

A

1) Decreased BP (low blood flow to kidneys)
2) Low sodium levels (sensed by the macula densa)
3) SNS activation of the JG cells via B1

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27
Q

Atrial Natriuretic Peptide (ANP) is released in response to _____ and causes _____

A

Overstretch of atrial cells due to excess fluid volume

ANP inhibits the secretion of renin, and thereby the actions of angiotensin II. Results in afferent dilation and efferent constriction as well as loss of sodium and water.

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28
Q

Urodilantin is released in response to

A

Released by the distal and collecting tubules in response to high circulating volume.

Acts by inhibiting salt and water reabsorption. I can’t really find anywhere how it does this, so it’s probably not important.

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29
Q

Urodilantin is similar to _____ in structure and function

A

ANP

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30
Q

How do osmotic diuretics work?

A

By increasing the osmolality of the filtrate, causing water to remain in the tubule, resulting in increased urine volume.

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31
Q

How do ACE inhibitors work?

A

They block the formation of angiotensin II (and thusly, aldosterone as well).

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32
Q

How do loop diuretics work and what patient population do they work well for?

A

Inhibit the Na/K/2Cl channels in the thick ascending loop and are good for those with impaired renal function.

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33
Q

How do thiazide-like diuretics work and what patient population do they work well for?

A

They block the Na/Cl symporter in the distal tubule. This increases the concentration of the filtrate, and water follows. These are good for those with normal kidney function.

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34
Q

Examples of potassium wasting diuretics

A

Osmotic, loop, and thiazide-like

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35
Q

Example of a potassium sparing diuretic

A

Aldosterone blocking agents

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36
Q

Renal considerations in infancy

A

Kidneys are immature

1) Low GFR
2) Reduced ability to concentrate urine (subject to volume depletion)

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37
Q

Renal considerations in the elderly

A

The kidneys begin to diminish in size and functions due to the loss of nephrons. Starts after the 4th decade, and significantly by the middle of the 6th decade.

This means

  • Low RBF
  • Low GFR
  • Decreased ability to concentrate urine
  • More susceptible to fluid loss and electrolyte imbalances

(sort of similar to infancy)

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38
Q

This synthetic molecule can be used to measure GFR

A

Inulin

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39
Q

When would you want to do a 24 hour urine collection?

A

To evaluate substances that are excreted in varying concentrations throughout the day (like protein)

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40
Q

The normal color of urine is due to

A

Urochrome pigments (urobilin)

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41
Q

Is normal urine slightly acidic or basic?

A

Slightly acidic

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42
Q

WBC casts are associated with

A

Renal infections (pyelonephritis)

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43
Q

RBC casts are associated with

A

Inflammation of the glomerulus (glomerulonephritis)

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44
Q

Epithelial casts are associated with

A

ATN, because they indicate the sloughing of tubular cells

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45
Q

Does urine osmolality and spec grav stay the same of fluctuate throughout the day?

A

It should normally fluctuate. If it does not fluctuate, it could indicate renal impairment.

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46
Q

How does creatinine enter the circulation?

A

It is the end result of muscle metabolism and is excreted ONLY by the kidney.

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47
Q

What affects creatinine levels in the body?

A

1) Rate of creatinine produced by the muscle (should be about constant)
2) Rate of creatinine excreted by the kidney (which is determined mostly by the GFR)

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48
Q

Plasma creatinine levels will rise proportionately to a fall in

A

GFR

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49
Q

Normal creatinine level

A

.7 - 1.5

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50
Q

Normal BUN level

A

10-20

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51
Q

Normal BUN:Creat ratio

A

10-20

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52
Q

Urea is the end product of

A

Protein metabolism. An increase in BUN may indicate a decrease in renal function.

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53
Q

Why is urea a poor measure of renal function?

A

Because it is influenced by hydration status, dietary protein intake, and rate of protein catabolism.

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54
Q

Why isn’t creatinine completely accurate in assessing GFR?

A

Because some is secreted into the lumen.

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55
Q

What is azotemia?

A

An elevation of both BUN and creat. It indicates a reduction of GFR.

56
Q

What is uremia?

A

Increase in BUN. Can indicate a failing excretory system and other metabolic or endocrine abnormalities.

57
Q

Where is renal pain felt?

A

The CVA and dematomes T10-L1.

58
Q

What causes renal pain?

A

Distention / inflammation of the renal capsule. It has a constant/dull quality.

59
Q

What test is a foundation for diagnosis of renal dysfunction?

A

Urinalysis

60
Q

Strong-smelling urine most likely indicates

A

High ammonia levels. If smelly and cloudy, it can indicate infection.

61
Q

What is renal agenesis what are the two types?

A

A failure of the kidneys to develop.

1) Unilateral agenesis
- The remaining kidney can fully compensate
2) Bilateral
- Incompatible with life

62
Q

What is renal hypoplasia?

A

Minimal kidney development.
The architecture is correct, but they kidneys are small and have a low amount of nephrons.
If has one normal: can compensate.
Requires lifelong kidney monitoring.

63
Q

Pathogenesis of PKD

A

Autosomal dominant defects of the PKD1 and PKD2 genes (located on 16 and 4 respectively).
Normally, these genes code for polycystins, which regulate the growth of the tubules and regulate intracellular calcium.
Defects in these causes defects in the formation of epithelial cells and their cilia, causing cyst formation and obstruction. Intracellularly, they will have high cAMP and low Ca++.

64
Q

Why is there low intracellular Ca in PKD?

A

Normally, the touching of the cilia from the filtrate sets off a cascade resulting in increased Ca levels. These cells have a lack of cilia, and will not have this cascade set off.

65
Q

Does PKD affect both kidneys or just one?

A

Either scenario can happen

66
Q

Is PKD dominant or recessive?

A

Both forms exist. However, the dominant form is responsible for the majority of cases in adults.

67
Q

Affect of the cysts in PKD

A

Fluid filled cysts expand and disrupt urine formation and flow. The person will have a decreased GFR and decreased ability to concentrate urine. This can lead to kidney failure and the person may need dialysis or transplantation.

68
Q

Manifestations of PKD

A

Pain (most common)
HTN
Paplation of large renal mass
Liver involvement

69
Q

Diagnosis and tx of PKD

A

Dx: U/S and genetic hisotry

Tx: BP management and supportive therapy (ex-dialysis if in ESRD)

70
Q

Symptoms of renal cell carcinoma

A

Asymptomatic until in advanced stage (because we can compensate until 75-90% of nephrons are lost). Mets may develop due to late diagnosis.
- CVA tenderness, hematuria, palpable mass

71
Q

Treatment of renal cell carcinoma

A

Nephrectomy.

Mets may be very resistant to chemo, radiation, and immunotherapy

72
Q

Body’s protective measures against UTI

A

Acidic pH
Presence of urea in the urine
Peeing (washes stuff away)
Unidirectional flow of urine (prevents reflux)
Men: bacteriostsic prostate secretions
Women: urethral glands that secrete mucous

73
Q

Causes of pyelonephritis

A

Infection of the renal pelvis

Caused by ascending infection from the lower urinary tract or from bacteremia.

74
Q

How is acute pyelonephritis diagnosed?

A

WBC casts indicative of upper UTI.

Need to treat promptly to avoid decreased renal function.

75
Q

Causes, S/S, dx, and tx of CHRONIC pyelonephritis

A

Reflux/obstruction/recurrent infections/stones etc cause chronic inflammation, leading to scarring and loss of functional nephrons. This can result in chronic kidney disease.

Manifests with abd/flank pain, fever, malaise, anorexia

Diagnosed with U/S or IV pyelography.

Tx: Correct the underlying process and extend antibiotic therapy

76
Q

Common causes of urinary obstruction

A

Stones (most common)
Tumors
BPH
Strictures of the ureters or urethra

77
Q

Complete obstruction will result in

A

Hydronephrosis (water in the kidney)
Decreased GFR (d/t increased pressure in Bowman’s space)
Ischemic kidney disease d/t increased intraluminal pressure
ATN
CKD

78
Q

Causes of kidney stones

A

Supersaturation (required)
Low UO
Abnormal urine pH

79
Q

Most kidney stones are made of

A 
Calcium crystals (70-80%)
Others: uric acid, struvite, cystine, and stones associated with certain meds
80
Q

How do glomerulopathies develop?

A

Damage from immune/inflammatory processes result in altered structure and function.
Hereditary and environmental factors may also play a role (metabolic/DM, infectious, hemodynamic, toxic, genetic, injuries, etc.)

81
Q

In reference to glomerulopathies, diffuse means ____ and global means _____

A

Diffuse: affects all glomeruli
Global: affects all parts of the glomerulus (the entire globe that is the glomerulus)

82
Q

Membranous glomerulopathy is

A

a thickening of the glomerular capillary walls

83
Q

Goodpasture syndrome

A

Rare autoimmune disease involving anti-GBM antibodies. Results is a nice linear deposition along the BM.

84
Q

A renal biopsy showing increased collagen would likely indicate

A

damage to mesangial cells

85
Q

Nephrotic syndrome

A

Indicates necrosis.
High protein loss (protein only!) due to loss of negative charges in filtration slits
Lose >3-3.5 grams of protein in 24 hours. Protein loss causes edema *****
Liver activity increases to correct oncotic pressure, but results in hyperlipidemia and hypercoagulability.

Treat with diuretics, anti-HTN, lipid lowering agents, and immunosuppresion. Basically treat the cause, and manage the SEs.

May resolve or progress to ESRD.

86
Q

Nephitic syndrome

A

Represents glomerular inflammation
Mild-moderate proteinura
Hematuria and RBC casts present

87
Q

Layers of the glomerulus

A

1) Inner capillary endothelium
2) Basement membrane
3) Outer capillary epithelium (podocytes)

88
Q

Pathogenesis and S/S of glomerulornephritis

A

Inflammation causes attraction of immune cells, resulting in lysosomal degradation of the basement membrane.
Mesangial cells may contract, reducing SA for filtration, causing a decreased GFR.

S/S: Proteinuria, azotemia, oliguria, edema, and HTN.

89
Q

Treatment for glomerulornephritis

A 
Steroids (may be due to autoimmune process)
Plasmapheresis (remove the antibodies)
Supportive measures (diet and fluid management)
Management of systemic and renal HTN
90
Q

Post-infectious acute glomerulornephritis pathogenesis

A

Follows group A beta-hemolytic strep infection (impetigo or throat).
Antigen/antibody complexes are formed are deposit in the GBM. This activates complement and release of inflammatory mediators that damage the cells of the glomerulus and cause menangial cell proliferation.

Will have smoky/coffee colored urine. Care is supportive.

91
Q

IgA nephropathy

A

This is another type of acute glomerulornephritis, called Berger disease

May occur after upper resp/GI viral infection. Abnormal IgA binds to mesangial cells, causing them to proliferate, secrete matrix, and produce oxidants and proteases.
Causes hematuria, but NOT proteinuria. HTN does NOT result.

92
Q

Chronic glomerulornephritis

A

Progressive course. Mesangial cells continue to proliferate and crowd the glomerulus, resulting in sclerosis and fibrosis of the kidney. Renal function slowly declines. Proteinuria occurs, and hematuria may occur as well.

Supportive care. Will ultimately need dialysis or transplant.

93
Q

Diseases that may cause nephrotic syndrome

A

Minimal change disease (lipoid nephrosis)
SLE
DM

94
Q

Minimal change disease

A

Also called Lipoid Nephrosis
Occurs is children
Allergic or immune condition results in decreased filtration (responds well to corticosteroids)
Foot processes fuse together and lose their negative charge->
Sudden onset of urine protein loss, hypoalbuminemia, and edema.

95
Q

What is acute kidney injury?

A

A sudden reduction in renal function (GFR), causing retention of creatinine and nitrogenous waste products, and disruptions in fluid, electrolyte, and acid-base balance.

96
Q

BUN:Creat ratio values and their meanings

A

> 20 = pre-renal. Low blood flow causes less filtration of both products. Slow movement allows more time for urea reabsoprtion.

10-20 = post-renal (Urinary obstrution). Increased pressure in the bowman’s space results in results in decreased filtration in general.

<10 = Intra-renal - the tubules are failing and unable to reabsorb urea.

97
Q

Causes of pre-renal ARF

A

Hypovolemia / hypotension, caused by:
- Heart failure, fever, vomiting, diarrhea, renal artery obstruction, burns, overuse of diuretics, ACE inhibitors, angiotensin II blockers, NSAIDs

98
Q

S/S and tx of pre-renal ARF

A

Low GFR, causes oliguria, high spec grav and osmolality, low urine sodium, and azotemia.

Tx is treating the cause, increasing perfusion (volume replacement), and/or dialysis.

99
Q

Both pre and post-renal ARF can lead to

A

ATN

100
Q

Phases of post-renal ARF

A

1) Early phase
- GFR able to be maintained via dilation of the afferent arteriole
- 12-24 hours
2) Late phase
- After 12-24 hours, afferent vasodilation ceases
- GFR falls progressively and may result in anuria
- phase continues until the obstruction is relieved
3) Recovery phase (after removal of obstruction)
- Pre-renal vessels relax
- Perfusion restored and GFR increases in surviving nephrons
- If calyces and collecting system were dilated, this is permanent

101
Q

Causes of intrarenal ARF

A

Two main causes:

  • Ischemia
  • Toxicity (contrast media or other drugs)
102
Q

Phases of ATN

A

1) Prodromal Phase
- Insult to kidney has occurred, but no symptoms yet
2) Oliguric Phase
- Low GFR causes oliguria, uremia, fluid excess, hyperkalemia, acidosis, and uremic syndrome
- From 1-2 days to 8 weeks, with urine output of 50-400mL/day.
- May require dialysis
3) Post-oliguric Phase
- Diuresis and resultant fluid-volume deficit** until the kidneys recover
- Kidneys are still damaged, however, so azotemia continues.
- Labs slowly normalize

Full recovery is when BUN and creat levels normalize. There is usually some residual renal insufficiency that persists.

103
Q

The progressive steps of chronic renal failure

A

Chronic kidney disease > chronic renal failure > ESRD (requires dialysis)

Renal failure is often linked with DM and HTN

104
Q

Chronic renal failure is defined as

A

Kidney damage/decrease in renal function for more than three months as based on blood tests, urinalysis, and imaging studies.

Can also be a GFR of less than 60 for more than 3 months.

105
Q

Risk factors for chronic renal failure

A 
DM
HTN
Recurrent pyelonephritis
Glomerularnephritis
PKD
Family hx of chronic renal failure
Exposure to toxins
Age over 65
Ethnicity
106
Q

Treatment for chronic renal failure (CKD) is aimed at

A

Aggressive HTN control
DM control
Management of ATN
ACE inhibitor and Angiotensin II blockers to decrease proteinuria

107
Q

Someone with CKD may be prescribed sodium bicarb if their pH is less than

A

7.30

108
Q

Why does anemia develop in CKD?

A

Decrease in EPO production

Uremia decreases RBC life-span

109
Q

What is cardiorenal anemia?

A

The combination of worsening CKD, anemia, and heart failure

110
Q

Electrolyte imbalances seen with CKD

A

Elevated potassium, phos, and mag. Acidosis (increased H+)

Decreased calcium.

111
Q

Why is wound healing difficult with CKD?

A

Edema and build-up of waste products.

112
Q

At what point is dialysis needed?

A

When uremia and hyperkalemia are unresponsive to other treatments.

This usually happens at around stage 5 ATN/CKD.

113
Q

Micturation is mediated via

A

the pons, gravity, peristalsis, and the nervous system.

114
Q

Effect of the pons on micturation

A

Causes relaxation of the internal sphincter and contraction of the bladder

115
Q

Effect of the cerebral cortex on micturation

A

Concious control of the external sphincter

116
Q

ANS innervation of the bladder

A

SNS (L1-2) - allows relaxation and filling

PSNS (L2-4)- causes bladder contraction and relaxation of internal sphincter

117
Q

Normal residual volume in the bladder after voiding

A

50-100mL

118
Q

Is incontinence a normal part of aging?

A

No

119
Q

Urge incontinence: definition and cause

A

Involuntary sudden leakage of urine immediately following the urge to urinate. This is due to an overactive detrussor muscle.

Causes: Idiopathic, bladder infection, radiation therapy, tumors or stones, CNS damage

120
Q

Stress Incontinence: definition and cause

A

Incontinence with increases in intra-abdominal pressure (laughing, exertion, etc).

Due to weak pelvic floor muscles or intrinsic urethral sphincter deficiency

121
Q

Overactive bladder syndrome

A

Increased urination frequency during the day and at night. Not necessarily associated with incontinence.

122
Q

Neurogenic bladder

A

Incontinence due to a disruption of communication of the nervous system involved in micturation

123
Q

Overflow incontinence

A

Bladder so full that it leaks.

Caused by urethral obstruction or inactive destrussor muscle.

124
Q

Functional incontinence

A

Unable to get to a toilet in time

125
Q

Enuresis (2 types)

A

Incontinence while asleep, usually referring to children bedwetting.

Primary: was never continent
Secondary: Was continent for at least 6 months and then became incontinent again

126
Q

Monosymptomatic enuresis

A

Nocturnal enuresis in the absence of lower urinary tract malfunction

127
Q

Nonmonosymptomatic enuresis

A

Day-time and night-time incontinence

128
Q

Causes of enuresis

A

ADH deficiency
Nocturnal overacitivity of the detrussor muscle
Immature/abnormal arousal mechanisms
Familial pattern

129
Q

Manifestations and tx of vesicoureteral reflux

A

Recurrent UTI
Voiding dysfunction
HTN in children

May resolve spontaneously or require surgery

130
Q

Uretal ectopy

A

Ureter implanted in an abnormal location or presence of a duplicate ureter.
Can reduce renal function and increase risk of infection
Usually requires surgical treatment

131
Q

Ureterocele (2 types)

A

Cystic dilation at the distal end of the ureter
Intracesical/orthotopic - entirely within the bladder

Extravesical/ectopic - neck of bladder or in the urethra.

May be single or duplex system (1 or 2 ureter for the single kidney)

132
Q

S/S and treatment of ureterocele

A

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

Needs surgery (endoscopic decompression, nephroureterotomy, or complete reconstruction)

133
Q

How does dietary calcium prevent kidney stone formation?

A

By binding oxalate and preventing absorption.

134
Q

What is hydronephrosis?

A

Dilation of the kidney with urine. Dilation of the pelvis and calyces, and thinning of the renal parenchyma.
Can lead to ARF.

135
Q

In autoregulation, the afferent arteriole will (constrict/dilate) in response to high BP

A

Constrict. Remember that the goal of autoregulation is to provide a constant GFR.

136
Q

Why is it important to manage HTN in kidney diseases?

A

To prevent further kidney damage

137
Q

Overview of the pathogenesis of glomerulonephritis

A

Although the pathogenesis is not fully understood, current evidence supports that most cases of glomerulonephritis (GN) are due to an immunologic response to a variety of different etiologic agents. The immunologic response, in turn, activates a number of biological processes (eg, complement activation, leukocyte recruitment, and release of growth factors and cytokines) that result in glomerular inflammation and injury. GN may be isolated to the kidney (primary glomerulonephritis) or be a component of a systemic disorder (secondary glomerulonephritis

Patho (14 decks)

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