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Advanced Pathophysiology > Renal > Flashcards

Renal Flashcards

1
Q

How does the R kidney positioning differ from the L?

A

The R kidney is located slightly lower d/t displacement by the liver.

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2
Q

What are the three major functions of the kidney?

A
  1. Filtration
  2. Reabsorption
  3. Secretion

(4.Excretion)

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3
Q

Differentiate between hydrostatic and oncotic pressures.

A

Hydrostatic pressure refers to the pushing of fluids against the vessel walls from within the vasculature and within the interstitial space.

Osmotic pressure refers to the pulling force exerted on the vessel walls from within the vasculature and within the interstitial space

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4
Q

What is thirst triggered by?

A

Increased concentration of extracellular fluid (increased osmolality)
Decreased circulating blood volume

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5
Q

The amount of fluid excreted in the urine is controlled primarily by which hormones?

A 
ADH
Aldosterone
Natriuretic Peptides (ANP and BNP)
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6
Q

Where is ADH synthesized and released?

A

Synthesized in the hypothalmus

Released by the posterior pituitary gland

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7
Q

What factors increase the release of ADH?

A
  • Increased osmolality of the extracellular fluid
  • Decreased circulating fluid volume
  • Pain
  • Nausea
  • Physiologic/psychologic stressors
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8
Q

How does ADH impact the concentration of filtrate in the collecting duct (and DCT)?

A

ADH stimulates the epithelial cells in the collecting duct to produce aquaporins causing water to be reabsorbed from the filtrate to the capillaries.

This happens via osmosis d/t the increased concentration of solutes (increased osmolality) in the capillary vs. the decreased concentration (hypotonic solution) present in the renal tubules.

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9
Q

Where is aldosterone synthesized and released from?

A

Adrenal cortex

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10
Q

What are the main stimuli for aldosterone release? (2)

A
  1. Angiotensin II (AII)- from RAAS, activated by decreased circulating blood volume
  2. Increased concentration of K ions in the plasma
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11
Q

How does aldosterone impact the concentration of the filtrate in the collecting duct? (3)

A
  1. Stimulates the Na-K pump
  2. Opens Na channels (increased Na in the blood pulls water into the vascular=increased blood volume)
  3. Open K channels (K moves into filtrate)
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12
Q

What hormones opposed the action of aldosterone?

A

ANP

BNP

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13
Q

When are ANP and BNP release?

A

ANP is released with the atrial cells are overstretched signaling an excess of volume.
BNP is released by the ventricles when EDV is elevated indicating an excess of volume (HF)

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14
Q

How do natriuretic peptides oppose the action of aldosterone?

A

ANP opposes AII. Promote fluid excretion by nautriuresis (moving Na into the urine so that water follows=decreased blood volume)

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15
Q

How many nephrons are there per kidney?

A

One million

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16
Q

Traces the flow of filtrate through the kidney.

A

Glomerulus to PCT to LoH to DCT to collecting duct

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17
Q

What are the general functions of the glomerulus?

A

The capillary net that filters plasma, making ultrafiltrate that is called tubular fluid once it enters the PCT

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18
Q

What are the general functions of the PCT?

A

Has cuboidal epithelial cells with brush border villus membrane to increase surface area and is the main site of reabsorption of water, lytes and nutrients (isotonic filtrate)

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19
Q

What is the general function of the thin descending Loop of Henle?

A

Impermeable to solutes but permeable to water. Concentrates fluid as well as diffuses water out. (hypertonic filtrate)

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20
Q

What is the general function of the thick ascending Loop of Henle?

A

Impermeable to water but has NaK2Cl active transporters that reabsorb more solutes and dilute the tubular fluid. (Hypotonic) Sets up and maintains interstitial concentration gradient

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21
Q

What is the general function of the DCT?

A

Electrolyte modifications. Sense concentraiton of Na and Cl via villi and signals juxtaglomerular cells via PGE to release renin. Aldosterone acts on late distal tubule principle cells.

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22
Q

What is the general function of the collecting ducts?

A

Site of free water reabsorption through water channels ( aquaporins)controlled by ADH.
Important to acid-base balance; allow H secretion and bicarb secretion when necessary

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23
Q

What are the functions of the kidney?(5)

A
  1. Remove toxins/waste from the body
  2. Maintain proper H2O and electrolyte balance of blood (excrete H20 and lytes, secrete renin)
  3. Maintain proper pH of blood (usually excrete H and create bicarb)
  4. Secrete EPO
  5. Activate vit D (vital to Ca absorption)
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24
Q

What is filtration?

A

The movement of substances out of the blood into the filtrate. Glomerulus into the PCT.

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25
Q

What is reabsorption?

A

The return of substances from filtrate now present in the tubular fluid back into the blood.

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26
Q

What is secretion?

A

The movement of substances out of peritubular blood via kidney tubule cells in tubular fluid.

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27
Q

What is the vasa recta?

A

Capillaries located around the LoH; absorb interstitial fluid without excessive removal of interstitial solute.

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28
Q

What is the renal corpuscle?

A

Glomerulus and Bowman’s space

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29
Q

What is the kidney’s release of renin stimulated by (RAAS stimulation)?

A

Decreased BP
Decreased fluid volume
Increased B1-Sympathetic

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30
Q

What is the RAAS inhibited by?

A

Increased BP
Increased fluid volume
Decreased B1-Sympathetic
ANP

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31
Q

What are the steps of the RAAS?

A

In response to decreased BP or volume renin is released by the kidneys.
Renin acts on the liver which release Angiotensinogen that is cleaved by the renin resulting in Angiotensin I which is converted via the lungs by ACE to Angiotensin II which stimulates the adrenal cortex to release Aldosterone. Aldosterone acts on the distal portion of the nephron to increase Na K ATP pumps to increased the reabsorption of Na and H2O=increased blood volume and BP

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32
Q

In addition to stimulated the release of Aldosterone what does Angiotensin II do?

A

Causes vasoconstriction

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33
Q

How are the capillaries of the glomerulus different from other capillary networks in the body?

A

Glomerular capillaries branch from and drain into arterioles

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34
Q

Why is there no oncotic pressure in Bowman’s space?

A

This area should be protein free which is indicative of decreased oncotic pressure

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35
Q

Why is the NFP in the efferent arteriole=0?

A

No filtration happens here.

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36
Q

What is the purpose of the podocytes?

A

Surround the fenestrated epithelium and are negatively charged, so they provide a barrier to movement of negatively charged ions

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37
Q

What do mesangial cells do?

A

Provide structural support for glomerular capillaries, secrete matrix proteins, phagocytose and regulate GFR

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38
Q

How do mesangial cells regulate GFR?

A

SMC:Contraction and relaxation which alters the available surface are for filtration and affects GFR

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39
Q

How does each nephron regulate its own GFR?

A

Tubuloglomerular feedback

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40
Q

What is the regulatory structure that controls tubuloglomerular feedback?

A

Juxtaglomerular apparatus

  1. Glomerulus
  2. Macula densa
  3. Juxtaglomerular cells
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41
Q

What does the macula densa do?

A

Located near the end of the ascending LoH in the DCT. Senses changes in the amount of NaCl. Increased NaCl inhibits renin release and a decreased load promotes renin release (decreased amount of tubular fluid moving by)

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42
Q

What do the juxtaglomerular cells do?

A

Surround afferent arteriole. Produce and release renin

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43
Q

How is bicarbonate reabsorbed?

A

Bicarb is converted to CO2 and H20 via carbonic anhydrase in the PCT. Carbonic anhydrase is then used to the catalyze the reverse reaction creating H and bicarb; bicarb is reabsorbed back into the blood via the Na HCO3 transporter and H is excreted in the urine

44
Q

What does decreased reabsorption cause?

A

Dilution of urine and overall increase in fluid volume

45
Q

How is sympathetic nerve activity related to the ‘fight or flight’ response in the kidneys?

A

Diverts blood from kidneys and GI tract. Increases fluid reabsorption to shut of ability to make urine (Na and H2O reabsorbed)

46
Q

What affect does in an increase in pressure sensed by baroreceptors in the afferent arteriole cause?

A

Inhibits renin release

47
Q

What are the 2 mechanisms of regulation of RBF and GFR?

A
  1. Autoregulation- myogenic mechanisms and tubuloglomerular feedback
  2. Neural regulation
  3. Hormonal regulation- RAAS, ADH, Natriuretic peptides
48
Q

How do osmotic diuretics work?

A

Increase osmolality of the filtrate causing more water to remain in the tubule which is excreted as urine

49
Q

How do ACE inhibitors cause diuresis?

A

Inhibit AII and Aldosterone. Inhibits reabsorption of Na which keeps more water in the filtrate to be excreted

50
Q

How do loop diuretics work?

A

Block the Na K 2Cl pumps on the ascending loop to keep solutes in the urine

51
Q

How do thiazide-like diuretics work?

A

Block Na Cl co-transporter in the DCT blocking Na reaborption

52
Q

How do aldosterone blocking agents work?

A

Decrease Na and H2O reabsorption and K excretion (potassium sparing)

53
Q

What are the different casts that may be found in urine and what do they indicate? (3)

A
  1. WBC- pylonephritis
  2. RBC- glomerulonephritis
  3. Epithelial casts- ATN
54
Q

Where is kidney associated pain most often felt?

A

CVA/flank pain; transmitted from T10-T12 and L1 via sympathetic afferent neurons

55
Q

What is agenesis?

A

Congenital abnormality. Kidneys don’t develop in the fetus.
Bilateral = incompatible with life
Unilateral= compensatory hypertrophy of functional kidney

56
Q

What is hypoplasia of the kidney?

A

Congenital abnormality. Some fetal kidney development. Could lead to pediatric ESRF.

57
Q

What causes cystic kidney disease?

A 
Genetically transmitted. 
Autosomal recessive (often lethal and do not make it to reproductive age= less common)
Autosomal dominate (Chromosome 16 PKD1 most common and Chromosome 4 PKD2)
58
Q

What is cystic kidney disease?

A

Characterized by fluid filled renal cysts, may expand and disrupt urine flow.

Decreased cilia formation of the epithelial cells in the nephron that should detect pressure and solute content passing through and stimulate Ca and cAMP. Decreased intracellular Ca and excessive intracellular cAMP causes reduction of normally function kidney tissue and development of cysts.

Decreased GFR and ability to concentrate urine

59
Q

What are the clinical manifestation of cystic kidney disease?

A
  1. Hypertension (decreased GFR=decreased urine=incr. volume)
  2. Pain (common)
  3. Concomitant cystic liver involvement
60
Q

What are common causes of secondary glomerular disorders?

A

Goodpasture syndrome
SLE
Diabetic neuropathy

61
Q

What type of urine is common of a patient with nephrotic syndrome?

A

Proteinuria d/t necrosis of the glomerulus
3-3.5g loss/day
Usually no hematuria(?)

62
Q

What type of urine is common of a patient with nephritic syndrome?

A

Mild to moderate proteinuria
*Hematuria and RBC casts present in sediment (RBCs are indicative of less severe injury because they are less negatively charged than protein)

63
Q

How can proteinuria eventually result in hyperlipidemia and hypercoagulability?

A

Proteinuria leads to hypoalbuminemia which stimulates the liver to increased fat production (hyperlipidemia) and clotting factor production (hypercoagulability)

64
Q

How can proteinuria cause generalized edema?

A

Proteinuria causes hypoalbumemia which decreases intravascular osmotic pressure allowing fluid to move into the interstitium causing generalized edema

65
Q

What is minimal change disease or MCD?

A
  • Lipoid nephrosis
  • Initiated by allergic or immune condition causing decreased GFR
  • Fusion of the glolmerular podocytes and decreased production of anions of the basement membrane =decreased barrier)
  • Occurs in children
  • Sudden onset of edema, nephrotic levels of proteinuria, and hypoalbuminemia
66
Q

What is acute glomerulonephritis?

A

Acute inflammation of the glomerulus.
Related to antibody deposition leading to inflammation which results in lysosomal degradation of the basement membrane.
GFR may fall d/t contraction of mesangial cells

67
Q

What are the clinical manifestations of acute glomerulonephritis?

A

Hematuria, proteinuria, oliguria, azotemia, edema and HTN

68
Q

What does membranous nephropathy describe?

A

Diffuse thickening of the glomerular basement membrane. (Glomerulonephritis)

69
Q

What is a common cause of postinfectious acute glomerulonephritis? (aka acute proliferative glomerulonephritis)

A 
Follows skin (impetigo) and throat infections 
*Group A beta-hemolytic streptococci

Developing countries, smoky/coffee-colored urine

70
Q

What is Berger disease?

A
  • Acute glomerulonephritis
  • IgA nephropathy (found in tracts)
  • Upper resp or GI viral infections
  • Complex deposition leading to mesangial injury
  • Hematuria presents in 1-2days
  • Proteinuria (but no HTN or edema)
  • Variable prognosis, could lead to ESRD
71
Q

What is indicative of chronic glomeruloneprhitis?

A

Sclerosis and fibrosis of the kidney

72
Q

What type of urine do patients with chronic glomerulonephritis present with?

A

Proteinuria with or without hematuria

73
Q

What does the sudden reduction of kidney function consistent with acute renal failure lead to?(4)

A
  • Disruption in fluid, lyte, and acid-base balance
  • Retention of nitrogenous waste
  • Increased serum Cr
  • Decreased GFR
74
Q

What are the three sites of disruption in acute renal failure?

A

Prerenal (decreased renal perfusion)
Intrarenal (parenchymal renal damage)
Postrenal (obstruction to urine flow)

75
Q

What happens to the BUN:Cr ration with each respective cause of acute renal failure?

A

Normal 10-20

Prerenal >20
Intrarenal <10
Postrenal 10-20 (equally affected)

76
Q

What will a patient present with d/t decreased GFR secondary to pre-renal acute renal failure?

A

Oliguria, high urine specific gravity and osmolality, low urine Na, azotemia

77
Q

What are the two possible pathological processes associated with intra-renal acute renal failure?

A
  1. Vascular- RBF decreased, hypoxia, vasoconstriction

2. Tubular- inflammation and reperfusion injury, causes casts, obstructs urine flow, tubular backleak

78
Q

Two most common causes of ATN?

A

Ischemia

Nephrotoxin

79
Q

Three phase of ATN include:

A
  • Prodromal phase- insult occurs
  • Oliguric phase- 1-2 to 8wks; oliguria, progressive uremia, decreased GFR, hypervolemia, hyperkalemia (?dialysis)
  • Postoliguric phase- recovery; diuresis, tubular function impaired and azotemia continues, fluid volume deficient until kidneys recover

Full recovery is defined as normal BUN/Cr, may take up to a year.

80
Q

Most common causes of chronic renal failure?

A
  • HTN
  • Diabetes
Recurrent pylonephritis
Glomerulonephritis
Polycystic Kidney Disease
Family hx of CKD
Toxin exposure 
Age over 65
Ethnicity
81
Q

What is chronic renal failure defined as?

A
  • Decreased kidney function or kidney damage of 3 months duration based on blood tests, urinalysis, and imaging
  • GFR <60ml/minute/1.73m2 for 3 months with or without indication of damage
82
Q

What causes relaxation of the internal sphincter and contraction of the bladder to enable urination?

A

Pons

83
Q

What role does the cerebral cortex play in urination?

A

Inhibits via conscious control of the external sphincter

84
Q

What role to sympathetic and parasympathetic nerves play in bladder function?

A

Sympathetic (L1-2)- allow relaxation and filling

Parasympathetic (S2-4)- cause bladder contraction and relaxation of the internal sphincter to initiate emptying

85
Q

To void:

A

The detrusor muscle of the bladder must contract and urethral sphincters must relax

86
Q

What is acute pylonephritis?

A

Infection of the renal pelvis/parenchyma usually from an ascending UTI

87
Q

What is chronic pylonephritis usually associated with?

A

Reflux or an obstructive process leading to persistent urine stasis
(chronic inflammation causes scarring and loss of functional nephrons)

88
Q

Common causes of urinary tract obstruction include:

A

*Stones
Tumors
Prostatic hypertrophy
Strictures of the ureters or urethra

89
Q

Why do renal calculi most often form?

A

Supersaturation of solutes (Ca and Phos), low urine volume, abnormal decreased urine pH

90
Q

Symptoms of kidney stone migration include:

A

Intense renal colic pain, abrupt and may radiate
N/V
Diaphoresis
Hematuria may be present

91
Q

What is cystitis and what could cause it?

A

Inflammation of the bladder lining (cystele)

Infection (most common, originates in urethra), chemical irritants, stones, trauma

92
Q

Dietary Calcium ______ kidney stones.

A

Prevents by binding oxalate and preventing absorption

93
Q

How can hyperparathyroidism lead to hypercalcemia and kidney stones?

A

PTH is release from the parathyroid gland and increases circulating Ca levels. If Ca is not bound it increases the risk for stone formation

94
Q

Hydronephrosis is:

A

Distention/dilation of the kidney with urine.

Marked dilation of the renal pelvis and calyces and thinning of the renal parenchyma=decreased function

95
Q

What can an overactive detrusor muscle causes?

A

Urge incontinence

96
Q

Stress incontinence is secondary to:

A

Increases in intra abdominal pressure d/t weakening of pelvic muscles or intrinsic urethral sphincter deficiency

97
Q

Overactive bladder syndrome is associated with:

A

Increased daytime frequency and nocturia

98
Q

When does neurogenic bladder occur?

A

Pathology that produces a disruption of nervous communication governing micturition

99
Q

Overflow incontinence can be caused by:

A

Underactive/inactive detrusor muscle

100
Q

Possible pathogenesis of enuresis:

A

Deficiency in ADH
Nocturnal overactivity of the detrusor muscle
Immature/abnormal arousal mechanisms (incr. symp, dec para)
Familial pattern

101
Q

Vesicoureteral Reflux is:

A

Congenital
Reflux of urine from the ureter-bladder junction

(may manifest as HTN in children)

102
Q

What is ureteral ectopy?

A

Congenital
Single ureter implanted in an abnormal location or a duplicate ureter
Increased risk for infection and reduced renal function

103
Q

What is ureterocele?

A

Cystic dilation at distal end of the ureter that feeds into the bladder
Causes ureteral and renal calyx dilation, reflux and infection
Surgical intervention necessary

(s/s- hydronephrosis, UTIs, voiding dysfxn, hematuria, urosepsis, FTT)

104
Q

Systemic hypertension leading to glomeruli dysfunction can lead to what pathologic change:

A

Obstruction of the renal tubule

105
Q

A mass of proliferating cells found in Bowman’s space is associated with what disease?

A

Crescentic glomerulonephritis/rapidly progressing glomerulonephritis

106
Q

Acute renal failure due to liver failure (hepatorenal syndrome) is due to:

A

Diminished intrarenal blood flow

107
Q

What three regulatory mechanisms are involved in tubuloglomerular feedback?

A
  1. Baroreceptor mechanism (if pressure low=stimulate renin)
  2. Macula densa (if Na in tubule low=stimulate renin)
  3. Sympathetic activity (if low=stimulate renin)

All are signs of low blood volume and pressure, renin release increases pressure.

Advanced Pathophysiology (12 decks)

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