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APP Part 2 > Renal > Flashcards

Renal Flashcards

1
Q

1/12 people in the US have ___
____ % of all women ages 20-45 will experience a UTI
____ adults over 20 have chronic kidney disease
____ % of kidney failure is caused by diabetes. ____ is the second leading cause of renal failure.
____ people with kidney failure die each year
- Kidney disease is the ___th leading cause of death in America
- There are___ people being kept alive through dialysis

A
  • 1/12 people in the US have renal or urinary tract disease
  • 13% of all women ages 20-45 will experience a UTI
  • 26 million adults over 20 have chronic kidney disease
  • 45% of kidney failure is caused by diabetes. HTN is the 2nd leading cause of renal failure
  • Over 87,000 ppl with kidney failure die each year
  • Kidney disease is the 9th leading cause of death in US
  • 367,000 ppl on dialysis (85 thou waiting for transplant, only 15 thou will get one).
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2
Q

malignant nephrosclerosis (symptoms and treatment)

A

Azotemia, proteinuria, and further hypertension that the kidney brings on itself
Treatment: anti-hypertensives and dialysis

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3
Q

What is the purpose of autoregulation?

2 mechanisms:

A
  • Maintains constant blood flow to the glomerulus and thus maintain GFR independent of systemic BP.
  • Kidneys autoregulate via myogenic mechanism and tubuloglomerular feedback (juxtaglomerular apparatus)
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4
Q

<p>How does sympathetic nervous system affect renin secretion</p>

A

<p>Increased sympathetic activity --> increased renin release</p>

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5
Q

Symptoms of chronic pyelonephritis

A
  • Chills, fever, headache, general malaise.

- Back pain, tenderness, dysuria, frequency/urgency of urination.

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6
Q

Clear cell carcinoma

A
  • Most common renal tumor in adults.
  • Normally asymptomatic due to large renal reserve.
  • Symptoms: pain, palpable mass, hematuria
  • Called clear cell carcinoma because cells are clear on a stain due to accumulation of lipids
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7
Q

<p>Membranous glomerulonephritis treatment</p>

A

<p>Steroids for immunomodulation</p>

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8
Q

<p>Focal glomerular disease</p>

A

<p>Only a few of the glomeruli in a histological section are affected</p>

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9
Q

<p>Minimal change disease treatment</p>

A

<p>Steroids</p>

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10
Q

<p>Treatment of post-renal ARF</p>

A

<p>Remove the obstruction</p>

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11
Q

<p>Proteinuria/albuminuria</p>

A
  • protein or albumin in urine

- first indication of glomerular disorder

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12
Q

<p>Diabetic nephropathy</p>

A
  • leading cause of kidney failure!
  • 30% of ppl with diabetes (both types) have diabetic nephropathy.
  • Treated with ACE inhibitors and angiotensin receptor blockers (ARBs). May require dialysis, though diabetic patients do worse on dialysis than non-diabetic patients.
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13
Q

<p>What is normal GFR</p>

A

100-125 ml/min.

Declines with age and in pathology.

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14
Q

<p>Anuria</p>

A

NO urine flow

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15
Q

Local/segmental glomerular disease

A

A portion of a glomerulus in a histological section is affected

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16
Q

Peritoneal dialysis

A
  • Uses the peritoneal membrane as the semipermeable membrane. By infusing and draining the peritoneal space with dialysis fluid we are able to take waste away without pumping blood in/out of the patient.
  • High risk of infection.
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17
Q

Focal segmental glomerulosclerosis histology

A

Part of the glomerulus shows scarring/sclerosing.

Tons of immunoglobulin present on the side of the glomerulus with sclerosis.

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18
Q

<p>What is BUN &amp;amp; how is it handled by kidney?</p>

A

Blood urea nitrogen.

Urea is filtered and reabsorbed.

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19
Q

<p>Treatment for pre-renal ARF</p>

A

improve renal perfusion, volume replacement, dialysis

Reversible disease with re-perfusion!

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20
Q

Why has kidney disease risen so rapidly in prevalence in recent years?

A

OBESITY, HT, Diabetes

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21
Q

Describe the renal vasculature (high level)

A

1 renal artery enters
1 renal vein exits
NO COLLATERALs

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22
Q

Urolithiasis

A

Stones found in the urinary tract

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23
Q

Proliferative glomerular disease

A

Increases cellular glomerulus (more cells present) - could increase number of immune cells in the glomerulus even though they should NOT be present

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24
Q

Chronic glomerulonephritis

A
  • All of the disease progress to this if left untreated.
  • The glomeruli solidify partially or wholly, the tubules atrophy, and the arteries show intimal thickening.
  • Thin cortex - very small amt of functioning tissue.
  • Histology: no Bowman’s space, no open capillaries, solidified and nonfunctional.
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25
Q

What does a BUN/Cr ratio

A
  • Intrarenal ARF.

- Something is wrong with the kidney/tubule; dec in transporter function decreases reabsorb of urea.

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26
Q

Causes of post-renal ARF

A

Tubular obstruction caused by insult (such as ischemia) –> increase in pressure –> reduced GFR

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27
Q

Where do obstructions occur in post-renal ARF?

A
  • Ureter system - cysts or tumors in abdomen can impinge on lumen of ureters/urethra
  • Kidney stones
  • Injury to tubule causing dead cells to slough off and obstruct the tubule
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28
Q

Minimal change disease mechanism

A

Unknown mechanism, but most commonly seen in children following a recent immune response, for example in illness or with a vaccination.

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29
Q

Membranous glomerulonephritis histology

A

Diffuse –> all glomeruli are affected

Increase in extracellular substances (thickened capillary loops)

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30
Q

IgA Nephropathy (Berger)

A
  • After a mucosal infection large amounts of IgA antibodies deposit on the surface of mesangial cells.
  • most common glomerular renal disease throughout the world.
  • Presents with a slightly thickened basement membrane and large deposits of IgA in the mesangium, causing capillaries to rupture.
  • Treat w/ steroids
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31
Q

<p>Most causes of kidney disease are primary or secondary?</p>

A

<p>secondary</p>

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32
Q

3 mechanisms that affect the renin-angiotensin system (tubuloglomerular feedback)

A
  • Baroreceptors in the afferent arteriole will sense pressure changes (increase in pressure = inhibits renin release)
  • Increase in SNS increase renin release
  • Macula densa cells in the distal tubule sense flow of NaCl through the DCT and stimulate renin if salt conct is high.
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33
Q

<p>Renin converts \_\_\_ to angiotensin I, which is converted to angiotensin II via \_\_\_.</p>

A

<p>Angiotensinogen

| ACE</p>

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34
Q

<p>Where does Angiotinsinogen come from? </p>

A

<p>made continuously in liver</p>

35
Q

5 functions of angiotensin II:

A

OVERALL: AngII increase BP through an increase in TPR and BV

  • Increase in SNS activity → inc. vasoconstriction and HR
  • Inc aldosterone secretion → inc na+ reabsorption → inc water reabsorption → increase BV
  • Direct increase in Na/water reabsorption → increase BV
  • Promotes vasoconstriction → TPR inc.
  • Promote release of ADH → water reabsorption → increase BV
36
Q

Causes of acute renal failure

A

Pre-renal: decreased renal perfusion
Intra-renal: Parenchymal renal disease
Post-renal: obstruction to urine flow

37
Q

Azotemia vs. Uremia

A
  • Azotemia: elevation of BUN and creatinine, related to decreased GFR
  • Uremia: manifestations of waste buildup; includes azotemia, acidosis, hyperkalemia (high K+), hypertension, anemia, hypocalcemia (low Ca2+)
38
Q

<p>Proteinuria/albuminuria:</p>

A

<p>more than 3 mg of protein in the uriner /day</p>

39
Q

<p>Hematuria:</p>

A

<p>blood in the urine</p>

40
Q

<p>Lipiduria:</p>

A

<p>lipids in the urine</p>

41
Q

<p>Oliguria:</p>

A

<p>decreased urine production</p>

42
Q

<p>Anuria:</p>

A

<p> no urine flow</p>

43
Q

<p>leukocytes in the urine</p>

A

Pyuria

44
Q

Chronic Kidney Disease (CKD):

A
  • NOT reversible (acute kidney disease IS reversible!)

- progressive loss of the ability to excrete waste, concentrate urine, and conserve electrolytes.

45
Q

Diffuse vs. focal

A

Diffuse – All glomeruli in the field are affected

Focal – only few of the glomeruli are affected

46
Q

<p>Local/Segmental vs. Global</p>

A

Local/Segmental – Portion of the glomerulus is affected

Global – Entire glomerulus is affected

47
Q

<p>Proliferative</p>

A

Increases in number of cells in the glomerulus

*could be increased number of immune cells in the glomerulus

48
Q

<p>Membranous</p>

A

Increase in glomerular basement membrane (not an increase in mesangeal cells).

49
Q

<p>Necrotizing </p>

A

Necrosis within glomerulus; death of tissue, build

up of dead tissue

50
Q

<p>Sclerotic </p>

A
  • Hardening/fibrosis within the glomerulus
  • Part or the entire glomerulus will fibrose over with a lot of scar tissue; this will affect the architecture of the glomerular basement membrane.
51
Q

nephrotic syndrome manifestations:

A
  1. edema – low oncotic pressure due to loss of plasma protein
  2. hypoalbuminemia – loss of protein
  3. hypercoagulable state – loss of coagulation cascade proteins
  4. decrease immunoglobulins – prot loss, susceptible to infection.
  5. Hyperlipoproteinemia
52
Q

FOCAL and GLOBAL disease

A

only SOME of the glomeruli in the field are affected BUT for each glomerulus that is affected, the ENTIRE glomerulus will be affected

53
Q

how do we tell Membranoproliferative Glomerularnephritis from Membranous Glomerularnephritis ?

A
  • in Membranous only GBM thickens
  • in Membranoproliferative GBM thickens AND the mesangial cells inc in number (remember proliferative in the name = inc in cell number)
54
Q

Nephritic syndrome is usually caused by _____

A

an inflammatory rupture of glomerular capillary

55
Q

Symptoms of nephritic syndrome

A

PHAROH
P: proteinuria
H: hematuria
A: azotemia: decrease in renal function leading to an increase in nitrogenous waste products
R: RBC cast in urine
O: Oliguria
H: hypertension because of decrease in renal function (increased blood volume)

56
Q

Key difference between nephrotic and nephritic syndrome

A

In nephritic rupture of capillary leads to an increase in proteinuria AND hematuria. In nephrotic only proteinuria.

57
Q

_____ is the most common glomerular renal disease throughout the world.

A

IgA Nephropathy

58
Q

CHRONIC KIDNEY DISEASE

A
  • a progressive loss of kidney SA/loss of nephrons
  • decreased ability to excrete waste, concentrate urine and conserve electrolytes
  • Causes — Primary CRF (problem within kidney) vs. Secondary CRF (disease outside of kidney causes damage)
59
Q

Primary Chronic Renal Failure (2 ex)

A

a problem with the kidney itself
• Chronic glomerulonephritis
• Interstitial nephritis

60
Q

Secondary Chronic Renal Failure (3 ex)

A

another pathological problem causes damage to kidney
• Hypertensive vascular disease
• Diabetes
• Partial urinary tract obstruction

61
Q

Chronic Renal Failure may continue to ____

A

end-stage renal disease (ESRD)

62
Q

4 Stages of chronic renal failure

A

1) Decreased renal reserve - GFR normal, NO effect
2) Renal insufficiency - GFR 20-30%, mild azotemia, nocturia, mild anemia.
3) Renal failure - below 20%, azotemia, acidosis, impaired urine dilution, severe anemia, hypernatremia, hyperkalemia.
4) End Stage RF - GFR below 5%, all organ systems feel the
effects.

63
Q

at what stage of CRF does a patient needs to start dialysis and be put on the transplant list?

A

Renal failure – GFR below 20%

64
Q

Proteinuria leads to…

A
  • decreased immunoglobulin
  • hypercoagulable state
  • hypoabluminemia (low protein in the blood)
  • low protein in blood = decreased oncotic pressure = edema
65
Q

Pros and Cons of peritoneal dialysis

A
  • Pro – cheaper, more accessible, blood doesnt have to leave body
  • Con – not as efficient, needs to be done a lot more, higher risk of infection
66
Q

Pros and Cons of hemodialysis

A
  • Pro – More efficient, depending on severity may only need a few times a week, lower risk of infection
  • Con – more expensive, blood needs to be pumped in and out into a dialyzer through AV fistula, needs to be done at a hospital
67
Q

Symptoms of uremia

A

anorexia, nausea, vomiting, diarrhea, weight loss, edema, and neurologic changes

68
Q

which part of the nephron can we see in the cortex vs. medulla?

A

cortex – all glomeruli and some proximal and distal convoluted tubule.
Medulla – LOH, and collecting ducts (PCT), more homogenous looking.

69
Q

podocytes are also known as _____

A

visceral epithelial cells

70
Q

GFR is dependent on…

A

Dependent on oncotic pressure, hydrostatic pressure, and Kf. Major determinant is glomerular capillary pressure (HP)

71
Q

ESRD counts are highest for ____, but rates are highest for ___, then ___

A

counts – highest for white

rates – highest for blacks, then native americans.

72
Q

Acute renal failure is defined as ____, results in an inc in ___.

A
  • a sudden decrease in GFR, resulting in an increase in plasma concentration of waste products (azotemia).
73
Q

ARF is characterized by: (3)

A
  • Reduced urine = oliguria/anuria
  • Retention of water, H+, minerals = metabolic acidosis
  • Retention of metabolic waste in blood (BUN, creatinine, etc) = azo
    (Sudden loss of renal function causes all of these)
74
Q

____ almost always evolves in the hospital

A

Acute renal failure

75
Q

ARF is divided into three parts:

A

Pre-Renal (Decreased renal perfusion)
Post-Renal (Obstruction to urine flow)
Parenchymal Renal Disease

76
Q

Pathogenesis of ARF (what can cause it)

A

any process that sharply decreases renal perfusion (Low BP):

  • Hypotension
  • Hypovolemia = volume depletion (fluid loss, bleeding, etc.)
  • Primary cardiac pump failure
  • Decreased systemic vascular resistance (sepsis = systemic vasodilation)
77
Q

In Acute Renal failure, how does kidney respond to renal hypoperfusion?

A

Dec GFR => increase Ang II, ADH, Aldosterone

Result: Na and water retention inc BV and BP

78
Q

Intrinsic ARF (intrarenal/parenchymal) affects 4 areas of kidney:

A

Glomerulus
Vessels
Interstitium
Tubules

79
Q

2 mechanisms of post-renal AFR:

A

Tubular obstruction – Insult (ischemia) causes cell of the tubules to slough off and a cast within the tubular lumen, leading to a retrograde increase in pressure and reduced GFR.
Tubular backleak– Backward flow of filtrate.

80
Q

Phases of post-renal ARF:

A 
Early Phase: (lasts only 12–24 hrs) Aff arteriole dilates to inc glomerular perfusion--reflex to maintain GFR despite rising tubular HP.
Late Phase: (After 12–24hrs) aff vasodilatation stops. perfusion continues to drop = GFR drop. May have anuria. Phase continues until obstruction is relieved. If prolonged, ischemia leads to permanent nephron loss.
Recovery Phase (after relief of urinary obstruction): release of pressure, pre-renal vessels relax, perfusion restored. *Dilatation of calyces, collecting system permanent.*
81
Q

BUN/Creatinine ratio in prerenal ARF:

A

Reduced blood flow causes elevated creatinine and BUN. Also, bc tubular flow is slower more BUN reabsorption (more Urea in blood) + more Crt secretion = lower Crt in blood. So ratio INC. >20/1

82
Q

We see a normal BUN/Creatinine ratio in what kind of ARF? Why?

A

Post-renal ARF, bc kidney function is normal, problem is AFTER filtration and processing of waste (trouble is getting that filtrate out). Normal ratio = 10-20/1

83
Q

BUN/Creatinine ratio in intra-renal ARF:

A
84
Q

Renal Osteodystrophy caused by ___

A

Elevated serum phosphate levels
Decreased serum calcium levels
Impaired activation of vitamin D
Hyperparathyriodism

APP Part 2 (9 decks)

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