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PATHO/PHARM II > Conditions Effecting the Urinary System and Pharmacotherapy > Flashcards

Conditions Effecting the Urinary System and Pharmacotherapy Flashcards

Exam 1: Just kill yourself already you idiot.

1
Q

Glomerulonephritis

A

inflammation of glomeruli and of the small blood vessels in the kidney

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2
Q

Causes of inflammation of the glomeruli

A

Primary glomerular injury- isolated to the kidney

Secondary glomerular injury- systemic disease (drugs, DM, HTN)

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3
Q

What are the main components of inflammation of glomeruli/

A

Immune mechanisms are the main component

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4
Q

Immune mechanisms are the main component of inflammation of glomeruli, what are the examples:

A

Antigen-antibody complexes, activated inflammatory response
* Complement activation, WBC recruitment, activated platelets, cytokine release  injury
to GBM
* Increased glomerular mem permeability  proteins & RBCs escape into urine
* Swelling & cell proliferation in Bowman’s space

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5
Q

Risk factors leading to inflammation of glomeruli?

A
  • Streptococcal infection, typically precedes (most common)
  • It affects children between the ages of 3 to 7 years, especially boys
  • Staphylococcus, Pneumococcus, varicella
  • Immunodeficiency
  • Inflammatory DX ~ SLE
  • Meds (eg NSAIDs)
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6
Q

Complications of inflammation of glomeruli?

A

CKD, renal failure are the leading cause

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7
Q

How long does it take for clinical manifestations of glomerulonephritis?

A

Sudden or gradual

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8
Q

What can occur before symptoms appear for glomerulonephritis?

A

Significant nephron function loss can occur before symptoms

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9
Q

How is symptoms presentation of glomerulonephritis?

A

Symptom presentation may be silent, mild, moderate or severe

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10
Q

What kind of disease is glomerulonephritis considered?

A

Severe or progressive disease  oliguria, htn, renal failure

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11
Q

What are two major signs and symptoms of severe glomerulonephritis?

A

Hematuria with red blood cell casts & Proteinuria (foamy urine) exceeding 3 to 5 g/day with albumin (macroalbuminuria) as the major protein

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12
Q

What is used to evaluate glomerulonephritis?`

A

Urinalysis

Renal biopsy

Reduced GFR

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13
Q

Urinalysis for glomerulonephritis should include:

A

proteinuria, rbcs, wbcs, casts

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14
Q

Renal biopsy for glomerulonephritis should find out:

A

Type of lesion, extent of renal injury

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15
Q

Reduced GFR: slide I don’t understand

A

Elevated plasma urea
* Cystatin C in blood
* Biomarker of kidney function
* Elevated creatinine concentration &
reduced CrC

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16
Q

Treatment of glomerulonephritis includes:

A

Treating Edema

High calorie, low protein diet

Antibiotics

Corticosteriods

Cytotoxic agents

ANticoagulants

BP management

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17
Q

To treat edema related to glomerulonephritis what should be done?

A

diuretics, dialysis, restrict Na & H2O
intake, I &O, daily weight

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18
Q

What should antibiotics be used for in glomerulonephritis?

A

mgmt of underlying infection causing
antigen-antibody response

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19
Q

What are corticosteroids used for in glomerulonephritis?

A

suppress the inflammatory
response, decrease Ab synthesis

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20
Q

What are cytotoxic agents used for in glomerulonephritis?

A

(cyclophosphamide) – suppress immune response

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21
Q

What are Anticoagulants used for in glomerulonephritis?

A

– fibrin crescent formation

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22
Q

Tetrad of manifestations of Nephrotic syndrome

A
  1. Proteinuria
  2. Hyperlipidemia (Dyslipidemia)
  3. Hypoalbuminemia
  4. Peripheral edema
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23
Q

What is the pathophysiology of nephrotic syndrome:

A
  1. Inflammation/damage of the glomerulus
  2. Proteins are able to pass to tubule (more permeable)
  3. Protein travels through tubule and becomes part of urine
  4. Protein loss is proteinuria w/wo hematuria
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24
Q

What types of proteins are lost in urine in nephrotic syndrome?

A

immunoglobulins

albumins

lipiduria

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25
Q

What would loss of protein lead to in nephrotic syndrome?

A

Edema-

Susceptibility to infection

Liver produces more cholesterol= hypercholesterolemia

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26
Q

Why would edema occur in nephrotic syndrome?

A

Hypoproteinemia would lead to reduced oncotic pressure. Water and electrolytes move to interstitial space. There are no solutes to hold the water and electrolytes in the vascular compartment.

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27
Q

What is nephritic syndrome?

A

Nephritic syndrome is hematuria and red blood cell casts in the urine.

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28
Q

What does nephritic syndrome usually occur with?

A

It occurs primarily with infection-related glomerulonephritis and rapidly progressive crescentic glomerulonephritis.

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29
Q

What is nephritic syndrome caused by:

A

It is caused by increased permeability of the glomerular filtration membrane with pore sizes large enough to allow the passage of red blood cells and protein.

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30
Q

Renal insufficiency

A

Decline in renal fxn to ≈25% of normal, GFR <30 ml/min, & mildly elevated serum creatinine (SCr) and urea

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31
Q

Kidney failure

A

Kidney failure refers to significant loss of renal function.

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32
Q

End Stage Kidney Disease

A

When less than 10% of kidney function remains, this is termed end-stage kidney disease (ESKD).

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33
Q

Uremia (uremic syndrome)

A

is a syndrome of renal failure and includes elevated blood urea and creatinine levels accompanied by fatigue, anorexia, nausea, vomiting, pruritus, and neurologic changes.

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34
Q

Uremia represents numerous consequences related to kidney failure, including:

A

retention of toxic wastes, deficiency states, electrolyte disorders, and immune activation promoting a proinflammatory state.

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35
Q

Azotemia

A

is characterized by increased blood urea nitrogen (BUN) levels (normal is 8 to 20 mg/dl) and frequently increased serum creatinine levels (normal is 0.7 to 1.4 mg/dl).

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36
Q

What do both azotemia and uremia indicate?

A

Both azotemia and uremia indicate an accumulation of nitrogenous waste products in the blood

37
Q

Acute kidney injury (AKI)

A

is a sudden decline in kidney function with a decrease in glomerular filtration and urine output with accumulation of nitrogenous waste products in the blood

38
Q

AKI can be classified as what?

A
  1. Prerenal
  2. Intrarenal
  3. Postrenal
39
Q

What is the most common reason for AKI?

A

Prerenal acute kidney injury is the most common reason for AKI and is caused by inadequate kidney perfusion.

40
Q

Prerenal acute renal failure

A

a condition that occurs when the blood supply to the kidneys is reduced or compromised

41
Q

Prerenal acute kidney injury causes include:

A

Hypovolemia

Renal Hypoperfusion/Renal Vasoconstriction

Systemic Vasodilation

Decreased arterial blood volume (decreased cardiac output)

42
Q

Poor perfusion of kidneys can occur because of:

A

Poor perfusion can result from hypotension, hypovolemia associated with hemorrhage or fluid loss (e.g., burns), sepsis, inadequate cardiac output (e.g., myocardial infarct [heart attack]), or renal vasoconstriction (e.g., caused by NSAIDs or radiocontrast agents) or renal artery stenosis.

43
Q

The GFR declines in Prerenal acute kidney injury why?

A

The GFR declines because of the decrease in glomerular filtration pressure.

44
Q

Failure to restore blood volume in prerenal acute kidney injury includes:

A

Failure to restore blood volume or blood pressure and oxygen delivery can cause ischemic cell injury and acute tubular necrosis or acute interstitial necrosis, a more severe form of AKI.

45
Q

Intrarenal acute kidney injury:

A

(disorders involving renal parenchymal or interstitial tissue)

a type of AKI that occurs when the kidney’s structure is damaged.

46
Q

Intrarenal acute kidney injury:

A

Acute tubular necrosis (postischemic or nephrotoxic)

Glomerulopathies

Acute interstitial necrosis (tumors or toxins)

Vascular damage

Malignant hypertension, vasculitis

Coagulation defects

Renal artery/vein occlusion

Bilateral acute pyelonephritis

47
Q

Post acute renal failure (ARF)

A

occurs when waste builds up in the kidneys due to an obstruction in the lower urinary tract

48
Q

Examples of obstructive uropathies that cause post renal AKI?

A

BPH
Renal calculi
Bladder/prostate cancer
Blood clots
Tumors

49
Q

What are characteristic findings of Post renal AKI?

A

Characteristic finding: flank pain & anuria followed by polyuria

50
Q

Post renal AKI: Prolonged mechanical obstruction leads to what?

A

Prolonged mechanical obstruction leads to tubular atrophy and irreversible kidney fibrosis

51
Q

Treatment of Post renal AKI?

A

Perform urinary catheterization
Prevent UTI.
Relieve obstruction
Treat reversible causes

52
Q

Four phases of AKI:

A
  1. Onset
  2. Oliguric
  3. Diuretic phase
  4. Recovery phase
53
Q

Onset phase of AKI

A

Onset phase: Kidney injury occurs.

54
Q

Oliguric (anuric) phase of AKI

A
  1. Oliguric (anuric) phase: Urine output decreases from renal tubule damage.
55
Q

Diuretic phase of AKI

A
  1. Diuretic phase: The kidneys try to heal and urine output increases, but tubule scarring and damage occur. The kidneys recover their ability to excrete waste but cannot concentrate the urine.
56
Q

Recovery phase of AKI

A

Tubular edema resolves and renal function improves.

57
Q

Chronic Kidney Disease (CKD)

A

Progressive loss of renal function, affects nearly all organ systems

58
Q

What are some qualities of Chronic Kidney Disease

A

Slow, progressive, and irreversible loss of kidney function & GF based on eGFR

59
Q

What do people with Chronic Kidney Disease require?

A

Requires dialysis or kidney transplantation to maintain life.

60
Q

AKI can progress to what?

A

AKI can progress to CKD or AKI on CKD

61
Q

Normal gfr values

A

Normal GFR 120 to 140 mL/min

62
Q

Stages of chronic kidney disease

A
  1. Normal kidney function (GFR > 90 mL/min)
  2. Mild CKD (GFR 60-89 mL/min)*
  3. Moderate (GFR 30-59 mL/min)
  4. Severe (GFR 15-29 mL/min)
  5. End stage (GFR less than 15)
63
Q

What occurs during stage 1- Normal kidney function (GFR > 90 mL/min)

A

Mild damage, reduced renal reserve

64
Q

What happens to the kidneys during stage 1- Normal kidney function (GFR > 90 mL/min)

A

Unaffected nephrons overwork to compensate for diseased nephrons

65
Q

What kind of symptoms are common in stage 1 of ckd?

A

Htn common, proteinuria, high Cr or no sx at all

66
Q

What is the kidney function in stage 1 of ckd?

A

Kidney function 90-100%

67
Q

What happens to nephrons in stage 2 of ckd?

A

Kidney nephron damage has occurred

68
Q

What happens to metabolic waste in stage 2 of ckd?

A

Slight elevation of metabolic waste in BUN/Cr

69
Q

What symptoms occur during stage 2 of ckd?

A

Inability to concentrate urine, polyuria and nocturia
Htn

70
Q

How is stage 3 of ckd divided?

A

split into two substages based on eGFR (3a & 3b):

71
Q

What happens to nephrons in the third stage of CKD?

A

Nephron damage continues with decreased nephrons

72
Q

What may be needed in stage 3 of ckd?

A

Restriction of fluids, proteins, electrolytes, including phosphorus, may be needed

73
Q

What occurs in stage 4 of CKD?

A

Erythropoietin deficiency, anemia, HyperPhos/K, Increased triglycerides, Met acidosis, Na+/H2O retention

74
Q

WHat occurs during stage 5 of ckd?

A

Oliguria occurs

Uremia (“urea in blood”) is the result and is fatal; classic marker

75
Q

What happens to BUN and Cr levels in CKD?

A

Excessive urea (BUN) and Cr builds up in the blood

76
Q

What is a classic marker of stage 5 - end stage ckd?

A

Uremia (“urea in blood”) is the result and is fatal; classic marker

77
Q

What are two factors known to advance renal disease?

A

proteinuria and angiotensin II activity

78
Q

How does proteinuria contribute to injury?

A

Proteinuria contributes to tubulointerstitial injury by accumulating in the interstitial space of the nephron tubules.

79
Q
A

Angiotensin II (from activation of the renin-angiotensin-aldosterone system [RAAS]) causes efferent arteriolar vasoconstriction and promotes glomerular hypertension and hyperfiltration. Hyperfiltration is also associated with hyperglycemia and diabetic nephropathy. The chronically high intraglomerular pressure increases glomerular capillary permeability, contributing to proteinuria. Angiotensin II also may promote systemic hypertension and the activity of inflammatory cells and growth factors that participate in tubulointerstitial fibrosis and scarring.

80
Q

Parathyroid acts on the kidneys to do what?

A

PTH acts on the kidneys to increase calcium reabsorption and decrease phosphate reabsorption

81
Q

Vitamin D works with PTH to do what?

A

Vitamin D, particularly its active form calcitriol, works with PTH to maintain calcium and phosphorus homeostasis by facilitating intestinal absorption of calcium and phosphate.

82
Q

slide 35

A
83
Q

Skeletal presentation of CKD?

A

Results are pathological fxs, bone pain, deformities of long bones

84
Q

What is the treatment of skeletal issues with CKD?

A

Activated Vitamin D

Phosphate binders work to bind phosphate in gut & excrete in stool

Phosphate-restricted diet
Activated Vit D replacement
Possible parathyroidectomy

85
Q

Cardiovascular presentation of CKD?

A

37

86
Q

Neuro clinical presentation of CKD?

A

Uremic encephalopathy from toxins in CSF

Spectrum of cognitive & consciousness changes

87
Q

What is the treatment of neuro problems with CKD?

A

Tx: dialysis/kidney transplant

88
Q

Slide 39

A
89
Q
A

PATHO/PHARM II (8 decks)

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