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Drug Action I > Block 4: Disorders of Kidney and Urinary Tract Function Phys > Flashcards

Block 4: Disorders of Kidney and Urinary Tract Function Phys Flashcards

1
Q

What are kidneys responsible for?

A

Urine production
Elimination
Endocrine function
Regulates BP, electrolyte, acid-base, RBC, and bone health

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2
Q

What is the difference between AKI and CKD?

A

AKI: Rapid decrease in kidney function
CKD: loss of kidney function over time → ESRD

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3
Q

What are some of function that are affected by kidney disorders?

A
  1. Fluid and electrolyte balance
  2. Acid-base balance
  3. Elimination of waste products
  4. Comport pain
  5. Perfusion
  6. Tissue integrity
  7. health promotion
  8. Metabolism
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4
Q

What is the difference between acidosis and alkalosis in regards to the kidneys?

A

Acidosis: kidneys reabsorb bicarbonate and more acid is excreted in the urine
Alkalosis: kidneys excrete more bicarbonate and there is reduced secretion of acid in the urine

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5
Q

What is the function of glomerulus?

A

Filtering unit of the kidney

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6
Q

What is Glomerulonephritis (GN)?

A

Inflammation of the glomeruli and capillaries caused by an immune response

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7
Q

What are the symptoms of GN?

A
  1. Proteinuria
  2. Hematuria
  3. Edema
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8
Q

What is primary vs secondary GN?

A

Primary: kidneys
Secondary: Result of another systemic illness (lupus, diabetes)

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9
Q

What are the types of glomerular disorders?

A
  1. Postinfectious (deposit of immune complexes in glomeruli)
  2. Systemic disease
  3. Toxin exposure
  4. Thrombosis
  5. Genetics
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10
Q

What is IgAN?

A

Leading cause of GN → Involves mesangial deposition of IgA in glomerulus and presence of crescents in some glomeruli

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11
Q

What are glomerular crescent?

A

Crescent-shaped scar that develops when a space or hole in the glomerular basement membrane becomes crowded with macrophages and other cells

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12
Q

What is RPGN?

A

Idiopathic and the result of anti-GBM antibodies

Pauci-immune type (with symptoms of systemic vasculitis)

Inflammation of blood vessels

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13
Q

What is nephritic syndrome?

A

Clinical presentation of hematuria, mild proteinuria, RBC casts and dysmorphic RBCs.

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14
Q

How do the types of nephritic syndrome differ?

A

Focal NS → fewer than half of the glomeruli in biopsy sample are diseased

Diffuse NS: Most or all of the glomeruli in a biopsy sample are diseased

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15
Q

What is acute GN?

A

Type of nephritic syndrome

Kidney changes result from deposition of antigen-antibody complexes in the glomerular membrane

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16
Q

What are the complexes of acute GN?

A
  1. External antigens (bacteria)
  2. Internal causes (lupus)
  3. Foreign proteins
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17
Q

Symptoms of acute GN?

A
  1. Hematuria
  2. RBC casts
  3. Edema
  4. Hypertension
  5. Pyuria (pus in the urine)
  6. Decreased renal function
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18
Q

Conditions involving acute GN

A
  1. Lupus nephritis
  2. Postinfectious glomerulonephritis
  3. Antiglomerular basement membrane disease
  4. Immunoglobin A nephropathy
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19
Q

What is nephrotic syndrome?

A

Acute GN worsens → proteinuria is >3 g/day

20
Q

What are the symptoms fo NS? Conditions?

A
  1. HLD
  2. Hypoalbuminermia
  3. Edema
  4. Urinary fatty casts
  5. RBCs and cast absence

Diabetic nephropathy

21
Q

Difference between nephritic and nephrotic syndrome?

A
22
Q

What is diabetic nephropathy?

A

Hyperglycemic-induced glomerulosclerosis → ESRD

23
Q

What is an early indication of diabetic nephropathy?

A

Mild albinuria → 10-15 yr after diagnosis of diabetes

24
Q

What are the types of proteinuria?

A
  1. Persistant mild albuminuria
  2. Tubular proteinuria (Smaller proteins)
25
Q

How can you detect proteinuria?

A

Dipstick assessment

26
Q

T/F: Tubular proteinuria is detectable via dipstick assessment?

A

False: proteins are small

27
Q

Describe the progressions of diabetic nephropathy?

A

Hyperglycemia → polyuria → increase RBF → Glomerular hypertrophy → Glomerular HTN → Hyperfiltration

28
Q

How does renal auto regulation or intrisic control work?

A

Maintains constant GFR when MAP is 80-180
Autoreg ceases when out of ranges

  1. Myogenic mechanism
  2. Tubuloglomerular feedback mechanism
29
Q

What is Tubuloglomerular feedback mechanism? How does it work?

A

Flow-dependent mechanism respond to filtrate NaCl concentration from the macula dense cells

If GFR Increase → filtrate flow rate Increase → Decrease reabsorption time → high filtrate NaCl levels → constriction of afferent arteriole → Decrease NFP & GFR → more time for NaCl reabsorption

Opposite with low GFR

30
Q

What happens during prolonged hyperglycemia?

A

Glycosylation of amino acids → advanced glycosylation end products → microvascular complications → hypoxia and increased oxidative stress → Proteinuria

31
Q

What can cause prolonged hyperglycemia?

A

Podocytopenia

32
Q

What is podocytopenia?

A

Reduction of podocytes

33
Q

Main manifestations of diabetic neuropathy?

A
  1. Albuminuria
  2. Hyperfiltration
  3. HTN
34
Q

How does HTN nephropathy differ from diabetic?

A

CKD from long standing HTN → ESRD and nephrosclerosis

35
Q

What are examples of essential (primary) HTN?

A
  1. Genetics
  2. Lifestyle
  3. Activation of RAA, and SNS
  4. Arterial stiffness
36
Q

What is the difference between primary and secondary HTN?

A

Primary: No clear cause
Secondary: From a med condition

37
Q

What occurs during HTN nephropathy?

A

Atherosclerosis → Reduction of BF to glomeruli → SNS stimulation → Activation of RAAS → renal renin production → increase BP

38
Q

How can HTN damage kidneys?

A
  1. Increase development of AS in afferent and efferent arterioles
  2. HBP damages fragile capillaries
  3. Waste product build up → decrease GFR → Proteinuria and microalbuminuria

Kidney responds by increasing systemic blood pressure

39
Q

What are the manifestations of HTN nephropathy?

A
  1. LV hypertrophy
  2. Ophthalmic changes
  3. Mild proteinuria
  4. Increased BUN and creatine
40
Q

What is nephrolithiasis?

A

Stone formation and aggregation of urinary crystals (Kidney stones)

41
Q

What is composition of a majority of kidney stones?

A

Calcium based

42
Q

What are the outcomes stones?

A
  1. Damage to the lining of the urinary tract.
  2. Decreased amounts of substances that allow crystals to aggregate.
  3. Slow urine flow that allows urine to crystallize.
43
Q

Describe the process of stone formation?

A
  1. Crystals are unable to dissolve because of their high concentration (supersaturation)
  2. Excretion of large amounts of calcium in kidneys, urinary pH, and lack of inhibitors
  3. Aggregation of crystals
  4. Nuclei formation
44
Q

What are the manifestations of renal calculi?

A
  1. Acute, unilateral flank pain
  2. Nausea, vomiting
  3. Hematuria
  4. Severe pain that comes and goes (renal colic)
45
Q
A

Drug Action I (32 decks)

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