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Renal, Urinary Systems, and Electrolytes Flashcards

1
Q

Hyperparathyroidism: Pathophysiology
How does primary hyperparathyroidism lead to osteoporosis?

A

Hypercalcemia and hypophosphotemia. Causing cortical thinning of the appendicular skeleton (eg, pectoral girdle, pelvic girdle, and limbs). Radiologically as subperiosteal erosions.
More advanced disease can present as osteitis fibrosa cystic, characterized by granular decalcification of the skull (“salt-and-pepper-skull), osteolytic cysts, and brown tumors.

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2
Q

Uworld: Physiology: Hypophosphatemia
What are some causes phosphate to decrease via internal redistribution?
3 points

A
  • increased insulin secretion (refeeding malnourished)
  • acute respiratory alkalosis (stimulate glycolysis)
  • hungry bone syndrome (after parathyroidectomy)
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3
Q

Uworld: Physiology: Hypophosphatemia
What are some causes phosphate to decrease through decreased intestinal absorption?
3 points

A
  • chronic poor intake
  • aluminum or magnesium containing antacids (bind phosphate)
  • steatorrhea or chronic diarrhea
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4
Q

Uworld: Physiology: Hypophosphatemia
What are some causes phosphate to decrease through increased urinary excretion?
4 points

A
  • primary and secondary hyper-PTH
  • vitamin D deficiency (decrease GI absorption, increased urinary excretion)
  • primary renal phosphate wasting syndromes
  • Fanconi syndrome
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5
Q

Pharmacology:
How does the drug Sevelamer help treat CKD?

A
  • Prevents GI Phosphate absorption, decreasing the serum levels and decrease parathyroid over activation (secondary hyperparathyroidism)
  • generally reserved for phosphate levels consistently greater than 5.5 mg/dL
  • AE include GI upset, fatigue, and joint pain
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6
Q

Pathology:
What is the makes up the protein matrix of all urinary casts?

A

Tamm-Horsfall mucoprotein

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7
Q

Pathology:
What type of hypersensitivity is Goodpasture syndrome and type 1 rapidly progressive glomerulonephritis?

A

Type 2

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8
Q

Pathology:
What type of hypersensitivity is Post-streptococcal glomerulonephritis, type 2 RPGN, and membranous glomerulopathy?

A

Type 3

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9
Q

Pathology:
What are the causes and findings for epithelial cell casts?

A

Causes:
- Acute tubular necrosis
- ethylene glycol toxicity
- heavy-metal poisoning
- acute rejection of transplant graft
Findings:
- desquamated tubular cells in a protein matrix

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10
Q

Pathology:
What are the causes and findings for red blood cell casts?

A

Causes:
- Glomerulonephritis: IgA nephropathy, PSGN, and goodpasture syndrome
- Malignant HTN
- vasculitis
- renal ischemia
Findings:
- clumps of dysmorphic RBCs with blebs and buds indicate RBCs are of glomerular origin versus bladder origin (eg, bladder cancer)

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11
Q

Pathology:
What are the causes and findings for white blood cell casts?

A

Causes:
- pyelonephritis
- interstitial nephritis
- lupus nephritis
Findings:
- WBC casts indicate inflammation in renal interstitial tubules, and/or glomeruli
- WBCs in urine indicate lower UTI

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12
Q

Pathology:
What are the causes and findings for Hyaline casts?

A

Causes:
- often seen in normal urine
- pyelonephritis
Findings:
- glassy looking
- composed of Tamm-Horsfall protein

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13
Q

Pathology:
What are the causes and findings for granular casts?

A

Causes:
- ATN
- chronic renal failure
- nephrotic syndrome
Findings:
- derived from the breakdown of cellular causes, especially epithelial casts

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14
Q

Pathology:
What are the causes and findings for fatty casts?

A

Causes:
- nephrotic syndrome
Finding:
- fat droplets in hyaline matrix
- Maltese-cross configuration due to presence of cholesterol (under polarized light)

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15
Q

Pathology:
What conditions manifest with nephrotic syndrome?
6 points

A
  • MCD
  • FSGN
  • Membranous glomerulopathy
  • Membranoproliferative glomeronephritis
  • Diabetic nephropathy
  • Lupus Nephropathy
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16
Q

Pathology:
What conditions manifest with nephritic syndrome?
7 points

A
  • acute proliferative glomerulonephritis (poststreptococcal/infectious)
  • Rapidly progressive glomerulonephritis (crescentic)
  • Anti-GBM disease Goodpasture syndrome
  • MPGN
  • IgA nephopathy (Berger disease)
  • Hereditary nephritis (Alport syndrome)
  • Lupus nephritis
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17
Q

Pathology:
What are the key findings of nephrotic syndrome?

A
  • Massive proteinuria ( > 3.5 g/24h)
  • Hypoalbuminemia (plasma albumin level < 3 g/dL)
  • Edema
  • Hyperlipidemia, urinary fatty casts, and hypercoagulation are also hallmarks
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18
Q

Pathology:
How would you describe membranous glomerulopathy?

A

Thick GBM but no proliferation

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19
Q

Pathology:
How would describe membranoproliferative glomerulonephritis?

A

Thich GBM with hypercellular glomeruli

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20
Q

Pathology:
How would you describe crescentic glomerulonephritis?

A

Proliferation of the parietal epithelial cell lining of Bowman capsule (forms a crescent)

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21
Q

Pathology:
Patients with nephrotic syndrome are at increased risk for what type of infections, why?

A
  • Encapsulated bacterial infections (Staphylococci and pneumococci)
  • loss of gamma-globulins
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22
Q

Pathology:
What is MCD usually preceded by?

A

Respiratory infections or routine immunization

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23
Q

Pathology:
What are some other names for MCD?

A
  • lipoid nephrosis
  • nil disease
  • foot process disease
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24
Q

Pathology:
How would diagnose MCD?

A

Light microscopy:
- no obvious chances but note a lipoid appearance in the PCT
Electron Microscopy:
- podocyte effacement and increased lipoproteins in the PCTs
- * Definitive dx is made when there is diffused effacement

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25
Q

Pharmacology:
How would you treat MCD?

A
  • Initial: High dose oral glucocorticoids (Prednisone) for up to 8 weeks
  • if relapse or recurrence then alkylating agent (ie cyclophosphamide or chlorambucil)
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26
Q

Pathology:
How does Focal Segmental Glomerulosclerosis present?

A
  • nephrotic syndrome
  • nonselective proteinuria
  • HTN
  • Associated with HIV, Heroin use, and sickle cell disease
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27
Q

Pathology:
How would you diagnose Focal Segmental Glomerulosclerosis?

A
  • light microscope: focal accumulation of hyaline material and segmental sclerosis
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28
Q

Pharmacology:
How would you treat Focal Segmental Glomeruloscleosis?

A
  • oral glucocorticoids
  • cyclophosphamide and cyclosporine
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29
Q

Pathology:
What is the leading cause of nephrotic syndrome of nephrotic syndrome?

A

Diffuse Membranous Glomerulopathy
- peak incidence ages from 30-50

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30
Q

Pathology:
How does Diffuse Membranous Glomerulopathy present?

A
  • nephrotic syndrome with nonselective proteinuria in otherwise HEALTHY patients
    Associated with
  • Systemic diseases: SLE and RA
  • STIs: Hep B, Hep C, ans syphilis
  • Less common infections: Schistosomiasis, malaria, and leprosy
  • Drugs: Penicillamine and Gold-containing compounds
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31
Q

Pathology:
How would you diagnose Diffuse membranous glomerulopathy?

A

Light Microscopy:
- diffuse GBM thickening due to subepithelial deposits
Electron Microscopy:
- spike and dome pattern IF staining IgG and C3

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32
Q

Pharmacology:
How would you treat Diffuse membranous glomerulopathy?

A
  • 40% have spontaneous remission
  • if severe then immunosuppressive therapy
  • Cyclophosphamide and cyclosporine with glucocorticoids to reduce proteinuria and slow the decline of GFR
  • Renal transplant is ESRD progresses
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33
Q

Pathology:
How does Membranoproliferative Glomerulomephritis occur?

A
  • idiopathic
  • more commonly secondary to monoclonal immunoglobulin deposition diseases, autoimmune (ie SLE), chronic thrombotic microangiopathies, or chronic infections
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34
Q

Pathology:
Describe Membranoproliferative Glomerulonephritis type 1:

A
  • occurs with 2/3 of cases
  • due to deposition of ICs (T3HS)
  • associated with Hep B, Hep C, and cryoglobulinemia
  • some cases have a nephritic presentation
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35
Q

Pathology:
Describe Membranoproliferative Glomerulonephritis type 2:

A
  • occurs in 1/3 of cases
  • often associated with C3 nephritic factor (C3NeF)
  • aka dense deposit disease due to the deposition between the laminate dense and sub endothelial space of the GBM
  • C3 is present, there are no IgG deposits
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36
Q

Pathology:
How does Membranoproliferative Glomerulonephritis present?

A
  • Type 1 presents with nephrotic syndrome
  • Type 2 can show either or both nephrotic/nephritic
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37
Q

Pathology:
How would you diagnose Membranoproliferative Glomerulonephritis?

A

Electron Microscopy:
- Type 1 shows sub endothelial electron dense deposits of IgG and C3. Ingrowth of the mesangium causes splitting of the GBM creating and ‘tram-track appearance’
- Type 2 shows intramembranous deposits and increased size of glomeruli, and increases cellularity of the mesangial cells. ‘Tram-track’ appearance.

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38
Q

Pharmacology:
How would you treat Membranoproliferative Glomerulonephritis?

A
  • no effective therapy
  • plasma exchange with Albumin can slow disease progression in some pts with circulating C3NeF
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39
Q

Pathology:
What is the first sign of Diabetic Nephropathy?

A

Microalbuminuria, can occur aboutt 5-10 years before other symptoms develop

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40
Q

Pathology:
How does Diabetic Nephropathy present?

A
  • HTN or Edema
  • complication may include arteriosclerosis of the renal artery and the efferent arterioles before the afferent.
  • left untreated, nephrotic-range proteinuria ultimately develops
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41
Q

Pathology:
How would you diagnose Diabetic Nephropathy?

A

Clinical grounds
- should be suspected in patients with diabetes and end-organ damage from DM such as retinopathy and neuropathy; and have a positive dipstick positive proteinuria.
Light Microscopy:
- Kimmelstiel-Wilson lesion / ‘wire loop’ lesions: signifies the thickening of the GBM and mesangial expansion

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42
Q

Pharmacology:
How do you treat Diabetic Nephropathy?

A
  • ACEi’s and ARB’s to counteract the hyper filtration.
  • Good glucose control
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43
Q

Pathology:
What is Renal Amyloidosis?

A
  • deposition of fibrous, insoluble proteins in a beta-pleated sheet conformation in the renal glomeruli. It is a multisystem disorder of protein folding
  • Two types: AL and AA
  • when immunoglobulin light chains lack the beta-pleated configuration, disease is then called light chain deposition disease
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44
Q

Pathology:
How does Renal Amyloidosis present?

A
  • nephrotic- range proteinuria, severe edema, and renal insufficiency
  • if amyloidosis is caused by a secondary disease (eg, multiple myeloma, TB, RA, etc.) the pt will also show signs and symptoms of the primary disease
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45
Q

Pathology:
How do you diagnoses renal amyloidosis?

A
  • definitive diagnosis is based on renal, abdominal fat pad, or rectal biopsy
    Light Microscopy:
  • Congo red apple-green birefringence under polarized light
  • mesangial expansion is present with amorphous hyaline material (amyloid) and thickening of the GBM
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46
Q

Pharmacology:
How do you treat renal amyloidosis?

A
  • combo of melphalan and prednisone
  • AA amyloidosis tx depends on underlying cause
  • transplantation is an option, but extra renal organ involvement may be a contraindication
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47
Q

Pathology:
Describe the presentation of Lupus Nephritis:

A
  • nephrotic or nephritic
  • weight gain, high BP
  • darker foamy urine
  • swelling around the eyes, legs, ankles, or fingers
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48
Q

Pathology:
How would you diagnose Lupus Nephritis?

A
  • diffuse proliferative nephritis (Class IV) is the most common type seen in SLE
  • renal Bx can categorize into 6 classes based on advancement
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49
Q

Pharmacology:
How would you treat Lupus Nephritis?

A
  • Class VI is usually resistant to treatment so focus on symptom management
  • general SLE treatment, increase dose on corticosteroids, immunosuppressant therapy
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50
Q

Pathology:
What are some distinct symptoms of Nephritic Syndrome?

A
  • hematourira
  • oliguria
  • azotemia (increased BUN and creatinine)
  • HTN
  • Mild proteinuria
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51
Q

Pathology:
What are some important serological markers in nephritic syndromes?

A
  • C3 levels
  • Anti-GBM titer
  • antineutrophil cytoplasmic antibody titer (ANCA)
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52
Q

Pathology:
How does Acute Proliferative Glomerulonephritis (PSGN) typically precede? How?

A
  • Precedes with infection with certain strains of Group A Beta-Hemolytic streptococci (GABHS)
  • secondary to immune-complex deposition in the glomerulus with resulting complement activation and inflammation
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53
Q

Pathology:
How does PSGN present?

A
  • Nephritic syndrome
  • usually 10 days after pharyngeal infection or,
  • 2-3 weeks after skin infection with GABHS
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54
Q

Pathology:
How do you diagnose PSGN?

A
  • serum chemistry: ASO titers or other streptococcal antibodies (anti-DNAase B), C3 levels tend to be low; ANCA and anti-GBM antibodies are negative
  • Urinalysis: ‘Smoky brown’ colored urine, RBCs and RBC casts, mild proteinuria
  • pathology: renal bx
  • light microscopy: hyper cellular and enlarged glomeruli
  • electron microscopy: characteristic sub epithelial electron-dense deposits (humps)
  • immunofluorescence: IgG and C3 coarse granular deposits, with a ‘lumpy-bumpy’ appearance.Pathology:
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55
Q

Pharmacology:
What is the treatment of PSGN?

A

Goal to maintain proper water and electrolyte balance.
- diuretics and other antihypertensive
- PCN to eradicate GABHS to prevent the progression to rheumatic fever

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56
Q

Pathology:
How many types of Rapidly Progressive Glomerulonephritis?

A

3

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57
Q

Pathology:
Describe RPGN Type 1:

A
  • associated with Goodpasture syndrome
  • IF findings: ANCA-negative, linear IgG and C3 deposits along the GBM
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58
Q

Pathology:
Describe RPGN Type 2:

A
  • associated with PSGN, SLE, IgA nephropathy, Henoch-Schönlein purpura
  • IF findings: ANCA-negative, granular ‘lumpy-bumpy’ deposits
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59
Q

Pathology:
Describe RPGN Type 3:

A
  • associated with granulomatosis with polyangiitis or idiopathic
  • IF findings: ANCA-positive, no deposits on the GBM
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60
Q

Pathology:
How would you diagnose RPGN?

A

Serum chemistry:
- BUN and creatinine may rise rapidly
- anti-GBM antibody positive is association with Goodpasture syndrome
- ANCA presence varies depending on cause
- complement levels may be decreased in some cases
Urinalysis: Blood (RBCs). protein. WBC (monocytes), and casts
Pathology: Renal biopsy
Light Microscopy: crescents signifying proliferation of glomerular parietal cells; Bowman space is filled with monocytes and macrophages. Large amounts of fibrin accumulate in the layers of the crescents.

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61
Q

Pathology:
Describe the pathophysiology in Goodpasture Syndrome:

A

antibodies against proteins in the GBM, resulting in symptoms isolated to the kidney, or including the lungs because of cross-reactivity (eg. alpha 2 chain of collagen type IV) seen in the alveolar and GBM.

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62
Q

Pathology
How does Goodpasture syndrome present?
4 points

A
  • Hematuria and other nephritic symptoms
  • subnephrotic range proteinuria
  • RPGN over the course of a few weeks
  • Pulmonary hemorrhage presenting with hemoptysis
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63
Q

Pathology:
How would you diagnose Goodpasture syndrome?

A
  • CXR shows bibasilar shadows
  • serum chemistry: positive for anti-GBM antibodies, ANCA negative most cases, C3 levels normal
  • Urinalysis: RBCs, RBC casts, and mild proteinuria
  • Light microscopy: Cellular accumulation in the Bowman space; crescent formation.
  • Immunifluorescence: Linear, ribbon-like deposits of IgG along the GBM
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64
Q

Pharmacology:
What is the treatment for Goodpasture syndrome?

A
  • emergency plasmapheresis until anti-GBM titers become negative
  • Prednisone and either cyclophosphamide or azathioprine started simultaneously to suppress formation of new GBM antibodies
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65
Q

Pathology:
What differentials can you think of if the patient presents with hemoptysis and hematuria?

A
  • Goodpasture syndrome
  • GPA (Wegener granulomatosis)
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66
Q

Pathology:
Describe IgA Nephropathy (Berger Disease):

A
  • usually affects children and young adults
  • caused by increased production or decreased clearance of IgA leading to deposition of the antibodies in the mesangial matrix
  • most common glomerulopathy worldwide
  • also can be a component to Henöch- Schönlein purpura
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67
Q

Pathology:
How does IgA Nephropathy (Berger Disease) present?

A
  • gross hematuria 24-48 hours after a nonspecific upper respiratory tract infection or GI infection
  • Hematuria typically lasts for several days and then spontaneously resolves, only to recur every few months
  • HTN is unusual at presentation
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68
Q

Pathology:
How would you diagnose IgA Nephropathy (Berger Disease)?

A
  • serum chemistry: ANCA- and anti-GBM are negative, C3 levels are normal
  • Urinalysis: Painless spontaneous hematuria
  • Light microscopy: can be normal, also show focal crescentic proliferative glomerulopathy
  • Immunifluorescence: Granular IgA deposits with specific distribution in mesangial cells
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69
Q

Pharmacology:
How would you treat IgA Nephropathy (Berger Disease)?

A
  • Modest prtoeinuria: Glucocorticoids
  • Severe disease: plasma exchange and immunosuppression or high dose Immunoglobulins
  • ACE inhibitors to slow the disease progression to ESRD
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70
Q

Pathology:
Describe the pathophysiology of Hereditary Nephritis (Alport Syndrome):

A
  • hereditaryL XLR
  • error in the synthesis of the alpha 5 chain of type 4 collagen
  • Sensorineural deafness, les dislocation, and early development of cataracts also show because of Type 4 collagen in other tissues
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71
Q

Pathology:
How does Alport Syndrome present?

A
  • between 5 a 20 year olds
  • asymptomatic, but also painless gross hematuria
  • family hx of nephritic syndrome and deafness in males
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72
Q

Pathology:
How do you diagnose Hereditary Nephritis (Alport Syndrome)?

A
  • serum Chemistry: ANCA- and anti-GBM negative, C3 levels are normal
  • Urinalysis: Gross hematuria, mild proteinuria
  • Light microscopy: Glomerular and mesangial proliferation. Foam cells
  • EM: Splitting of the laminate dense (component of GBM)
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73
Q

Pharmacology:
How do you treat Hereditary Nephritis (Alport Syndrome)?

A

No specific therapy
- ACEIs and ARBs to slow the progression
- Renal transplantation
- Males more severe, females typically carriers

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74
Q

Pathology:
Describe the definition of Granulomatosis with polyangitis (GPA):

A
  • formerly Wegener granulomatosis
  • its a systemic disease that presents as focal necrotizing vasculitis and necrotizing granulomas in both in the upper and lower respiratory tract (lungs)
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75
Q

Pathology:
Describe the presentation of Granulomatosis with polyangitis:

A
  • nonspecific symptoms: fever, arthralgia, lethargy, and malaise
  • nephritic symptoms
  • mild proteinuria
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76
Q

Pathology:
Describe how you would diagnose granulomatosis with polyangitis:

A
  • cytoplasmic staining ANCA (c-ANCA) positive (80% with renal involvement)
  • Bx is required and demonstrates focal, segmental necrotizing glomerulonephritis with occasional crescent formation
  • anti-GBM is negative and complement levels are normal
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77
Q

Pharmacology:
Describe the treatment of granulomatosis with polyangitis:

A
  • glucocorticoids and cyclophosphamide
  • plasma exchange can be life saving
  • dialysis and renal transplantation
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78
Q

Pathology:
What is the mnemonic for GPA/Wegener granulomatosis?

A

3 C’s
- c-ANCA
- Corticosteroids
- Cyclophosphamide

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79
Q

Pathology:
How many different types of renal stones are there?

A

5;
- Calcium oxalate
- calcium phosphate
- struvite (magnesium ammonium phosphate)
- uric acid
- cystine

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80
Q

Pathology:
Describe how calcium oxalate stones can form:

A
  • most common, in the setting of high calcium concentrations
  • high [Ca2+] from excess GI absorption, excess renal excretion, and/or excess bone resorption
  • hyperoxaluria can also be a cause ( hereditary primary hyperoxaluria, high vitamin C intake, IBD, ethylene glycol (antifreeze) ingestion
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81
Q

Pathology:
Describe how calcium phosphate stones can form:

A
  • setting of immobilization or bone-mineral disease
  • hypercalcemia secondary to hyperparathyroidism, vitamin D intoxication, and sarcoidosis, milk-alkali syndrome
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82
Q

Pathology:
Which organisms contribute to struvite stones?

A
  • urease positive organisms ie Proteus vulgaris, staphylococci, Klebisella, and Pseudomonas
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83
Q

Pathology:
What would cause uric acid stones?

A
  • gout or diseases that cause rapid cell turnover (leukemia, myeloproliferative diseases)
  • forms in acidic urine
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84
Q

Pathology:
What would cause cystine stones?

A
  • genetic defects in the PCT resorption of cystine, ornithine, lysine, or arginine
  • forms in acidic urine
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85
Q

Pathology:
What is the appearance of a calcium oxalate stone?

A
  • Radiology: Radiopaque
  • Appearance: Envelope or octahedron
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86
Q

Pathology:
What is the appearance of a calcium phosphate stone?

A
  • Radiology: Radiopaque
  • Appearance: amorphous
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87
Q

Pathology:
What is the appearance of a struvite (ammonium magnesium phosphate) stone?

A
  • Radiology: Radiopaque
  • Appearance: rectangular prism, like coffin lids
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88
Q

Pathology:
What is the appearance of a uric acid stone?

A
  • Radiology: Radiolucent
  • Appearance: yellow or red-brown, diamond or rhombus
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89
Q

Pathology:
What is the appearance of a cystine stone?

A
  • Radiology: Faintly opaque, ground glass
  • Appearance: flat, yellow, hexagonal
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90
Q

Pathology:
What are the most common cause of UTIs in women?

A

Escherichia coli is most common, followed by Staphylococcus saprophyticus

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91
Q

Pathology:
Sterile pyuria in the setting of a negative urine culture suggests what?

A

Infection by Neisseria gonorrheae or Chlamydia trachomatis

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92
Q

Pharmacology:
Which medications can be used to treat an acute UTI in a pregnant woman?

A
  • first line normally is Nitrofurantoin
  • Cephalexin, amoxicillin, and amoxicillin-clavulanate can also be used
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93
Q

Pathology:
What is the treatment for acute pyelonephritis?

A

Oral or IV antibiotics such as TMP/SMX and ciprofloxacin

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94
Q

Pathology:
What would cause chronic pyelonephritis?

A

Structural abnormalities such as obstructions (ie stones, BPH. or congenital ureteripelvic junction obstruction) or Vesicourethral Reflux in children

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95
Q

Pharmacology:
How would you treat chronic pyelonephritis?

A
  • TMP/SMX
  • Nitrofurantoin
  • surgical repair
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96
Q

Pathology:
What could you see in the light micrograph of a renal biopsy in a pt with chronic pyelonephritis?

A

Thyroidization

97
Q

Pathology:
How does Diffuse Cortical Necrosis develop?

A

Infarction of the cortices of the kidney secondary to ischemia. Often multifactorial and can progress to AKI, especially in the 3rd trimester of pregnancy.

98
Q

Pathology:
Which conditions associated with Diffuse Cortical Necrosis?

A
  • Abruptio placentae
  • Eclampsia/preeclampsia
  • Septic shock
  • Hemolytic-uremic syndrome (in children)
99
Q

Pathology:
How does Renal papillary necrosis present?

A

Polyuria, rust-colored urine, AKI, and flank pain

100
Q

Pathology:
What are some conditions associated with renal papillary necrosis?

A
  • Diabetes Mellitus
  • Acute pyelonephritis
  • Chronic analgesic use, especially those containing phenacetin
  • sickle cell disease/trait
    ** Mneumonic: SAAD Papa
101
Q

Pathology:
How would you diagnose renal papillary necrosis?

A

UA: sediment, casts, blood, and necrotic renal papillae. Plain radiographs may show a ring of calcification, especially in disease resulting from analgesic use.

102
Q

Pathology:
What is the mnemonic for the indication for dialysis?

A

AEIOU:
- metabolic Acidosis
- Electrolyte abnormalities (hyperkalemia)
- Intoxicants (eg, ethylene glycol, methanol, and Li)
- fluid Overload
- Uremia (including uremic pericarditis)

103
Q

Pathology:
Describe AKI:

A

Abrupt onset decrease in renal function as measured by GFR leading to reduced ability to maintain serum electrolytes and excrete nitrogenous waste.

104
Q

Pharmacology:
How would you treat AKI?

A
  • maintain fluid and electrolyte balance and avoid nephrotoxic medications.
  • Treat obstruction if indicated.
105
Q

Pathology:
What are some terms to keep in mind associated with AKI or CKI?

A
  • Glomerular filtration rate (GFR)
  • Azotemia
  • Uremia
  • Oliguria
  • Anuria
  • Polyuria
106
Q

Pathology:
What are some findings with uremia?

A

Encephalopathy, platelet dysfunction/bleeding, pericarditis, anorexia, and vomiting. Most often seen in the setting of renal symptoms secondary to AKI/CKI.

107
Q

Pathology:
What are the variables needing to be aware of with Prerenal Kidney Injury?

A
  • Urine osmolality (mOsm/kg): > 500
  • Urine Na (mEq/L): < 20
  • FE_Na: < 1%
  • BUN/Cr ratio: > 20
108
Q

Pathology:
What are the variables needing to be aware of with Renal Kidney Injury?

A
  • Urine osmolality (mOsm/kg): < 350
  • Urine Na (mEq/L): > 40
  • FE_Na: > 2%
  • BUN/Cr ratio: < 15
109
Q

Pathology:
What are the variables needing to be aware of with Postrenal Kidney Injury?

A
  • Urine osmolality (mOsm/kg): < 350
  • Urine Na (mEq/L): Variable
  • FE_Na: > 4%
  • BUN/Cr ratio: > 15
110
Q

Pathology:
What would a patient show to suspect a type of kidney injury?

A

Azotemia, Oliguria/anuria

111
Q

Pathology:
Where is the problem with Prerenal Kidney injury? What is the cause?

A
  • Problem: the body
  • Cause: Hypovolemia (sepsis, shock, heart failure)
112
Q

Pathology:
Where is the problem with Renal Kidney injury? What is the cause?

A
  • Problem: the Bean; Tubular or glomerular
  • Cause: Tubular: ATN, Interstitial nephritis; Glomerular: Nephritic and Nephrotic Syndromes
113
Q

Pathology:
Where is the problem with Postrenal Kidney injury? What is the cause?

A
  • Problem: Beyond- Urinary Tract
  • Cause: Obstruction- BPH, Cancer, Stones, Obstructed urinary catheter, Congenital obstructions
114
Q

Pathology:
What is the most common cause of AKI?

A

Acute Tubular Necrosis, can be ischemic or nephrotoxic.

115
Q

Pathology:
What are some associations with Acute Tubular Necrosis?

A

Muddy brown casts, Rhabdomyolysis, and crush injury.

116
Q

Pathology:
What are the three stages of ATN?

A

Inciting event
Oliguric phase
Polyuric phase

117
Q

Pathology:
Why is the oliguric phase dangerous?

A

The oliguric, or maintenance phase, is dangerous because many patients may become hypovolemic and/or hyperkalemic.

118
Q

Pathology:
How does the polyuric phase develop?

A

If the oliguric stage is left untreated longer than 2 weeks. AKA the recovery phase, notable for polyuria and electrolyte wasting due to re-epithelialization of the nephron while the tubules are still damaged.
** Hypokalemia is a major risk due to a large loss of dissolved solutes during this phase.

119
Q

Pathology:
How is ATN diagnosed?

A
  • Azotemia
  • FE_Na > 1%
  • Muddy brown casts
120
Q

Pharmacology:
How can you prevent contrast nephropathy?

A

Fluid bolus and N-Acetylcysteine

121
Q

Pathology:
How would you describe CKD?

A

Substantial decrease in renal function, usually less than 20% of normal GFR over the the course of 6 months or more. Can be asymptomatic for many years, followed by increasing uremia and associated symptoms as GFR drops below 60 mL/min.

122
Q

Pathology:
Describe the etiology of Nephrotoxic ATN:
Where is the damage?

A
  • Drugs: NSAIDs, radiocontrast, cyclophosphamide, ahminoglycosides, diuretics, and heavy metals
  • Disease: rhabdomyolysis, hemolysis, gout, pseudo gout, and multiple myeloma
  • Damage: PCT
123
Q

Pathology:
Describe the etiology of Ischemic ATN:
Where is the damage?

A
  • Decreased blood flow
  • Damage: Straight segment of PCT, medullary segment of TAL, tubular BM are disrupted
124
Q

Pathology:
Describe the causes of Prerenal CKD:

A
  • renal artery stenosis, embolism of both kidneys
125
Q

Pathology:
Describe the causes of Parenchymal CKD: 8 points

A
  • DM
  • SLE
  • HTN
  • Amyloidosis
  • Chronic glomerulonephritis
  • chronic tubulointerstitial nephritis
  • adult polycystic kidney disease
  • renal cancer
126
Q

Pathology:
Describe the causes of Postrenal CKD:

A

Chronic urinary tract obstruction

127
Q

Pathology:
What is the pathophysiology of Autosomal Dominant Polycystic Kidney Disease?

A

Mutations in PKD1 or PKD2 on chromosomes 16 and 4 respectively

128
Q

Pathology:
How does ADPCKD present?

A

40s with flank pain, intermittent hematuria, a palpable abdominal/flank pain, HTN, and a positive hx of kidney disease.

129
Q

Pharmacology:
How is ADPCKD treated?

A

Supportive, antihypertensives, diuretics, and a low salt diet. Prompt antibiotics to treat UTIs, dialysis and renal transplant if ESRD.

130
Q

Pathology:
What condition(s) are associated with ADPCKD?

A

Saccular aneurysms affecting the Circle of Willis, leading to a high incidence of SAH

131
Q

Pathology:
What is the pathogenesis of ARPCKD?

A

Mutation of PKHD1

132
Q

Pathology:
How does ARPCKD present?

A

Neonates present with enlarged kidneys at birth. Maternal oligohydramnios leads to Potter facies and pulmonary hypoplasia in newborns.

133
Q

Pathology:
What medications can cause Fanconi syndrome?

A
  • expired tetracyclines
  • tenofovir
  • ifosfamide
134
Q

Pathology:
What are some consequences of renal failure? 8 points

A
  • uremic syndrome
  • hyperkalemia
  • metabolic acidosis
  • Na H2O retention
  • Renal osteodystrophy
  • anemia
  • HTN
  • Fanconi Syndrome
135
Q

Pathology:
What is Fanconi Syndrome?

A

A state where there is loss of function to the PCT’s transporters.

136
Q

Pathology:
What are some inherited disorders that can lead to Fanconi syndrome?

A
  • Wilson disease
  • tyrosinemia
  • cystinosis
  • Glycogen storage diseases
137
Q

Pathology:
What are some non inherited disorders that can manifest Fanconi Syndrome?

A
  • expired tetracyclines, ifosfamide, and tenofovir
  • lead poisoning
  • ischemia
  • multiple myeloma
138
Q

Pathology:
How does Fanconi Syndrome present?

A
  • symptoms of acidosis (type 2 RTA) (defective bicarb reabsorption)
  • polyuria and polydipsia (defect in Na and H2O reabsorption)
  • renal glycosuria (Na+/glucose cotransporters, **normal serum glucose)
  • children: failure to thrive and/or rickets (hypophosphatemia due to dysfunction of the Na+/Phosphate cotransporter)
139
Q

Pathology:
Describe Bartter Syndrome:

A

Rare autosomal recessive disorder where mutations affect the transporters of the thick ascending limb of Henle.

140
Q

Pathology:
How does Bartter Syndrome present?

A
  • symptoms similar to pts taking loop diuretics
  • presents in early life with neonatal polyuria or polyhydramnios and postnatal volume depletion
  • growth delays
  • electrolyte abnormalities including hypokalemia, hypochloremic metabolic alkalosis, and hypercalciuria
141
Q

Pathology:
How would you diagnose Bartter Syndrome?

A
  • Made clinically
  • rule out vomitting and diuretic abuse
  • polyuria in the setting of volume depletion and multiple electrolyte abnormalities
  • high renin and aldosterone
  • genetic tests
142
Q

Pathology:
How can you treat Bartter Syndrome?

A
  • NSAIDs decrease RBF, GFR, and urinary sodium wasting
  • Potassium supplements and high fluid diet
143
Q

Pathology:
What is the prognosis of Bertter Syndrome?

A
  • prognosis is good with supportive care
  • often there is short stature and ongoing need for high fluid intake, high sodium intake, and high potassium intake.
  • Pts with significant hypercalciuria and can develop nephrocalcinosis, tubulointerstiaial scarring and eventual CKD and ESRD
144
Q

Pathology:
Describe Gitelman Syndrome:

A

Rare autosomal recessive disorder making defective Na+-Cl- cotransporter in the DCT which are thiazide- sensitive.
So rare it is diagnosed until late childhood or early adulthood.

145
Q

Pathology:
How does Gitelman syndrome present?

A
  • Similar to those seen in pts using thiazide diuretics
  • cramp and severe fatigue
  • hypochoremic metabolic alkalosis, hypokalemia, and hypocalciuria, and hypomagnesemia
  • No HTN
146
Q

Pathology:
How is Gitelman Syndrome diagnosed?

A
  • clinical diagnosis
  • electrolyte abnormalities with volume depletion
  • hypokalemia
  • hypochloremic metabolic alkalosis
  • hypocalciuria ( vs Bartter syndrome )
  • polyuria
  • elevated urine sodium and FE_Na
  • rule out vomitting and diuretic abuse
147
Q

Pharmacology:
How do you treat Gitelman Syndrome?

A
  • NSAIDs to decrease RBF, GFR, and urinary sodium wasting
  • High sodium, high potassium, and high fluid diet
148
Q

Pathology:
What is the prognosis of Gitelman Syndrome?

A

Prognosis is excellent, no risk of tubulointerstitial scarring and ESRD.

149
Q

Pathology:
Descibe Liddle Syndrome:

A

Autosomal dominant disorder; severe HTN due to gain of function mutation in the collecting duct epithelial sodium channel (ENaC).
Excess sodium reabsorption increases ECF volume and causes hypertension and hypokalemia.

150
Q

Pathology:
How doesLiddle Syndrome present?

A
  • frequently asymptomatic
  • hypokalemia
  • metabolic alkalosis with HTN
  • presentation is similar to hyperldosteronism, but is independent of mineralocorticoids
151
Q

Pathology:
How would you diagnose Liddle Syndrome?

A
  • persistent HTN
  • hypokalemia
  • metabolic alkalosis
  • genetic testing
152
Q

Pharmacology:
How would you treat Liddle Syndrome?

A

ENaC antagonists: Amiloride or triamterene

153
Q

Pathology:
Describe Renal Cell Carcinoma:

A
  • most common primary tumor in adults
  • arises from epithelium of the PCT
  • Has three common forms: Clear-cell carcinomas, papillary renal cell carcinomas, and chromophore renal carcinomas
154
Q

Pathology:
What are the risk factors for renal cell carcinoma?

A

Smoking, exposure to cadmium, petroleum, gasoline, asbestos, lead, acquired cystic disease from chronic dialysis

155
Q

Pathology:
Describe clear cell carcinoma:

A
  • 1st type of RCC amounting to 80% of cases of RCC
  • has clear or granular cytoplasm
  • genetic defect on chromosome 3 VHL gene (tumor suppressor)
156
Q

Pathology:
Describe Papillary renal cell carcinoma:

A
  • 2nd type of RCC amounting to 15% of RCC cases
  • have a papillary growth pattern and affects the PCTs
  • defect in the MET gene on chromosome 7 (photo-oncogene)
  • familial forma also exhibit trisomy of chromosome 7
157
Q

Pathology:
Describe Chromophobe renal carcinomas:

A
  • 3rd type of RCC amounting to <5% of RCC cases
  • affects the cortical collecting ducts, staining dark
  • loss of an entire chromosome, frequently chromosome 1, 2, 6, 10, 13, 17, 21
158
Q

Pathology:
How does RCC present?

A
  • painless hematuria
  • palpable flank mass
  • flank pain
    ** does not need to fulfill triad
159
Q

Pathology:
How and where does RCC spread?

A

Hematogenously via the renal vein and IVC to the bones or lungs. Spread to the left renal vein can cause left-sided varicocele because blocks left spermatic vein drainage.

160
Q

Pathology:
Describe the paraneoplastic syndromes associated with RCC:

A
  • hypercalcemia due to high levels of PTHrP
  • polycythemia from excess EPO production
161
Q

Pathology:
What cancer is associated with Schistosomiasis?

A

Squamous cell carcinoma of the Bladder

162
Q

Pathology:
What are the risk factors associated with bladder tumors?

A

Exposures to Beta-naphthylamine, cigarette smoking, cyclophosphamide, and phenacetin (analgesic), also Aniline dyes (Aromatic amines)

163
Q

Pathology:
Describe a Wilms tumor (Nephroblastoma):

A
  • most common primary tumor of the kidney in children between 2 and 5 years
  • loss of WT1 of chromosome 11, a tumor suppressor gene lost from a two-hit mechanism
164
Q

Pathology:
Describe how a Wilms Tumor presents:

A
  • large, palpable abdominal mass
  • HTN: due to excessive renin secretion
  • Beckwith-Wiedemann syndrome: enlarged organs, hemi hypertrophy of extremities
  • WAGR complex: Wilms tumor, Aniridia (absence of iris), Genitourinary malformation, and mental-motor retardation
  • Denys-Drash syndrome: gonadal dysgenesis, renal abnormalities eg. diffuse mesangial sclerosis, and wilms tumor
  • abdominal pain, fever, and hematuria
165
Q

Pharmacology:
What is the treatment of Wilms tumor/nephroblastoma?

A

Nephrectomy with chemotherapy (vincristine, actinomycin D, and doxorubicin if lung metastases are found)
Abdominal radiation can be used in selected patients.

166
Q

Pathology:
Describe Neuroblastoma:

A
  • most common extracranial solid tumor in children
  • most common tumor in the first year of life
  • arises from malignant transformation of cells of the sympathetic nervous system of neural crest cell origin most often in the adrenal glands
  • a small number of cases are familial and are caused by a mutation in the anaplastic lymphoma kinase (ALK) gene
  • most have an amplification of N-myc gene
  • also shows spontaneous regression
167
Q

Pathology:
How does a Neuroblastoma present?

A
  • rapidly growing abdominal mass
  • constitutional symptoms: fatigue, fever, and loss of appetite
  • if compression of the renal artery is present then HTN
168
Q

Pathology:
How is a Neuroblastoma diagnosed?

A
  • urine catecholamines and catecholamine degradation products (vanillylmandelic acid VMA)
  • calcification on CT
  • positive metaiodobenzylguanidine (mIBG) scan
169
Q

Pathology:
What serum value is considered hypernatremia?

A

> 145 mEq/L

170
Q

Pathology:
Describe the presentation of Hypernatremia:

A

Excessive thirst, doughy skin, and mental status changes (confusion, seizures, and muscle twitching)
Neurologic symptoms include irritability, delirium, and. coma.

171
Q

Pathology:
Describe the causes of Hypernatremia:

A

Hypertonic saline, diabetic ketoacidosis, and central or nephrogenic DI, medications (diuretics, lithiums, or sodium-containing drugs)

172
Q

Equation:
What is the formula to determine the amount of fluid to give for IV hydration?

A

Free water deficit = Total body water * [(Plasma Na/140) - 1]

173
Q

Pathology:
Describe how hyponatremia presents:

A

Headaches, nausea, muscle cramps, depressed reflexes, and disorientation, beware of central pontine myelinolysis (CPM) during correction.

174
Q

Pathology:
What are the causes of hyponatremia?

A

Skin or GI losses, SIADH, water intoxication, and liver or heart failure.

175
Q

Pathology:
Describe the presentation of hyperkalemia:

A

Palpitations, muscle weakness, peaked T waves, widened QRS interval, flattened P waves, ventricular fibrillation (COD)

176
Q

Pathology:
What are the causes of hyperkalemia?

A

Lab error (hemolysis), acute or chronic kidney injury, crush injury, hypoaldosteronism

177
Q

Pathology:
How does hypokalemia present?

A

Fatigue, muscle weakness, hyporeflexia, intestinal ileum, flattened T waves, U waves, prolonged PR interval, ST-segment depression

178
Q

Pathology:
What causes hypokalemia?

A

Jnsulin, diuretics, vomiting, hyperaldosteronism, hypomagnesemia, type 1 and 2 RTA, and alkalosis

179
Q

Pathology:
How does hypercalcemia present?

A

“Renal stones, abdominal groans, painful bones, and psychiatric moans,” QT-segment shortening

180
Q

Pathology:
What causes hypercalcemia?

A

Malignancy, hyperparathyroidism, granulomatous disease, renal failure, and milk-alkali syndrome

181
Q

Pathology:
How does hypocalcemia present?

A

Muscle cramps, depression, tetany, convulsions; QT-segment prolongation; Chvostek and Trousseau signs

182
Q

Pathology:
What causes hypocalcemia?

A

DiGeorge syndrome (in children), hypoparathyroidism (following Parathyroidectomy, furosemide, and vitamin D deficiency
Pseudohypoparathyrosidism, vitamin D deficiency, osteomalacia, rickets, and diuretics (furosemide)

183
Q

Pathology:
How does hypomagnesemia present?

A

Often asymptomatic; anorexia, nausea, vomiting, lethargy, personality changes
Hypocalcemia and hypokalemia because low Mg2+ decreases PTH release and increases intracellular K+ efflux.

184
Q

Pathology:
What causes hypomagnesemia?

A

Dietary deficiency difficult to correct hypocalcemia or hypokalemia in the setting of hypomagnesemia.

185
Q

Pathology:
What serum sodium level is considered hyponatremic?

A

< 136 mEq/L

186
Q

Pathology:
What is considered a normal serum osmolality for sodium?

A

280-295 mOsm/kg, considered isotonic

187
Q

Pathology:
What are the causes of a hypotonic hyponatremic and hypovolemic with a FeNa <1%?

A

Extrarenal salt loss:
Dehydration, diarrhea, vomiting

188
Q

Pathology:
What are the causes of a hypotonic hyponatremic and hypovolemic with a FeNa >2%?

A

Renal salt loss:
- ACEi’s Nephropathies, mineralocorticoid deficiency

189
Q

Pathology:
What are the causes of a hypotonic hyponatremic and hypovolemic that is euvolemic?

A

SIADH
Postoperative hyponatremia
Hypothyroidism
Psychogenic polydipsia
Beer potomania

190
Q

Pathology:
What are the causes of a hypotonic hyponatremic and hypovolemic that is hypervolemic?

A

Edematous states:
- CHF
- liver disease
- nephrotic syndrome
- Oliguric renal failure

191
Q

Pathology:
What are the causes of a isotonic hyponatremia?

A
  • Hyperproteinemia
  • hyperlipidemia (chylomicrons, triglycerides, rarely cholesterol)
192
Q

Pathology:
What are the causes of a hypertonic hyponatremia?

A
  • Hyperglycemia
  • mannitol, sorbitol, glycerol, maltose
  • radiocontrast agents
193
Q

Pathology:
What is the serum value for hyperkalemia?

A

> 5.0 mEq/L
- RMP less negative and cell is more excitable

194
Q

Pathology:
What are the symptoms of Central pontine myelinolysis (CPM)?

A
  • sudden para or quadriparxsis
  • dysphagia
  • dysarthria
  • double vision
  • loss of consciousness
195
Q

Pharmacology:
How would you treat hyperkalemia?

A
  • Calcium gluconate: first to stabilize the myocardium
  • Insulin: with concurrent glucose infusion; increases potassium uptake
  • Beta agonists (drives K+ into cells)
  • if academic, administer bicarbonate
  • if residual renal function; furosemide + IV fluids
  • Sodium polystyrene solfonate (causes excretion of K+ from the GI tract)
196
Q

Pathology:
What is the serum value for hypokalemia?

A

< 3.6 mEq/L
- making the RMP more negative and cells are less excitable

197
Q

Pathology:
What is the serum value for hypercalcemia?

A

> 10.2 mg/dL, increasing th threshold and thus cells are less excitable (acidosis has a similar effect)

198
Q

Pharmacology:
What is the treatment for hypercalcemia?

A
  • treat the underlying cause
  • hydrate with IV normal saline, furosemide, and bisphosphonates to inhibit bone resorption by osteoclasts
  • hemodialysis if severe
199
Q

Pathology:
What is the serum value for hypocalcemia?

A

< 8.5 mg/dL
Decreasing the threshold potential and thus cells are more excitable (alkalosis has a similar effect)

200
Q

Pharmacology:
What is the treatment for hypocalcemia?

A

IV Calcium gloconate
PO calcium and vitamin D in less severe cases

201
Q

Pathology:
What is the serum value for hypomagnesemia?

A

< 1.5 mEq/L

202
Q

Pharmacology:
What is the treatment of hypomagnesemia?

A

Magnesium Sulfate

203
Q

Pharmacology:
What is the goal of using diuretics?

A
  • increase urine volume
  • first line tx for HTN, edematous states ie CHF, nephrosis, and cirrhosis
204
Q

Pharmacology:
What are some side effects of diuretics?

A
  • volume depletion
  • hypokalemia (loop diuretics and thiazides)
  • hyponatremia
  • hyperglycemia (thiazides)
  • metabolic acidosis (acetazolamide and K+ sparing diuretics (spiranolactone)
  • metabolic alkalosis (loop diuretics and thiazides)
  • hypercalciuria (loop diuretics)
205
Q

Pharmacology:
What are the five main classes of diuretics?

A
  1. Osmotic agents: Mannitol and urea (tx for SIADH)
  2. Carbonic anhydrase inhibitors: acetazolamide
  3. Loop agents: furosemide, bumetanide, and ethacrynic acid
  4. Thiazides: HCTZ and metalazone
  5. Potassium-sparring agents: spiranolactone, eplerenone, triamterene, and amiloride
206
Q

Pharmacology:
Describe the MOA of Carbonic anhydrase inhibitors:
What are the examples?
What are the electrolyte changes?

A

Ex: Acetazolamide
Inhibits carbonic anhydrase in PCT, blocks Na+/H+ exchange. Also prevents Na/HCO3 reabsorption, leading to diuresis
- hyperchloremic metabolic acidosis ( increase Cl- and H+)
- hypokalemia

207
Q

Pharmacology:
Describe the MOA of Osmotic agents:
What are the examples?
What are the electrolyte changes?

A

Ex: Mannitol and urea
Increases tubular fluid osmolarity in entire tubule
- Hypernatremia

208
Q

Pharmacology:
Describe the MOA of Loop agents:
What are the examples?
What are the electrolyte changes?

A

Ex: Furosemide, bumetannide, ethacrynic acid
Inhibits Na+ - K+ - 2Cl- transporter in TAL of loop of henle. Decreases positive luminal potential, leading to increased excretion of calcium and magnesium.
- hypokalemia
- hyponatremia
- hyperuricemia
- hypocalcemia
- hypomagnesemia
- metabolic alkalosis

209
Q

Pharmacology:
Describe the MOA of Thiazide diuretics:
What are the examples?
What are the electrolyte changes?

A

Ex: HCTZ, metolazone
Blocka Na+ - Cl- cotransport in DCT
- hyperglycemia
- hyperlipidemia
- hyperuricemia
- hypercalcemia
- hypokalemia
- hyponatremia
- metabolic alkalosis

210
Q

Pharmacology:
Describe the MOA of Potassium sparring agents:
What are the examples?
What are the electrolyte changes?

A

Ex: Spironolactone, eplerenone, amiloride, triamterene
Spironolactone and eplerenone are competitive aldosterone receptor antagonists in the late DCT and collecting tubule.
Other agents block Na+ channels (ENaC) in the DCT and collecting tubule, reducing Na+ reabsorption.
- hyperchloremic metabolic acidosis
- hyperkalemia

211
Q

Pharmacology:
What are the uses of Osmotic agents?

A
  • reduction of intraocular or intracranial pressure
  • increases excretion of water more than sodium
  • urinary excretion of metabolic toxins
212
Q

Pharmacology:
What are the side effects of osmotic agents?

A
  • dehydration without adequate water intake
  • increased ECF volume, leading to pulmonary edema
213
Q

Pharmacology:
What diuretic medication is contraindicated in pulmonary edema?

A

Osmotic agent Mannitol

214
Q

Pharmacology:
What are the uses of Carbonic Anhydrase inhibitors?

A
  • glaucoma (decreases production of aqueous humor)
  • acute mountain sickness (stimulates ventilation via metabolic acidosis)
  • elimination of acidic toxins (alkalinizes urine, excreting weak acids)
  • Pseudotumor cerebri ( decreases CSF production)
  • corrects alkalosis
215
Q

Pharmacology:
What are some side effects of carbonic anhydrase inhibitors?

A
  • renal stones (calcium phosphate)
  • Potassium wasting (increased Na+ delivery to distal nephron increases K+ exertion)
  • Hypochloremic metabolic acidosis
216
Q

Pharmacology:
What are the side effects of loop diuretics outside of the electrolyte anomalies?

A
  • ototoxicity
  • renal calculi (hypercalciuria)
  • SEVERE dehydration
  • allergic reactions (all loop diuretics are solfonamide derivatives except ethacrynic acid)
217
Q

Pharmacology:
What are the uses for Loop diuretics?

A
  • pulmonary or other edema
  • hypercelcemia
  • hyperkalemia
  • HTN
  • pseudotumor cerebri
  • volume overload in AKI
218
Q

Pharmacology:
What are the uses of Thiazide diuretics?

A
  • first line tx of HTN, CHF, nephrosis, hypercalciuria, and nephrogenic DI
  • thiazides reduce ECF volume -> activates RAAS -> increase proximal reabsorption of NaCl and H2O -> decrease delivery of fluid to distal nephron -> decrease urine output
219
Q

Pharmacology:
What are the uses of K sparring diuretics: Spironolactone and eplerenone?

A
  • primary hyperaldosteronism (Conn syndrome)
  • Edematous states caused by secondary hyperaldosteronism (cirrhosis, nephrotic syndrome, and cardiac failure)
  • anti androgen activity can be useful for tx of PCOS and hirsutism
220
Q

Pharmacology:
What are the uses of K sparring diuretics: Amiloride and triamterene?

A
  • counteract K+ loss caused by other diuretics
  • adjunct therapy to other diuretics to treat edema or HTN
221
Q

Pharmacology:
What are some side effects to K sparring agents outside of electrolyte anomalies?

A
  • Gynecomastia (spironolactone)
  • impotence (males)
  • abnormal menses (females)
222
Q

Pharmacology:
What are some side effects to thiazide diuretics outside of the electrolyte anomalies?

A
  • dehydration
  • allergic reactions (sulfonamide derivatives)
  • thiazides increase Li+ reabsorption in the proximal tubules, possibly causing Li+ toxicity
223
Q

Pharmacology:
Describe the MOA, Uses, and side effects of ADH medications Vasopressin and Desmopression):

A
  • MOA: up regulates selective water channels (aquaporin 2) in apical membrane of collecting ducts
  • uses: central DI, enuresis (bedwetting)
  • AE: Vasoconstriction, headaches, nausea
224
Q

Pharmacology:
Describe the MOA, Uses, and side effects of ADH antagonist medication Demeclocycline:

A
  • MOA: non selectively inhibits action of ADH in collecting ducts by decreasing cAMP levels. Member of the tetracycline family of antibiotics.
  • Uses: SIADH, decrease IV fluid volume in heart or liver failure
  • side effects: nephrogenic DI and renal failure
225
Q

Pharmacology:
Describe the MOA, Uses, and side effects of ADH antagonist medication Tolvaptan:

A
  • MOA: competitively inhibits arginine vasopressin receptor 2, thus promoting excretion of free water
  • uses: SIADH, decrease IV fluid in heart and liver failure
  • AE: GI upset, polyuria, polydipsia, renal failure
226
Q

Pharmacology:
What are the side effects of ACE inhibitors?

A
  • dry cough (bradykinin)
  • teratogenic (don’t give to pregnant women)
  • hypotension
  • acute renal failure ( pts with BL RAS)
  • hyperkalemia
  • angioedema (bradykinin)
227
Q

Pharmacology:
Where do ARBs act upon?

A

Angiotensin II receptors at vascular smooth muscle and adrenal glands.

228
Q

Pharmacology:
What are the side effects of ARBs?

A
  • hypotension
  • teratogenic
  • acute renal failure
  • hyperkalemia
229
Q

Pharmacology:
Which antihypertensives are nephrotoxic?
What is the toxic renal actions?

A
  • ACEi’s and ARB’s
  • fetal renal toxicity (teratogenic)
230
Q

Pharmacology:
Which antibiotics are nephrotoxic?
What is the toxic renal actions?

A
  • Aminoglycosides (eg gentamycin, neomycin), Beta-lactams (eg, methicillin), sulfonamides (eg, sulfamethoxazole), trimethoprim, rifampin
  • range form mild renal impairment to ATN (aminoglycosides) or AIN
231
Q

Pharmacology:
Which antiviral are nephrotoxic?
What is the toxic renal actions?

A
  • acyclovir, ganciclovir, and foscarnet
  • formation of urinary crystals (acyclovir) and transient renal dysfunction
232
Q

Pharmacology:
Which antifungals are nephrotoxic?
What is the toxic renal actions?

A
  • amphotericin B, polymyxin
  • Dose related nephrotoxicity (direct. acute tubular injury)
233
Q

Pharmacology:
Which anti-inflammatories are nephrotoxic?
What is the toxic renal actions?

A
  • NSAIDs (eg, ibuprofen, indomethacin, naproxen), COX-2 inhibitors (eg, refecoxib)
  • AIN, renal papillary necrosis, direct tubular injury due to ischemia
  • inhibition of COX isoenzymes inhibits renal PGI2 production, leading to altered excretion of Na+, edema, and HTN
234
Q

Pharmacology:
Which immunosuppressives are nephrotoxic?
What is the toxic renal actions?

A
  • cyclosporine, tacrolimus (FK506)
  • dose related nephrotoxicity (direct acute tubular injury)
235
Q

Pharmacology:
Which chemotherapeutics are nephrotoxic?
What is the toxic renal actions?

A
  • Cisplatin, cyclophosphamide, ifosfamide
  • dose related nephrotoxicity (cisplatin and ifosfamide), hemorrhagic cystitis (cyclophosphamide and ifosfamide)
236
Q

Pharmacology:
Which radiocontrast dyes are nephrotoxic?
What is the toxic renal actions?

A
  • iodinated contract agents
  • ATN/ contact-induced nephropathy, usually in pts with CKD (eg, DB nephropathy) are at higher risk for CIN
237
Q

Pharmacology:
Which endogenous toxins are nephrotoxic?
What is the toxic renal actions?

A
  • myoglobin (rhabdomyolysis, hemoglobin (hemolysis)
  • ATN, oliguria
238
Q

Pharmacology:
Which exogenous toxins are nephrotoxic?
What is the toxic renal actions?

A
  • ethylene glycol, heavy metals (arsenic, lead)
  • renal failure at high doses, ATN, oliguria,
    precipitation of calcium oxalate stones (ethylene glycol)
239
Q

Pharmacology:
What is the toxic renal actions of Lithium?

A

Nephrogenic diabetes insipidus and tubulointerstitial fibrosis.

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