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PATHO/PHARM II > Mod 2 > Flashcards

Mod 2 Flashcards

Exam 1- Lec 2

1
Q

Glomerulonephritis

A

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

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2
Q

Basic causes of inflammation of glomeruli?

A

Primary glomerular injury

Secondary glomerular injury

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3
Q

Primary glomerular injury

A

isolated to the kidney

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4
Q

Secondary glomerular injury

A

systemic disease (eg; drugs, DM, HTN, toxins, SLE, HF, HIV)

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5
Q

What is the main component of Glomerulonephritis?

A

Immune mechanisms are main component

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6
Q

Immune mechanisms that are main component include to glomerulonephritis:

A

Antigen-antibody complexes, activated inflammatory response

Complement activation, WBC recruitment, activated platelets, cytokine release _ injury to GBM

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7
Q

Increased glomerular membrane permeability leads to what?

A

Increased glomerular mem permeability –> proteins & RBCs escape into urine

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8
Q

What happens to bowman’s capsule in glomerulonephritis?

A

Swelling and cell proliferation in Bowman’s space

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9
Q

Immune mechanisms that are main component lead to:

A

Result: injury to the glomerulus

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10
Q

Risk factors that lead to glomerulonephritis: What is the most common?

A

Streptococcal infection, typically precedes (most common)

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11
Q

Risk factors that lead to glomerulonephritis: Who does it effect the most?

A

It affects children between the ages of 3 to 7 years, especially boys

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12
Q

Risk factors that lead to glomerulonephritis: what other bacterial infections?

A

Staphylococcus, Pneumococcus, varicella

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13
Q

Risk factors that lead to glomerulonephritis: What other problems?

A

Immunodeficiency
Inflammatory DX ~ SLE

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14
Q

Risk factors that lead to glomerulonephritis: Use of what would increase glomerulonephritis?

A

Meds (eg NSAIDs)

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15
Q

Complications related to glomerulonephritis include?

A

CKD & renal failure, leading cause

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16
Q

Clinical Manifestations: How does glomerulonephritis appear? Sudden or gradual?

A

Sudden or gradual

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17
Q

Clinical Manifestations: What can occur before appearance of symptoms of glomerulonephritis?

A

Significant nephron function loss can occur before symptoms

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18
Q

Glomerulonephritis Clinical Manifestations: How can symptom appearance be?

A

Symptom presentation may be silent, mild, moderate or severe

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19
Q

Glomerulonephritis Clinical Manifestations: severe or progressive disease can lead to what symptoms?

A

Severe or progressive disease –> oliguria, htn, renal failure

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20
Q

Clinical Manifestations: What are two major symptoms of glomerulonephritis?

A
  1. Hematuria with red blood cell casts
  2. Proteinuria (foamy urine) exceeding 3 to 5 g/day with albumin (macroalbuminuria) as the major protein
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21
Q

Clinical Manifestations: How much protein must be in the urine for severe glomerulonephritis?

A

Proteinuria (foamy urine) exceeding 3 to 5 g/day with albumin (macroalbuminuria) as the major protein

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22
Q

Diagnosing glomerulonephritis includes what tests?

A

Urinalysis – proteinuria, rbcs, wbcs, casts

Renal biopsy – type of lesion, extent of renal injury

Reduced GFR

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23
Q

Diagnosing glomerulonephritis: Reduced GFR

A

Elevated plasma urea
Cystatin C in blood

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24
Q

Cystatin C

A

Biomarker of kidney function
Elevated creatinine concentration & reduced CrCl

high= kidney no functioning

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25
Q

Treatment for glomerulonephritis includes treating:

A

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

High calorie, low protein diet

Abx – mgmt of underlying infection causing antigen-antibody response

Corticosteroids – suppress the inflammatory response, decrease Ab synthesis

Cytotoxic agents (cyclophosphamide) – suppress immune response

Anticoagulants – fibrin crescent formation
BP management ~ agents for HTN

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26
Q

What is used to treat edema in glomerulonephritis?

A

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

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27
Q

What are antibiotics used for in glomerulonephritis?

A

Abx – mgmt of underlying infection causing antigen-antibody response

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28
Q

What are glucocorticoids used for in glomerulonephritis?

A

Corticosteroids – suppress the inflammatory response, decrease Ab synthesis

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29
Q

What are cytotoxic agents used for in glomerulonephritis treatment?

A

Cytotoxic agents (cyclophosphamide) – suppress immune response

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30
Q

What are anticoagulants used for in glomerulonephritis treatment?

A

Anticoagulants – fibrin crescent formation

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31
Q

Tetrad of manifestations of Nephrotic syndrome

A
  1. Proteinuria
  2. Hyperlipidemia (Dyslipidemia)
  3. Hypoalbuminemia
  4. Peripheral edema
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32
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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33
Q

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

A

immunoglobulins

albumins

lipiduria

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34
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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35
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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36
Q

NephrITIC syndrome

A

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

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37
Q

Basic function of the kidney:

A
  1. Water, electrolyte, acid-basis homeostasis
  2. Excretion of nitrogenous metabolic wastes: urea, uric acid, creatinine
  3. Detoxifying drugs, toxins, & their metabolites
  4. Regulation of ECF & blood pressure: RAAS, renal prostaglandins, sodium & fluid balance
  5. Secretion of erythropoietin to stimulate RBC production
  6. Endocrine control of Ca-PO4 metabolism (Vit D activation, PO4 excretion)
  7. Hormone catabolism: insulin, glucagon, PTH, calcitonin, gH
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38
Q

Renal insufficiency how is renal function, GFR, ScCr?

A

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

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39
Q

Consequences of uremia:

A

Consequences: retention of toxic wastes, electrolyte disorders, deficiency states, immune activation  proinflammatory state

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39
Q

End-stage kidney disease (ESRD):

A

<10% of kidney fxn remains

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39
Q

Uremia (uremic syndrome):

A

↑ blood Urea & Scr,

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40
Q

What does Uremia (uremic syndrome) lead to?

A

fatigue, anorexia, pruritis, n/v, neurologic sx

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41
Q

Azotemia:

What does it lead to for lab values

A

Accumulation of nitrogen waste.

↑ BUN & Creatine

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42
Q

Oliguria

A

Oliguria: urine flow < 400ml/day,

but UO may exceed this in AKI

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43
Q

Anuria:

A

complete cessation of urine flow is uncommon in AKI (<50cc/24hrs)

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44
Q

Acute Kidney Injury (AKI)

A

Sudden decline in kidney function

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45
Q

What is the patho of Acute Kidney Disease?

A

Accumulation of nitrogenous waste products in blood due to reduced gf

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46
Q

How long does it take acute kidney disease to occur?

A

Occurs over a few hours to a few days

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47
Q

Acute Kidney Injury is permanent? What does it require?

A

Reversible, may require dialysis or progress to chronic

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48
Q

What are three classifications of Acute Kidney Injury?

A

3 classifications
(prerenal,
intrarenal,
postrenal)

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49
Q

Kidney Disease Improving Global Outcomes (KDIGO) workgroup defines AKI as:
(having to do with SCr)

A

increase in SCr by 0.3 mg/dL or more within 48 hours

increase in SCr to 1.5x baseline or more within the past 7 days

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50
Q

Kidney Disease Improving Global Outcomes (KDIGO) workgroup defines AKI as: (having to do with urine output)

A

Urine output less than 0.5 mL/kg/hour for 6 hours

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51
Q

Prerenal AKI Causes/Compensation:

A

Hypovolemia
Renal

Hypoperfusion/Renal Vasoconstriction

Systemic Vasodilation

Decreased Arterial Blood Volume (decreased cardiac output)

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52
Q

Intrarenal AKI Causes/Compensation:

Caused by

A

Glomerulopathies

Systemic disease/Type III Hypersensitivity

Hypercalcemia

Multiple myeloma

Acute tubular necrosis (most common)

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53
Q

What is the most common cause of Intrarenal AKI?

A

Acute tubular necrosis (most common)

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54
Q

Acute tubular necrosis- What is it and what happens?

A

Death of renal tubular epithelial cells

Membrane of tubular epithelium destroyed, cells slough off and plug the tubules.

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55
Q

Slide 22

A

I dont’ understand

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56
Q

Post renal AKI

A

Obstructive uropathies

Neurogenic bladder

As the flow of urine obstructed, urine refluxes into the renal pelvis, results in impaired nephron function.

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57
Q

Post renal AKI: As flow of urine is obstructed, what happens?

A

As the flow of urine obstructed, urine refluxes into the renal pelvis, results in impaired nephron function.

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57
Q

Obstructive uropathies that cause postrenal AKI?

A

Obstructive uropathies:

BPH
Renal calculi
Bladder/prostate cancer
Blood clots
Tumors

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58
Q

What are characteristic findings of post renal AKI?

A

Characteristic finding: flank pain & anuria followed by polyuria

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59
Q

Post renal AKI: Prolonged mechanical obstruction leads to what?

A

Prolonged mechanical obstruction leads to tubular atrophy and irreversible kidney fibrosis

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60
Q

Postrenal AKI treatment includes:

A

Perform urinary catheterization
Prevent UTI.
Relieve obstruction
Treat reversible causes

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61
Q

Four phases of AKI:

A
  1. Onset phase
  2. Oliguric phase
  3. Diuretic phase
  4. Recovery phase
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62
Q

Four phases of AKI: Onset phase

A

Kidney injury occurs.

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63
Q

Four phases of AKI: Oliguric (anuric) phase:

A

Urine output decreases from renal tubule damage.

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64
Q

Four phases of AKI: Diuretic phase:

A

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.

65
Q

Four phases of AKI: Recovery phase

A

Tubular edema resolves and renal function improves.

66
Q

Chronic Kidney Disease (CKD)

A

Progressive loss of renal function, affects nearly all organ systems

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

67
Q

Chronic Kidney Disease (CKD) requires what for survival?

A

Requires dialysis or kidney transplantation to maintain life.

68
Q

What can AKI progress to?

A

AKI can progress to CKD or AKI on CKD

69
Q

Chronic Kidney Disease is associated with?

A

A/W htn, diabetes, intrinsic kidney disease, SLE, pyelo, chr glomeruloneph, obs uropathy

70
Q

Normal GFR value

A

Normal GFR 120 to 140 mL/min

71
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)
72
Q

Stages of Chronic Kidney Disease:
Stage 1: Normal kidney function (GFR > 90 mL/min)

How is kidney?

A

Mild damage, reduced renal reserve

73
Q

Stages of Chronic Kidney Disease:
Stage 1: Normal kidney function (GFR > 90 mL/min)

How are nephrons?

A

Unaffected nephrons overwork to compensate for diseased nephrons

74
Q

Stages of Chronic Kidney Disease:
Stage 1: Normal kidney function (GFR > 90 mL/min)

What is symptoms are common?

A

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

75
Q

Stages of Chronic Kidney Disease:
Stage 2: Mild CKD (GFR 60-89 mL/min)*

How are nephrons?

A

Kidney nephron damage has occurred

76
Q

Stages of Chronic Kidney Disease:
Stage 2: Mild CKD (GFR 60-89 mL/min)*

How are lab values?

A

Slight elevation of metabolic waste in BUN/Cr

77
Q

Stages of Chronic Kidney Disease:
Stage 2: Mild CKD (GFR 60-89 mL/min)*

What are common symptoms?

A

Inability to concentrate urine, polyuria and nocturia

Htn

78
Q

Stages of Chronic Kidney Disease:
Stage 3: Moderate (GFR 30-59 mL/min)

How is it divided?

A

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

79
Q

Stages of Chronic Kidney Disease:
Stage 3: Moderate (GFR 30-59 mL/min)

How are nephrons?

A

Nephron damage continues with decreased nephrons

80
Q

Stages of Chronic Kidney Disease:
Stage 3: Moderate (GFR 30-59 mL/min)

What may be needed to be done in this stage?

A

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

81
Q

Stages of Chronic Kidney Disease:
Stage 4: Severe (GFR 15-29 mL/min)

What occurs?

A

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

82
Q

Stages of Chronic Kidney Disease:
Stage 5: End stage (GFR less than 15)

What are common symptoms?

A

Oliguria occurs

83
Q

Stages of Chronic Kidney Disease:
Stage 5: End stage (GFR less than 15)

How are lab values?

A

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

84
Q

Stages of Chronic Kidney Disease:
Stage 5: End stage (GFR less than 15)

What is a fatal, classic marker?

A

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

85
Q

Patho of Chronic Kidney Disease:

First two steps:

A
  1. Gradual loss of renal function
  2. Kidneys can adapt to the loss of nephron mass to a point
86
Q

Patho of Chronic Kidney Disease:

When are alterations in Na and water apparent in CKD?

A

Alterations in Na & H2O not apparent until GFR < 25%

87
Q

Patho of Chronic Kidney Disease:
How are changes in serum creatinine and urea in chronic kidney disease?

A

Changes in Scr & urea are minimal early, but rise as the disease progresses & GFR ↓

88
Q

Patho of Chronic Kidney Disease:
What is done to maintain GFR by nephrons?

A

Compensatory hypertrophy & hyperfunction of nephrons to maintain GFR (aka hyperfiltration)

89
Q

Patho of CKD you read it

A

Ang II (from RAAS activation)  renal arteriole vasoconstriction  glomerular htn & hyperfiltration  ↑’s capillary permeability, inflammation & fibrosis in the interstitial tissue of kidneys proteinuria (albuminuria)

90
Q

What is used to treat chronic kidney disease?

A

ACE inhibitors dilate glomerular arterioles and reduce glomerular hydrostatic pressure

91
Q

Vitamin D/parathyroid hormone

A
92
Q

Parathyroid hormone acts on the kidneys to do what?

A

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

93
Q

What is the active form of vitamin D?

A

calcitriol

94
Q

How does active vitamin D (calcitriol) work with PTH?

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.

95
Q

What does PTH do to vitamin D? What is the result?

A

PTH stimulates the conversion of vitamin D to its active form in renal tubular cells, enhancing calcium reabsorption.

96
Q

What is needed for bone health and mineral balance?

A

This intricate interplay between the parathyroid glands and vitamin D is crucial for maintaining bone health and overall mineral balance

97
Q

Osteodystrophy with renal failure

A

Slide 35

98
Q

Clinical Presentation of CKD and Treatment: What does it include?

List 6

A

Skeletal

Cardiovascular

Neuro

Integumentary

Hematological

GI

99
Q

Clinical Presentation of CKD
What does it include?

List 4

A

Electrolyte/Acid-Base Imbalance

Metabolic Changes

Reproductive System

Risk for infection

100
Q

Clinical Presentation of CKD:

Skeletal

A

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

101
Q

Clinical Presentation of CKD:

Skeletal: What is the treatment of skeletal issues?

A

Activated Vitamin D
Phosphate binders
Phosphate-restricted diet
Activated Vit D replacement
Possible parathyroidectomy

102
Q

Clinical Presentation of CKD:
Skeletal:
What do phosphate binders do as treatment for skeletal probs?

A

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

103
Q

Clinical Presentation of CKD:
Cardiovascular issues?

Name 3

A

Htn: fluid overload & excess Na+ (can also lead to pulmonary complications)

Renin-angiotensin-aldosterone system (RAAS) can become inappropriately elevated, even when there is an elevated volume status

Uremic toxins –> changes in myocardial contractility, irritability

104
Q

Clinical Presentation of CKD:
Cardiovascular issues?

Name 3:

A

Calcification of coronary arteries, valves, vascular tissue d/t derangement of Ca & P

Hyperkalemia

Anemia – due to ↓’d Epo –> increase demands on heart

Dyslipidemia- uremia causes deficiency in lipoprotein & triglyceride lipase

105
Q

Clinical Presentation of CKD:
Cardiovascular issues- What is the treatment?

A

Tx: diuretics to reduce volume (not K sparing), dialysis, avoid Mg because impaired magnesium excretion

106
Q

Clinical Presentation of CKD:
Neuro

A

Uremic encephalopathy from toxins in CSF

Spectrum of cognitive & consciousness changes

107
Q

Clinical Presentation of CKD:
Neuro:

What are spectrum of cog and consciousness changes?

A

From mild defects in thinking & memory to confusion, disorientation, coma, convulsions

Peripheral neuropathy

Muscle cramps, twitching

Autonomic nervous system: barometers in carotids & and aorta do not respond (burned out)

108
Q

Clinical Presentation of CKD:
Neuro: What is the treatment?

A

Tx: dialysis/kidney transplant

109
Q

What is the general appearance of someone with CKD? (behavior and lower extremity)

A

Tired, weak, malaise, lethargy, dizziness from anemia

Lower extremity edema

Wt △

110
Q

What is the general appearance of someone with CKD?

Skin color

A

sallow skin color – unhealthy yellow or pale brown from retained urinary pigments

111
Q

Clinical Presentation of CKD: Integumentary
How does the skin feel? Why?

A

Itching, crawling skin from phosphate deposits, uric acid, urea

112
Q

Clinical Presentation of CKD: Integumentary

Other issues of the skin that can occur?

A

Anemia - pallor
Bleeding into skin - ecchymosis
Uremic frost (seen with BUN levels >200 mg/dL)
Persistent pruritis
Jaundice
Calciphylaxis

113
Q

What is the treatment for skin issues of CKD?

A

Tx: Dialysis

114
Q

Clinical Presentation of CKD: Hematological

Why does anemia occur?

A

Anemia related to decreased production of erythropoietin increasing demands for cardiac output and adding to cardiac workload.

115
Q

Clinical Presentation of CKD: Hematological- What happens to RBCs lifespan?

What happens to blood in total?

A

Decreased RBC lifespan secondary to dialysis & uremia

Blood loss from dialysis

Abnormal bleeding and bruising

116
Q

Clinical Presentation of CKD: Hematological- What occurs that leads to increased infection?

A

Leukocytosis and altered immune response, leading to increased infection risk, especially in the respiratory and urinary tracts

117
Q

Clinical Presentation of CKD: Hematological-probs

What is the treatment?

A

Tx: Erythropoietin injections, transfusions

118
Q

Clinical Presentation of CKD: GI

A

Anorexia (d/t toxin buildup), N/V (inability of the body to rid itself of toxins)

Uremic colitis (diarrhea)

Stomatitis
Constipation
Uremic gastritis (possible GI bleeding)

119
Q

Clinical Presentation of CKD: GI-

What happens to sense of taste?

A

Metallic taste in mouth and changes in taste due to the buildup of urea in the body

120
Q

Clinical Presentation of CKD: GI-
What is the treatment for GI issues?

A

Tx: Protein-restricted diets

121
Q

Clinical Presentation of CKD:
What is the Acid-Base Imbalance that occurs?

What does this result in?

A

Metabolic acidosis, related to H+ ion retention

results in Kussmaul’s resp –> blow off CO2

122
Q

Clinical Presentation of CKD:
What is the Electrolyte Imbalance that occurs?

A

Hyperkalemia

Sodium& water balance

Hypocalcemia

Hyperphosphatemia

Hypermagnesemia

123
Q

Clinical Presentation of CKD:

Electrolyte imbalance
Why does Hyperkalemia occur?

A

Hyperkalemia r/t decreased filtering ability & met acidosis

124
Q

Clinical Presentation of CKD:

Electrolyte imbalance
Why does sodium and water imbalance occur?

A

Sodium& water balance
Fluid volume excess/edema
Na & water retained

125
Q

Clinical Presentation of CKD:

Electrolyte imbalance
Why does hypocalcemia lead to symptom-wise?

Hypocalcemia response is the same as what other electrolyte imbalance?

A

positive Chvostek and/or Trouseau’s signs
SPTH compensatory response

Hyperphosphatemia, same symptoms as patient with hypocalcemia
Normal level 2.5 to 4.5 mg/dL

126
Q

Clinical Presentation of CKD:
What does hypomagnesemia cause?

A

Hypermagnesemia causing decreased respirations

127
Q

Clinical Presentation of CKD:
Reproductive system

A

Decreased fertility
Infrequent or absent menses
Decreased libido
Impotence, infertility

128
Q

Clinical Presentation of CKD:
Metabolic changes that occur?

Urea/creatinine

Carbs

lipids

insulin

A

Urea and creatinine excretion are disrupted by kidney dysfunction
Carbohydrate intolerance
Hyperlipidemia
Insulin resistance

129
Q

Management of CKD: What is given for skeletal?

A

Vitamin D to ↓ PTH,
dietary phosphorus restriction, administer phosphorus-binding drugs

130
Q

Management of CKD: What is given for Hematological

A

Dialysis, Epo & Fe supplementation, blood transfusion

131
Q

Management of CKD: What is given for Cardiac?

A

Ace-Is, ARBs, Ca-Ch blockers, Diuretics, Beta blockers;
bilateral nephrectomy,
transplant;
limit Na & fluids;
dialysis

132
Q

Management of CKD: What is given for GI treatment?

A

Protein-restricted diet for relief of n/v, antidiarrheals, antiemetics, laxatives (none containing Mg)

133
Q

Management of CKD: What is given for neuro treatment?

A

dialysis, anticonvulsants

134
Q

Management of CKD: What is given for Integumentary treatment?

A

dialysis

135
Q

Management of CKD: What is given for Hyperkalemia?

A

Sodium polyesterate exchange resin: Na for K, sodium zirconium (K+ binder - captures K+ and exchanges it for hydrogen and sodium), IV Dextrose + insulin if K life-threatening, Ca gluconate for cardiac irritability

136
Q

Principles & Stressors Associated with Hemodialysis

A

Read it no time now

137
Q

Pharmacology for renal failure:

A
  1. Erythropoietin (Epogen, Procrit)
  2. Calcitriol (Rocaltrol) Vit D analog
  3. Phosphate Binders for Patients on Dialysis
  4. Cinacalcet [Sensipar]
138
Q

Erythropoietin (Epogen, Procrit)- What does it do?

A

Stimulates erythrocyte production in bone marrow in anemia associated with CRF

139
Q

Erythropoietin (Epogen, Procrit)- How is it administered?

A

IV or Sq

140
Q

Erythropoietin (Epogen, Procrit) : What is it used for?

A

Maintenance of erythrocyte counts
Partial reversal of anemia in CRF

141
Q

What does Erythropoietin (Epogen, Procrit) reduce the need for what?

What is needed for the med to work?

A

Reduced need for transfusions but NOT eliminated

Iron stores must be adequate for med to work- may need iron supplementation

142
Q

What does Erythropoietin (Epogen, Procrit) adverse effects?

A

Htn (already common in RF) – directly r/t rise in Hct

Monitor BP

Stroke, HF, thrombosis, MI

143
Q

Administration of erythropoetin means you should monitor what?

A

Monitor Hgb, reduce dosing or d/c if: Levels approach 11 gm/dL or Increases > 1 gm/dL within 2wks

144
Q

Calcitriol (Rocaltrol) Vit D analog: MOA

A

Active form of Vitamin D, promotes absorption of Ca, decreases PTH concentrations

145
Q

Calcitriol (Rocaltrol) Vit D analog: What is it used for?

A

Hypocalcemia in pts with CKD

146
Q

Calcitriol (Rocaltrol) Vit D analog: Pks

A

well absorbed from GIT, widely dist.
Stored in liver, fat, muscle, skin, bones.

147
Q

Calcitriol (Rocaltrol) Vit D analog: How should it be administered?

A

Adm: with or without food, risk for GI discomfort if taken w/food

148
Q

Calcitriol (Rocaltrol) Vit D analog: Contraindications?

A

hypercalcemia, Vit D toxicity

149
Q

Calcitriol (Rocaltrol) Vit D analog: Adverse reactions?

What does this mean you assess patient for?

A

ADRs: Toxicity - Hypercalcemia, Hypercalciuria, Hyperphosphatemia.

Assess pt for weakness, fatigue, n/v, abdominal cramping, constipation, bone pain

150
Q

Calcitriol (Rocaltrol) Vit D analog: Nursing indications?

A

Nsg Indications: Monitor serum calcium & phosphorus

151
Q

Phosphate Binders for Patients on Dialysis: What is it used to treat?

A

Used to treat hyperphosphatemia in ESRD

152
Q

Phosphate Binders for Patients on Dialysis: MOA?

A

Binds to dietary phosphate to form calcium phosphate complex, preventing its absorption

Phosphorus excreted in feces  decreased levels

153
Q

Phosphate Binders for Patients on Dialysis: How should it be taken?

A

Take with meals to bind with phosphate from ingested food to reduce the amount of phosphate absorbed from GIT

  • This helps control phosphate levels in the blood more effectively.
154
Q

Calcium-based phosphate binders
increase the risk for what?

A

Increase risk of hypercalcemia

155
Q

Calcium-free phosphate binders

A

Sevelamer carbonate [Renvela] 800mg
Sevelamer hydrochloride [Renagel] 400mg

Both bind drugs with bile salts in the intestines so they decrease cholesterol synthesis

Do not increase risk of hypercalcemia but are more costly

156
Q

Cinacalcet [Sensipar]- what is it approved for?

A

Approved for secondary hyperparathyroidism caused by CKD

157
Q

Cinacalcet [Sensipar]- what kind of drug is it?

A

Calcimimetic drug

158
Q

Calcimimetic drug

A

mimics the action of calcium by increasing the sensitivity of the calcium-sensing receptors (CaSR) on the surface of the parathyroid gland to extracellular calcium.

159
Q

What does Cinacalcet [Sensipar] do to CASr receptors?

A

By binding to and activating CaSR, cinacalcet enhances the receptor’s sensitivity to calcium. This means that the parathyroid glands respond to lower calcium levels in the blood.

160
Q

What happens when CaSR is activated?

A

When the CaSR is activated, it inhibits the release of parathyroid hormone (PTH).

161
Q

By reducing excessive PTH secretion, what does cinacalcet do?

A

By reducing excessive PTH secretion, cinacalcet helps prevent the complications associated with SPTH, such as bone disease and vascular calcification.

162
Q

How does Cinacalcet [Sensipar] control calcium levels?

A

Controls serum calcium levels by reducing PTH-induced calcium release from bones and increasing renal calcium excretion.

163
Q

Cinacalcet [Sensipar] Pks

A

Oral, absorption increased by food, highly bound to plasma proteins, undergoes hepatic met, excreted in urine

164
Q

Cinacalcet [Sensipar] Adverse reactions:

What are symptoms of this?

A

Hypocalcemia

S/sx hypocalcemia: cramping, convulsions, paresthesias, tetany

PATHO/PHARM II (27 decks)

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