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
2
Q
Basic causes of inflammation of glomeruli?
A
Primary glomerular injury
Secondary glomerular injury
3
Q
Primary glomerular injury
A
isolated to the kidney
4
Q
Secondary glomerular injury
A
systemic disease (eg; drugs, DM, HTN, toxins, SLE, HF, HIV)
5
Q
What is the main component of Glomerulonephritis?
A
Immune mechanisms are main component
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
7
Q
Increased glomerular membrane permeability leads to what?
A
Increased glomerular mem permeability –> proteins & RBCs escape into urine
8
Q
What happens to bowman’s capsule in glomerulonephritis?
A
Swelling and cell proliferation in Bowman’s space
9
Q
Immune mechanisms that are main component lead to:
A
Result: injury to the glomerulus
10
Q
Risk factors that lead to glomerulonephritis: What is the most common?
A
Streptococcal infection, typically precedes (most common)
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
12
Q
Risk factors that lead to glomerulonephritis: what other bacterial infections?
A
Staphylococcus, Pneumococcus, varicella
13
Q
Risk factors that lead to glomerulonephritis: What other problems?
A
Immunodeficiency
Inflammatory DX ~ SLE
14
Q
Risk factors that lead to glomerulonephritis: Use of what would increase glomerulonephritis?
A
Meds (eg NSAIDs)
15
Q
Complications related to glomerulonephritis include?
A
CKD & renal failure, leading cause
16
Q
Clinical Manifestations: How does glomerulonephritis appear? Sudden or gradual?
A
Sudden or gradual
17
Q
Clinical Manifestations: What can occur before appearance of symptoms of glomerulonephritis?
A
Significant nephron function loss can occur before symptoms
18
Q
Glomerulonephritis Clinical Manifestations: How can symptom appearance be?
A
Symptom presentation may be silent, mild, moderate or severe
19
Q
Glomerulonephritis Clinical Manifestations: severe or progressive disease can lead to what symptoms?
A
Severe or progressive disease –> oliguria, htn, renal failure
20
Q
Clinical Manifestations: What are two major symptoms of glomerulonephritis?
A
- Hematuria with red blood cell casts
- Proteinuria (foamy urine) exceeding 3 to 5 g/day with albumin (macroalbuminuria) as the major protein
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
22
Q
Diagnosing glomerulonephritis includes what tests?
A
Urinalysis – proteinuria, rbcs, wbcs, casts
Renal biopsy – type of lesion, extent of renal injury
Reduced GFR
23
Q
Diagnosing glomerulonephritis: Reduced GFR
A
Elevated plasma urea
Cystatin C in blood
24
Q
Cystatin C
A
Biomarker of kidney function
Elevated creatinine concentration & reduced CrCl
high= kidney no functioning
25
Treatment for glomerulonephritis includes treating:
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
26
What is used to treat edema in glomerulonephritis?
Edema – diuretics, dialysis, restrict Na & H2O intake, I &O, daily weight
27
What are antibiotics used for in glomerulonephritis?
Abx – mgmt of underlying infection causing antigen-antibody response
28
What are glucocorticoids used for in glomerulonephritis?
Corticosteroids – suppress the inflammatory response, decrease Ab synthesis
29
What are cytotoxic agents used for in glomerulonephritis treatment?
Cytotoxic agents (cyclophosphamide) – suppress immune response
30
What are anticoagulants used for in glomerulonephritis treatment?
Anticoagulants – fibrin crescent formation
31
Tetrad of manifestations of Nephrotic syndrome
1. Proteinuria
2. Hyperlipidemia (Dyslipidemia)
3. Hypoalbuminemia
4. Peripheral edema
32
What is the pathophysiology of nephrotic syndrome:
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
33
What types of proteins are lost in urine in nephrotic syndrome?
immunoglobulins
albumins
lipiduria
34
What would loss of protein lead to in nephrotic syndrome?
Edema-
Susceptibility to infection
Liver produces more cholesterol= hypercholesterolemia
35
Why would edema occur in nephrotic syndrome?
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.
36
NephrITIC syndrome
Nephritic syndrome is hematuria and red blood cell casts in the urine.
37
Basic function of the kidney:
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
38
Renal insufficiency how is renal function, GFR, ScCr?
decline in renal fxn to ≈25% of normal, GFR <30 ml/min, & mildly elevated serum creatinine (SCr) and urea
39
Consequences of uremia:
Consequences: retention of toxic wastes, electrolyte disorders, deficiency states, immune activation proinflammatory state
39
End-stage kidney disease (ESRD):
<10% of kidney fxn remains
39
Uremia (uremic syndrome):
↑ blood Urea & Scr,
40
What does Uremia (uremic syndrome) lead to?
fatigue, anorexia, pruritis, n/v, neurologic sx
41
Azotemia:
What does it lead to for lab values
Accumulation of nitrogen waste.
↑ BUN & Creatine
42
Oliguria
Oliguria: urine flow < 400ml/day,
but UO may exceed this in AKI
43
Anuria:
complete cessation of urine flow is uncommon in AKI (<50cc/24hrs)
44
Acute Kidney Injury (AKI)
Sudden decline in kidney function
45
What is the patho of Acute Kidney Disease?
Accumulation of nitrogenous waste products in blood due to reduced gf
46
How long does it take acute kidney disease to occur?
Occurs over a few hours to a few days
47
Acute Kidney Injury is permanent? What does it require?
Reversible, may require dialysis or progress to chronic
48
What are three classifications of Acute Kidney Injury?
3 classifications
(prerenal,
intrarenal,
postrenal)
49
Kidney Disease Improving Global Outcomes (KDIGO) workgroup defines AKI as:
(having to do with SCr)
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
50
Kidney Disease Improving Global Outcomes (KDIGO) workgroup defines AKI as: (having to do with urine output)
Urine output less than 0.5 mL/kg/hour for 6 hours
51
Prerenal AKI Causes/Compensation:
Hypovolemia
Renal
Hypoperfusion/Renal Vasoconstriction
Systemic Vasodilation
Decreased Arterial Blood Volume (decreased cardiac output)
52
Intrarenal AKI Causes/Compensation:
Caused by
Glomerulopathies
Systemic disease/Type III Hypersensitivity
Hypercalcemia
Multiple myeloma
Acute tubular necrosis (most common)
53
What is the most common cause of Intrarenal AKI?
Acute tubular necrosis (most common)
54
Acute tubular necrosis- What is it and what happens?
Death of renal tubular epithelial cells
Membrane of tubular epithelium destroyed, cells slough off and plug the tubules.
55
Slide 22
I dont' understand
56
Post renal AKI
Obstructive uropathies
Neurogenic bladder
As the flow of urine obstructed, urine refluxes into the renal pelvis, results in impaired nephron function.
57
Post renal AKI: As flow of urine is obstructed, what happens?
As the flow of urine obstructed, urine refluxes into the renal pelvis, results in impaired nephron function.
57
Obstructive uropathies that cause postrenal AKI?
Obstructive uropathies:
BPH
Renal calculi
Bladder/prostate cancer
Blood clots
Tumors
58
What are characteristic findings of post renal AKI?
Characteristic finding: flank pain & anuria followed by polyuria
59
Post renal AKI: Prolonged mechanical obstruction leads to what?
Prolonged mechanical obstruction leads to tubular atrophy and irreversible kidney fibrosis
60
Postrenal AKI treatment includes:
Perform urinary catheterization
Prevent UTI.
Relieve obstruction
Treat reversible causes
61
Four phases of AKI:
1. Onset phase
2. Oliguric phase
3. Diuretic phase
4. Recovery phase
62
Four phases of AKI: Onset phase
Kidney injury occurs.
63
Four phases of AKI: Oliguric (anuric) phase:
Urine output decreases from renal tubule damage.
64
Four phases of AKI: Diuretic phase:
The kidneys try to heal and urine output increases, but tubule scarring and damage occur. The kidneys recover their ability to excrete waste but cannot concentrate the urine.
65
Four phases of AKI: Recovery phase
Tubular edema resolves and renal function improves.
66
Chronic Kidney Disease (CKD)
Progressive loss of renal function, affects nearly all organ systems
Slow, progressive, and irreversible loss of kidney function & GF based on eGFR
67
Chronic Kidney Disease (CKD) requires what for survival?
Requires dialysis or kidney transplantation to maintain life.
68
What can AKI progress to?
AKI can progress to CKD or AKI on CKD
69
Chronic Kidney Disease is associated with?
A/W htn, diabetes, intrinsic kidney disease, SLE, pyelo, chr glomeruloneph, obs uropathy
70
Normal GFR value
Normal GFR 120 to 140 mL/min
71
Stages of Chronic Kidney Disease
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
Stages of Chronic Kidney Disease:
Stage 1: Normal kidney function (GFR > 90 mL/min)
How is kidney?
Mild damage, reduced renal reserve
73
Stages of Chronic Kidney Disease:
Stage 1: Normal kidney function (GFR > 90 mL/min)
How are nephrons?
Unaffected nephrons overwork to compensate for diseased nephrons
74
Stages of Chronic Kidney Disease:
Stage 1: Normal kidney function (GFR > 90 mL/min)
What is symptoms are common?
Htn common, proteinuria, high Cr or no sx at all
75
Stages of Chronic Kidney Disease:
Stage 2: Mild CKD (GFR 60-89 mL/min)*
How are nephrons?
Kidney nephron damage has occurred
76
Stages of Chronic Kidney Disease:
Stage 2: Mild CKD (GFR 60-89 mL/min)*
How are lab values?
Slight elevation of metabolic waste in BUN/Cr
77
Stages of Chronic Kidney Disease:
Stage 2: Mild CKD (GFR 60-89 mL/min)*
What are common symptoms?
Inability to concentrate urine, polyuria and nocturia
Htn
78
Stages of Chronic Kidney Disease:
Stage 3: Moderate (GFR 30-59 mL/min)
How is it divided?
split into two substages based on eGFR (3a & 3b):
79
Stages of Chronic Kidney Disease:
Stage 3: Moderate (GFR 30-59 mL/min)
How are nephrons?
Nephron damage continues with decreased nephrons
80
Stages of Chronic Kidney Disease:
Stage 3: Moderate (GFR 30-59 mL/min)
What may be needed to be done in this stage?
Restriction of fluids, proteins, electrolytes, including phosphorus, may be needed
81
Stages of Chronic Kidney Disease:
Stage 4: Severe (GFR 15-29 mL/min)
What occurs?
Erythropoietin deficiency, anemia, HyperPhos/K, Increased triglycerides, Met acidosis, Na+/H2O retention
82
Stages of Chronic Kidney Disease:
Stage 5: End stage (GFR less than 15)
What are common symptoms?
Oliguria occurs
83
Stages of Chronic Kidney Disease:
Stage 5: End stage (GFR less than 15)
How are lab values?
Excessive urea (BUN) and Cr builds up in the blood
84
Stages of Chronic Kidney Disease:
Stage 5: End stage (GFR less than 15)
What is a fatal, classic marker?
Uremia (“urea in blood”) is the result and is fatal; classic marker
85
Patho of Chronic Kidney Disease:
First two steps:
1. Gradual loss of renal function
2. Kidneys can adapt to the loss of nephron mass to a point
86
Patho of Chronic Kidney Disease:
When are alterations in Na and water apparent in CKD?
Alterations in Na & H2O not apparent until GFR < 25%
87
Patho of Chronic Kidney Disease:
How are changes in serum creatinine and urea in chronic kidney disease?
Changes in Scr & urea are minimal early, but rise as the disease progresses & GFR ↓
88
Patho of Chronic Kidney Disease:
What is done to maintain GFR by nephrons?
Compensatory hypertrophy & hyperfunction of nephrons to maintain GFR (aka hyperfiltration)
89
Patho of CKD you read it
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
What is used to treat chronic kidney disease?
ACE inhibitors dilate glomerular arterioles and reduce glomerular hydrostatic pressure
91
Vitamin D/parathyroid hormone
92
Parathyroid hormone acts on the kidneys to do what?
PTH acts on the kidneys to increase calcium reabsorption and decrease phosphate reabsorption
93
What is the active form of vitamin D?
calcitriol
94
How does active vitamin D (calcitriol) work with PTH?
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
What does PTH do to vitamin D? What is the result?
PTH stimulates the conversion of vitamin D to its active form in renal tubular cells, enhancing calcium reabsorption.
96
What is needed for bone health and mineral balance?
This intricate interplay between the parathyroid glands and vitamin D is crucial for maintaining bone health and overall mineral balance
97
Osteodystrophy with renal failure
Slide 35
98
Clinical Presentation of CKD and Treatment: What does it include?
List 6
Skeletal
Cardiovascular
Neuro
Integumentary
Hematological
GI
99
Clinical Presentation of CKD
What does it include?
List 4
Electrolyte/Acid-Base Imbalance
Metabolic Changes
Reproductive System
Risk for infection
100
Clinical Presentation of CKD:
Skeletal
Results are pathological fxs, bone pain, deformities of long bones
101
Clinical Presentation of CKD:
Skeletal: What is the treatment of skeletal issues?
Activated Vitamin D
Phosphate binders
Phosphate-restricted diet
Activated Vit D replacement
Possible parathyroidectomy
102
Clinical Presentation of CKD:
Skeletal:
What do phosphate binders do as treatment for skeletal probs?
Phosphate binders work to bind phosphate in gut & excrete in stool
103
Clinical Presentation of CKD:
Cardiovascular issues?
Name 3
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
Clinical Presentation of CKD:
Cardiovascular issues?
Name 3:
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
Clinical Presentation of CKD:
Cardiovascular issues- What is the treatment?
Tx: diuretics to reduce volume (not K sparing), dialysis, avoid Mg because impaired magnesium excretion
106
Clinical Presentation of CKD:
Neuro
Uremic encephalopathy from toxins in CSF
Spectrum of cognitive & consciousness changes
107
Clinical Presentation of CKD:
Neuro:
What are spectrum of cog and consciousness changes?
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
Clinical Presentation of CKD:
Neuro: What is the treatment?
Tx: dialysis/kidney transplant
109
What is the general appearance of someone with CKD? (behavior and lower extremity)
Tired, weak, malaise, lethargy, dizziness from anemia
Lower extremity edema
Wt △
110
What is the general appearance of someone with CKD?
Skin color
sallow skin color – unhealthy yellow or pale brown from retained urinary pigments
111
Clinical Presentation of CKD: Integumentary
How does the skin feel? Why?
Itching, crawling skin from phosphate deposits, uric acid, urea
112
Clinical Presentation of CKD: Integumentary
Other issues of the skin that can occur?
Anemia - pallor
Bleeding into skin - ecchymosis
Uremic frost (seen with BUN levels >200 mg/dL)
Persistent pruritis
Jaundice
Calciphylaxis
113
What is the treatment for skin issues of CKD?
Tx: Dialysis
114
Clinical Presentation of CKD: Hematological
Why does anemia occur?
Anemia related to decreased production of erythropoietin increasing demands for cardiac output and adding to cardiac workload.
115
Clinical Presentation of CKD: Hematological- What happens to RBCs lifespan?
What happens to blood in total?
Decreased RBC lifespan secondary to dialysis & uremia
Blood loss from dialysis
Abnormal bleeding and bruising
116
Clinical Presentation of CKD: Hematological- What occurs that leads to increased infection?
Leukocytosis and altered immune response, leading to increased infection risk, especially in the respiratory and urinary tracts
117
Clinical Presentation of CKD: Hematological-probs
What is the treatment?
Tx: Erythropoietin injections, transfusions
118
Clinical Presentation of CKD: GI
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
Clinical Presentation of CKD: GI-
What happens to sense of taste?
Metallic taste in mouth and changes in taste due to the buildup of urea in the body
120
Clinical Presentation of CKD: GI-
What is the treatment for GI issues?
Tx: Protein-restricted diets
121
Clinical Presentation of CKD:
What is the Acid-Base Imbalance that occurs?
What does this result in?
Metabolic acidosis, related to H+ ion retention
results in Kussmaul’s resp --> blow off CO2
122
Clinical Presentation of CKD:
What is the Electrolyte Imbalance that occurs?
Hyperkalemia
Sodium& water balance
Hypocalcemia
Hyperphosphatemia
Hypermagnesemia
123
Clinical Presentation of CKD:
Electrolyte imbalance
Why does Hyperkalemia occur?
Hyperkalemia r/t decreased filtering ability & met acidosis
124
Clinical Presentation of CKD:
Electrolyte imbalance
Why does sodium and water imbalance occur?
Sodium& water balance
Fluid volume excess/edema
Na & water retained
125
Clinical Presentation of CKD:
Electrolyte imbalance
Why does hypocalcemia lead to symptom-wise?
Hypocalcemia response is the same as what other electrolyte imbalance?
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
Clinical Presentation of CKD:
What does hypomagnesemia cause?
Hypermagnesemia causing decreased respirations
127
Clinical Presentation of CKD:
Reproductive system
Decreased fertility
Infrequent or absent menses
Decreased libido
Impotence, infertility
128
Clinical Presentation of CKD:
Metabolic changes that occur?
Urea/creatinine
Carbs
lipids
insulin
Urea and creatinine excretion are disrupted by kidney dysfunction
Carbohydrate intolerance
Hyperlipidemia
Insulin resistance
129
Management of CKD: What is given for skeletal?
Vitamin D to ↓ PTH,
dietary phosphorus restriction, administer phosphorus-binding drugs
130
Management of CKD: What is given for Hematological
Dialysis, Epo & Fe supplementation, blood transfusion
131
Management of CKD: What is given for Cardiac?
Ace-Is, ARBs, Ca-Ch blockers, Diuretics, Beta blockers;
bilateral nephrectomy,
transplant;
limit Na & fluids;
dialysis
132
Management of CKD: What is given for GI treatment?
Protein-restricted diet for relief of n/v, antidiarrheals, antiemetics, laxatives (none containing Mg)
133
Management of CKD: What is given for neuro treatment?
dialysis, anticonvulsants
134
Management of CKD: What is given for Integumentary treatment?
dialysis
135
Management of CKD: What is given for Hyperkalemia?
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
Principles & Stressors Associated with Hemodialysis
Read it no time now
137
Pharmacology for renal failure:
1. Erythropoietin (Epogen, Procrit)
2. Calcitriol (Rocaltrol) Vit D analog
3. Phosphate Binders for Patients on Dialysis
4. Cinacalcet [Sensipar]
138
Erythropoietin (Epogen, Procrit)- What does it do?
Stimulates erythrocyte production in bone marrow in anemia associated with CRF
139
Erythropoietin (Epogen, Procrit)- How is it administered?
IV or Sq
140
Erythropoietin (Epogen, Procrit) : What is it used for?
Maintenance of erythrocyte counts
Partial reversal of anemia in CRF
141
What does Erythropoietin (Epogen, Procrit) reduce the need for what?
What is needed for the med to work?
Reduced need for transfusions but NOT eliminated
Iron stores must be adequate for med to work- may need iron supplementation
142
What does Erythropoietin (Epogen, Procrit) adverse effects?
Htn (already common in RF) – directly r/t rise in Hct
Monitor BP
Stroke, HF, thrombosis, MI
143
Administration of erythropoetin means you should monitor what?
Monitor Hgb, reduce dosing or d/c if: Levels approach 11 gm/dL or Increases > 1 gm/dL within 2wks
144
Calcitriol (Rocaltrol) Vit D analog: MOA
Active form of Vitamin D, promotes absorption of Ca, decreases PTH concentrations
145
Calcitriol (Rocaltrol) Vit D analog: What is it used for?
Hypocalcemia in pts with CKD
146
Calcitriol (Rocaltrol) Vit D analog: Pks
well absorbed from GIT, widely dist.
Stored in liver, fat, muscle, skin, bones.
147
Calcitriol (Rocaltrol) Vit D analog: How should it be administered?
Adm: with or without food, risk for GI discomfort if taken w/food
148
Calcitriol (Rocaltrol) Vit D analog: Contraindications?
hypercalcemia, Vit D toxicity
149
Calcitriol (Rocaltrol) Vit D analog: Adverse reactions?
What does this mean you assess patient for?
ADRs: Toxicity - Hypercalcemia, Hypercalciuria, Hyperphosphatemia.
Assess pt for weakness, fatigue, n/v, abdominal cramping, constipation, bone pain
150
Calcitriol (Rocaltrol) Vit D analog: Nursing indications?
Nsg Indications: Monitor serum calcium & phosphorus
151
Phosphate Binders for Patients on Dialysis: What is it used to treat?
Used to treat hyperphosphatemia in ESRD
152
Phosphate Binders for Patients on Dialysis: MOA?
Binds to dietary phosphate to form calcium phosphate complex, preventing its absorption
Phosphorus excreted in feces decreased levels
153
Phosphate Binders for Patients on Dialysis: How should it be taken?
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
Calcium-based phosphate binders
increase the risk for what?
Increase risk of hypercalcemia
155
Calcium-free phosphate binders
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
Cinacalcet [Sensipar]- what is it approved for?
Approved for secondary hyperparathyroidism caused by CKD
157
Cinacalcet [Sensipar]- what kind of drug is it?
Calcimimetic drug
158
Calcimimetic drug
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
What does Cinacalcet [Sensipar] do to CASr receptors?
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
What happens when CaSR is activated?
When the CaSR is activated, it inhibits the release of parathyroid hormone (PTH).
161
By reducing excessive PTH secretion, what does cinacalcet do?
By reducing excessive PTH secretion, cinacalcet helps prevent the complications associated with SPTH, such as bone disease and vascular calcification.
162
How does Cinacalcet [Sensipar] control calcium levels?
Controls serum calcium levels by reducing PTH-induced calcium release from bones and increasing renal calcium excretion.
163
Cinacalcet [Sensipar] Pks
Oral, absorption increased by food, highly bound to plasma proteins, undergoes hepatic met, excreted in urine
164
Cinacalcet [Sensipar] Adverse reactions:
What are symptoms of this?
Hypocalcemia
S/sx hypocalcemia: cramping, convulsions, paresthesias, tetany
