Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Renal > Renal pharm > Flashcards

Renal pharm Flashcards

1
Q

acute kidney injury- nephrotoxicity

A

occurs after exposure to drugs, medical procedures, and toxins.
High incidence of acute kidney injury in patients receiving antibiotics, chemotherapy, or radiocontrast dyes.
Also a complications of tharacic surgery
Chronic kidney disease develops in 20-30% of acute kidney survivors
Current treatment involves fluid and blood pressure maintenance and hemdialysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Mechamism of acute kidney injury

A
  1. Arterial occlusion (transplant surgery), Hypotension (volume depletion), Shock (cardiogenic septic)
  2. Renal ischemia (reperfuision)
  3. Microvascular dysfunction, excess vasoconstriction, inflammation, oxidative stress, endothelial injury, endothelial-leukocyte interactions
  4. Mismatch between O2 consumption and O2 supply
  5. Renal tissue hypoxia
  6. Tubular necrosis and apoptosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Emerging pharmacological agents moa for acute kidney injury

A
  1. Antiapoptotic (Caspase inhibitors, Minocycline)
  2. Anti inflammatory (Adenosine A2A agonist, Phosphatidylserine binding protein)
  3. Antisepsis (Insulin)
  4. Growth Factor (recombinant erythropoietin)
  5. Vasodilator (Fenoldopam-dopamine, ANP, Nitro oleic acid analogs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Chronic kidney disease causes and treatments

A

Diabetic nephropathy, HTN, Glomerulonephritis, HIV nephropathy, Reflux nephropathy in children, Polycystic kidney disease, kidney infection and obstructions

Treatment for chronic kidney disease, inhibit RAAS

RAAS inhibitors decrease progression of albuminuria, GFR decline, risk of ESRD

Beneficial effects of inhibitors: only in part due to BP reduction, extend to CKD regardless of etiology, occur with both ACEis and ARBs, together better than alone

NSAIDs damage the kidney further, may interact with ACEs and ANG receptor antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Treatment of diabetic nephropathy

A

Management of primary disorder paramount, Good glycemic control (HbA1C<7%), BP coontrol under140
Meds to minimize Proteinuria (Acei and ARBs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

anemia in chronic kidney diseases

A

Erythropoietin- glycosylated protein hormone produced primarily in the kidney

REgulates RBC production by production by reducing apoptosis and stimulating differentiation and proliferation of erythroid progenitor cells. Deficient in End stage renal disease (ESRD)

Symptoms: Fatigue and decreased cognition, causes (Kidney releases ETP in response to hypoxia in endothelial cells of peritubular capillaries–> bone marrow–> RBCs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Epoetin

A

IV or Sub Q
Human recombinant synthesized, response more rapid with IV but greater response with subQ, E poetin half lige (4-6 hours) administered 2-3 times/wk

SE: NVD, headache, influenza like symptoms, HTN ( dose dependent and can be severe leading to encephalopathy and seizures, thrombosis of arteriovenous shunts, Pure red cell aplasia subQ admin in renal failure could have Antibodies of Epoetin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Hypocalcemia in CKD

A

CKD–> low renal phosphorous clearance–> hyperphosphatemia and increased FGF23–> reduced Vit D–> hypocalcemia, 2’ hyyperPTH

excitability of nerves and muscles and regulates permeability of cell membranes, also integrity of cell membranes

Ca essential for excitation and coupling of all types of muscles, exciteation and secretion of endocrine and exocrine glands, and release of NT from nerve ending, Intracellular messenger for hormones, autacoids and transmitters, impulse generation and condution in heart, coagulation of blood, structural function of bone and teeth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Plasma calcium

A

regulated by 3 hormones, PTH calcitonin, and calcitriol (vit D) 9-11 mg/dl

40% bound to plama protein- 10% citratem carbonate and phosphate and 50% is free ionized and important form, Hypoalbuminemia (no drecrease in calcium concentration)
Acidosis- favors ionization, alkalosis disfavors ionization hyper ventilation precipitates tetany and laryngospasm in calcium deficiency

Causes secondary hyperpth ( due to decreased vit D3, dec serum calcium, increased phosphorous)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

calcitriol and vit D analogs moa

A

enhancement of absorption of Calcium and Po4 from intestine, by increasing the synthesis of calcium channels and a carrier calcium binding protein CaBP or calbindin
Binds to cytoplasmic vit D receptor (VDR)- translocation increased synthesis of mRna- regulation of protein synthesis

Calcitriol also enhances recruitment and differentiation of osteoclast precursor for remodeling- resorption of calcium and PO4 from bone, also enhances renal tubular REAB of calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

SE of Calcitriol

A

increases intestinal absorption of Ca and phosphate and increases Ca and phosphate mobilization from bone, calcitriol can result in Hyper Ca and PO4

Second and 3rd generation of Vit D analogs have more affinity to the kidney and a lower incidence of Hyper Ca and PO4, and better PTH control

Ergocalciferol is inactive (needs hydroxylation in kidney)
Kidney disease- the hydroxylated active forms (alfacalcidol or calcitriol need to be used)
Alafacalcidol and calcitriol have really short half lives, paricalcitol requires IV injection, unwanted effect (excessive dosing leads to hypercalcemia

Signs and treatment of vit D- fractures and hyper PTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Phosphate binders

A

Calcium carbonate, calcium acetate, lanthanum carbonate

GI - phosphate absorption by reacting with phosphate and form insoluble compound

Sevelamer- calcium and aluminum free polymeric structure (GI se/hypercalcemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

bisphosphonates- hypercalcemia

A

RONATES

Bisphosphonates are pyrophosphate analogs that bind to hydroxyapatite in bone to inhibit bone resorption

Zoledondrates can suppress bone rresorption for up to a year after a single dose, removed by kidney, unwanted SE (GIT osteonecrosis of jaw)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Calcitonin

A

Produced by parafollicular or C cells of the thyroid gland, secreted when plasma calcium level rises, main action is the lowering of plasma calcium by limiting bone resorption and it increases phosphate excretion in the urine, intramuscular or subQ injection- half life 20 minutes

SE: facial flushing in most patients, neural (headaches, dizziness), GI (nausea, vomiting abdominal pain, diarrhea), taste disturbance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

hyperuricemia and gout in kidney disease

A

Kidney eliminates urate from plasma, 8-12% of Urate filtered load is excreted

Colchicine (reduces inflammation, given every 6-12 hrs, ) Unwanted side effects (GIT and rash)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Hyperuricemia and gout in kidney disease,

A

Xanthane Oxidase inhibitor - oral
Allorpurinol- purine
Febuxostat: Non- purine, competitve enzyme inhibitors, variable half life 1-15 hours (renal excretion), SE: GI upset, acute gout (release of Urate from tissue deposits, HS to allopurinol rashes especially in renal disease pts), Drug interaction inhibit metabolism of azathioprine

Rasbuircase iv admin, recombinant version of enzyme urate oxidase, metabolized by peptide hydrolysis in plamsa, used 1’ as prophylaxis during chemo (CKD), SE: fever NVD, HS hemolysis

17
Q

Renal replacement therapy and transplantation

A

you want a living donor,, malignant skin tumors, CVD, need immunosuppression to combat kidney transplant rejection

18
Q

Renal transplant, calcineurin inhibitors

A

Origin: Cyclosporine (small cyclic polypeptide, fungal origin), Tacroolimus (macrolide isolated from streptomyces)

MOA: bind to cytosolic receptor proteins, cyclophillin (cyclosporine), FKBP12 (tacrolimus)
Complex binds to and inhibits action of calcineurin, inhibits the transcription of cytokines, such as IL2 that aare essential for T cell activation and proliferation

Cyclosporine (oral or IV): concentrates in tissue- liver kidney, spleen, bone marrow, MEtabolized extensively by CYP3A4 in liver, long half life (27 hrs)

19
Q

Cyclosporine SE

A

Nephrotoxic, HTN and fluid retention, hepatic dysfunction, tremor, headache, fatigue, NVD, Hypertrichosis, gum hypertrophy, Hyper Lipidemia, Hypo magnesium, kalemia

20
Q

tacrolimus

A

calcineurin inhibitor
oral IV, more water soluble metabolized by liver, highly variable half life, monitor trough blood concentration essential, doesnt stimulate TGF B, unwanted side effects (pleural and pericardial effusions, cardiomyopathy in children)

21
Q

calcineurin inhibitor side effects

A

Hepatotoxicity: liver function should be monitored at regular intervals

Cardiovasular (HTN HLIP): fewer tacrolimus- treated patients require antihypertensive meds, Tacrolimus impact on lipid levels is less than that seen with cyclosporine

Glucose intolerance: recent studies indicate little differences tacrolimus and cyclosporine

Neurotoxicity (Tremor headache, insomnia, paresthesia)- seem more with tacrolimus

22
Q

calcineurin

A

Nephrotoxic agents (NSAIDs, vancomycin, Ganciclovir, aminoglycosides)- monitor renal function, NSAIDs may have increased nephrotoxicity with hepatic impairment

Potassium-sparing diuretics (hyperkalemia has been reported)

Antacids (magnesium and aluminum antacids may inhibit absorption of CNIs) if necessary should be taken 2hrs after CNI dose

HMG CoA reductase inhibitors (increased risk of rhabdomyolysis, BM suppression)

23
Q

mTOR sirolimus

A

Macrolide, Sirolimus binds to FKBP12, complex binds and modulates the activity of mTOR, blocks signal 3 (inhibition of cytokine/ IL2 induced cell cycle progression from G1 to S phase)

Oral Gut absorption odulated P gp, metabolized by intestinal and liver CYP450, very long half life (60 hrs)

24
Q

Antiproliferative Agents- mycophenolate Mofetil

A 
Mycophenolic acid (MPA): isolated from penicillim
Mycophenolate mofetil MMF: a prodrug of MPA

MOA: Competitive reversible, inhibition of IMPDH a critical rate limiting enzyme in de novoe purine synthesis
Lymphocytes dependent on de novo pathway vs salvage pathway utilized by other cell types, Inhibits proliferation of B and T cells

25
Q

Azathioprine

A

Purine analogue, metabolized in the liver to 6 mercaptopurine and then TIMP, TMP decreases synthesis of DNA precursors and also incorporate into DNA, More nonspecific effects than mycophenolate mofetil, effects on DNA synthesis not limited to lympoid cells, blocks CD28 co stimulation of T cells

Oral, short half life 3-5hrs, (bone marrow suppression leucopenia, thrombocytopenia, HS reactions, malaise, dizziness, GIT, fever rash hypotension, opportunistic infection, alopecia, small risk for lympomaas

26
Q

Basiliximab

A

Very long half life, given immediately prior to surgery and 4 days following, Unwanted side effects (HS reactions rarely occur)

27
Q

Belatacept

A

Fusion protein binds CD80 and CD86, blocks co stimulatory action with CD 28 on T cell activation
Used fro renal transplantation in pts for Ebstein Barr virus

Very long half life (8-10 days)
Unwanted SE: HS reactions, lymphoproliferative disorder in those with/o exposure to EBV

28
Q

Corticosteroids prednisolone

A

inhibits NFkB, activate inflammatory, reduces T cell proliferation and increases,

29
Q

rituximab for nephrotic syndrome

A

b cell depletion, anti cd20, toxicity

30
Q

polycystic kidney disease

A

tolvaptan, vasopressin 2 receptor antagonist for hyponatremia in CHF, and cirrhosis

Renal (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions