Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
38 Cards in this Set
- Front
- Back
|
Describe the functions of the kidney
|
Excretory: waste products, water, drugs
Regulatory: Control of body Fluid volume, composition, acid/base and blood pressure. Endocrine: production of erythropoietin, renin and prostaglandins Metabolic: metabolism of Vitamin D, Insulin and other small proteins. |
|
|
What are the factors that effect the excretory and regulatory function of the kidney?
|
Renal Blood Flow (1.3 L/min)
Glomerular Filtration (1 million Nephrons per kidney Tubular Function (reabsorbtion or secretion) |
|
|
Name the products that the kidney synthesizes
|
Renin
Erythropoietin Calcitriol (1,25-Dihydroxyvitamin D3) Bioactive agents: PG, adenosine, endothelin. |
|
|
What does the kidney metabolize
|
breakdown of many peptide hormones such as insulin
|
|
|
Describe glomerular filtration. What are the 3 factors that affect filtration?
|
Process by which plasma is filtered at the glomerulus and formation of urine (ultrafiltration) is initiated. Factors influencing filtration are:
1. Renal Plasma Flow (60% of blood flow) 2. Permeability and total surface area of glomeruli (Filtration Membrane) 3. Starlings Forces - Albumin protein keeps fluid in the vessels. a .Capillary Hydrostatic Pressure b. Hydrostatic pressure in Bowmans Space c. Plasma Oncotic Pressure |
|
|
Name the 3 layers of the filtration membrane
|
Fenestrated Endothelial Cell (blood side)
Basement Membrane Epithelial Cell with filtration slits between foot processes (urine side) |
|
|
1. What is the blood supply rate?
2. Plasma flow rate? 3. How much of protein free ultrafiltrate of plasma is filtered? 4. How much of water and electrolytes reabsorbed by tubules? 5. How much urine? |
1. 1.3 L/min - GFR at normal
2. 0.8 L/min 3. 180 L 4. 99% 5. 1.5 L |
|
|
What does the filtration membrane prevent? Why is the GFR so large?
|
Loss of protein in ultrafiltrate.
Physical barrier (<5200 mol wgt) Electrostatic Forces. (Anionic charge on albumin retards its ultrafiltration) Why is GFR so large? To maintain homeostasis of waste products present in plasma in low concentration. (e.g. urea) |
|
|
What is used as a markers for GFR?
|
Creatinine Clearance rate - number of cc of blood that are completely clreared of creatinine per min.
Normal GFR is 120 cc/ min. This falls with increasing age and w/ any process that affects the determinants of filtration |
|
|
Formula for GFR or Creatinine Clearance?
|
Ucr X V / Pcr .
-larger someone is, the higher the GFR. - falls w/inreasing age but still should have normal function. |
|
|
Name and describe each stage of chronic kidney disease
|
Stage I GFR > 90 ml/min/1.73m²
Diagnosis and Treatment, Slow progression, CVD risk reduction Stage II GFR 60-90 ml/min/1.73m² Estimating progression Stage III GFR 30-59 ml/min/1.73m² Evaluating and treating complications Stage IV GFR 15-29 ml/min/1.73m² Preparation for kidney replacement therapy Stage V GFR <15 ml/min/1.73m² (Replacement if uremia is present) |
|
|
What are some limitations of creatinine clearance?
|
1. incomplete urine collection.
Creatinine excretion is constant -Expect 20-25 mg/kg/day in men and 15-20 in women. If urine Cr is low due to incomplete collection -- CC is underestimated 2. ingestion of cooked meats increases plasma Cr (CC underestimated) and low muscle mass dec. Cr production. 3. increase tubular sec. of creatinine as renal fcn declines Note: Pt must be stable in order to use this as a good estimate |
|
|
What can we say about plasma creatinine and GFR in a steady state?
|
Creatinine excretion = creatinine production.
GFR x Pcr = constant. Pcr varies inversely with GFR. Pcr = 0.8-1.3 in men and 0.6-1.0 in women. -Reciprocal relationship between GFR + Pcr is valid in steady state only. -initial elevation in Pcr rep. major loss in GFR -this relationship is dependent on rate of creatinine production = muscle mass + meat and protein intake |
|
|
What is needed to monitor patients of kidney dysfunction?
|
Serial measurement of Pcr is needed to monitor patients with kidney dysfunction.
A rise in Pcr indicates disease progression, whereas a fall suggests recovery of renal function. Stable Pcr usually means stable renal function |
|
|
What do the Cockroft Gault equation and MDRD equation help you estimate?
|
Both used to estimate creatinine clearance formulas..
Takes into account age, lean body weight for Cockcroft. MDRD - Pcr, age, urine, and albumin |
|
|
What do non steroidal antiinflammatory drugs do? What considerations are there for antibiotics?
|
Reduce GFR in particular clinical settings (e.g when dehydrated or when combined with ACE
inhibitors). They can also lead to life threatening hyperkalemia in patients with renal failure. Antibiotics needs to be dose adjusted! Ex. Pen G needs to be halved for patients w/ GFR < 10 cc/min. |
|
|
Describe acute renal failure
|
Sudden decrease in renal function usually manifested by an increase in BUN and serum creatinine and sometimes associated with oliguria
Oliguria is defined as urine output < 400 ml/day or 20 ml/hour. 5% of inpatients and 15% of ICU patients develop ARF. 50%-70% mortality rate. ARF can be prevented in many settings. ** reversible. Most common cause is dehydration |
|
|
Prerenal azotemia
|
It is an elevation of the Pcr and BUN due to “effective” volume depletion resulting in diminished renal perfusion.
The kidney’s intrinsic ability to function remains intact. Potentially reversible when diagnosed early and treated effectively by giving them fluids. Patients with established CRF can develop superimposed prerenal azotemia. ** Most commonly caused by volume depletion |
|
|
What are some causes of the pre renal state?
|
Blood loss, Volume depletion
Hypotension CHF, Cirrhosis Medication effects (diuretics, antihypertensives, ACE inhibitors) Atherosclerosis of renal vessels, thrombosis, embolus, dissection of aorta |
|
|
What is the most common cause of renal failure in hospitalized patients? What may happen is pre renal milieu is severe? How about is most severe cases of volume depletion?
|
-Pre renal failure - may develop as a result of Acute Tubular nerosis. Usually resolves in 2 weeks though patients may require dialysis.
In the most severe cases of volume depletion, patients may develop “Acute Cortical Necrosis” and require lifelong dialysis. |
|
|
What does uremia genreally do with respect to absorption of drugs?
|
Generally, uremia decreases GI absorption of drugs by alkalizing effect of NH3 buffering gastric acid (FeSO4)
Antacid use can cause chelation and formation of nonabsorbable complexes (Digoxin, antibiotics) Uremia can alter protein binding of drugs which leads to increase in “active drug” and enhanced bioavailability (Dilantin) |
|
|
What are some side effects of nsaids?
|
salt and water retention (common) (edema in 3-5%)
hyperkalemia Acute renal failure Papillary necrosis Interstitial Nephritis (I.N) Nephrotic Syndrome with I.N. |
|
|
Reduced GFR occurs as a result of?
|
Glomerular lesions (crescentic glomerulonephritis)
Interstitial Nephritis (NSAID’s or antibiotics) Vascular lesions (malignant hypertension, thrombotic angiopathies) Tubular lesions (ATN: volume depletion, ischemia, antibiotics (gentamicin, amphotericin), chemotherapy cisplatin) |
|
|
Acute Intersitial Nephritis
|
10-15% of Acute Renal Failure
Usually drug induced Penicillin analogues, sulfonamides and NSAIDs **Marked leukocytes infiltrate in interstitium, esp EOSINOPHILS. Develops 5-7 days after exposure. Hypersensitivity triad of fever, rash and eosinophilia occurring in the setting of ARF. Hypersensitivity triad present in the minority of patients. (30% with penicillin) -hypertension + edema aren't prominent features -Urine analysis: hematuria, WBC, eosinophiluria, proteinuria -Often resolve spontaneously once the med is stopped -steroids may be beneficial |
|
|
What is post streptococcal GN?
|
Most common form of glomerulonephritis in children.
Diagnosis: Glomerular injury (hematuria, proteinuria) Identification of nephritogenic organism (strep) A rise in antibody titres to streptococcal products after a latent period following signs of infection (2 weeks) Immune complex glomerulonephritis immune deposits seen on biopsy specimen low C3 latent period antibody response |
|
|
Post renal failure
|
Obstruction
Most common cause in males is prostate disorders Most common cause in females is cervical cancer. Other causes: Single kidney: stone, clot etc As long as obstruction is not longstanding, renal function recovers rapidly with relief of the obstruction. Surgical (transurethral resection of prostate) Medical (alpha blockers) Foley catheter Nephrostomy tube Ureteral stents |
|
|
Acute renal failure symptoms
|
In general there are no symptoms from acute renal failure until renal failure is advanced.
Most patients are diagnosed with blood tests performed to evaluate other complaints. Symptoms are usully manifestations of the underlying etiology. Often times painless, and don't realize until its very late or have routine blood work done. |
|
|
Acute renal failure complications
|
Persistent low GFR with
Progressive azotemia: dialysis Persistent volume overload: dialysis Hyperkalemia: Kayexelate, Dialysis Persistent acidosis: Bicarbonate, Dialysis |
|
|
Describe risk factors of hypertension
|
-BP 140/90 on 2 occasions. Higher the BP, the greater your chance of MI, heart failure, and kidney disease.
Age: 50 % of adults >65 have a systolic blood pressure > 140 diastolic pressure > 90 Race: Nearly twice as common in African Americans and for a given level of hypertension this group also develops more severe end-organ damage. Salt Sensitivity: Not all hypertensives are salt sensitive. Other Cardiovascular Risk Factors: Diabetes, Smoking, family history etc. |
|
|
Secondary causes of hypertension
|
Renal Disease (all forms- account for 80% )
Salt and water retention (chronic renal disease, Liddles Syndrome) Hyperreninemia: RAS, Page Kidney, Vasculitis. Endocrine: Cushings, Pheochromocytoma, Conns Syndrome, Liquorice ingestion (chewing tobacco), Acromegaly, Reninomas, Congenital Adrenal Hyperplasia, Thyroid disorders, Hyperparathyroidism, Exogenous hormones (glucocorticoids, mineralocorticoids, OCP, Sympathomimetics. |
|
|
End organ damage of hypertension
|
Cardiovascular: Hypertensive Heart Disease, LVH, Heart Failure, Dissecting Aneurysm, CAD, PVD.
Stroke (hemorrhagic, ischemic), TIA. Kidney: Hypertensive Nephrosclerosis Eye: CRAO, Hemorrhage, Papilledema with malignant hypertension. Nose: Epistaxis Malignant Hypertension |
|
|
Significance of hypertension in dental care?
|
Dentists may be the first to identify the problem and can recommend evaluation or treatment by physicians
Use of NO or anxiolytics may be necessary for patients with “white coat hypertension” Use of epinephrine (a vasoconstrictor) for local anesthesia has been debated, but thought to be safe for all but those with the most severe CVD Patients with consistent SBP>160/100 should be referred for medical evaluation Patients with >180/110 require medical consultation as hospitalization may be required No published recommendations for Urgent dental care and BP, but most dental clinicians use <180/110 as a cutoff to proceed. |
|
|
How do the following meds affect dental care?
1. multiple BP meds 2. Clonidine, Beta blockers, a1 blockers, diuretics 3. Calcium channel blockers 4. ACE inhibitors |
Multiple BP meds can cause orthostatic hypotension, so sit upright for a few minutes after long procedure
Clonidine, β-blockers, α1-blockers, diuretics can all lead to xerostomia which can lead to caries, candidiasis, and difficulty with mastication/swallowing Calcium channel blockers can lead to Gingival overgrowth (Nifedipine most cited) Numerous medications have been linked with “lichenoid reactions” (oral lesions resembling lichen planus) ACE-inhibitors can lead to cough/loss of taste and infrequently, “scalded mouth syndrome” (burning sensation) |
|
|
Conservative therapy for hypertension?
|
Weight reduction in obese patients (Diabetics)
Moderate Alcohol Consumption Reduce sodium intake to <100 mmol/day (2.3g sodium, <6g salt) Regular exercise Smoking Cessation Potassium intake of 60-100 mmol/day (2.4-4g Avoid Decongestants. |
|
|
Treatment for hypertension
|
Despite the elusive etiology of most cases of hypertension, pharmacotherapy of this disease can significantly reduce morbidity and mortality.
Since 1972 there has been a decrease in age adjusted cardiovascular mortality rates. CAD reduced by 50% Stroke by 57% Reduction in diastolic pressure by 6 mm Hg in large trials reduced the risk of stroke by 40% |
|
|
What meds should you stay away from for those with kidney disease?
|
NSAIDs - generally they are metabolized in the kidney. Opiates partially both liver and kidney.
Oxycodone, dialaudid probably better to use. |
|
|
Complications of using NSAIDs for a long time?
|
-Edema
-High potassium levels -nephrotic syndrome - spill 3 g of protein per day in the urine. -intersistial nephritis - blood in urine, WBC in urine -papillary necrosis |
|
|
Drug dosing w/ renal impairment
|
In patients with kidney disease cognizance of the degree of renal impairment is important when dosing chemicals. (Elderly!)
Medication doses and intervals often need reducing in renal insufficiency, and occasionally need supplementation in dialysis patients Generally, uremia decreases GI absorption of drugs by alkalizing effect of NH3 buffering gastric acid (FeSO4) Antacid use can cause chelation and formation of nonabsorbable complexes (Digoxin, antibiotics) Uremia can alter protein binding of drugs which leads to increase in “active drug” and enhanced bioavailability (Dilantin) |
