Renal Flashcards

Question

Juxtaglomerular apparatus

Answer 1

JG cells= smooth muscle cells of afferent arteriole - Secrete renin when renal BP low Macula densa= DCT NaCl sensor - Induce JG cells to secrete renin in response to low NaCl in DCT Renin converts Angiotensinogen (liver) to angiotensin I--> lungs (ACE)--> angiotensin II + Increased sympathetic tone (Beta-1) ** Beta-blockers (Beta-1 selective, like metoprolol) can decrease BP--> inhibiting B1 receptors of JGA--> decreased renin release

Answer 2

Erythropoietin | - Released by interstitial cells in peritubular capillary bed in response to hypoxia

Answer 3

Converted by PCT cells from 25-OH to 1,25-OH2 (active form) - PTH enhances activity of enzyme (1-alpha-hydroxylase) ** PTH secreted in response to low plasma [Ca+2] or [vit D] or high plasma [Phosphate]

Answer 4

DO Insulin LAB work: - Digitalis - hyperOsmolarity - Insulin deficiency - Lysis of cells - Acidosis - Beta-adrenergic antagonist

Answer 5

Low serum [Na+] - Nausea, malaise, stupor, coma High serum [Na+] - Irritability, stupor, coma

Answer 6

Low serum [K+] - ECG: U waves, Flattened T waves - Arrhythmias, muscle weakness High serum [K+] - Wide QRS, peaked T waves - Arrhythmias, muscle weakness

Answer 7

Low [Ca+2] - Tetany, seizures High [Ca+2] - Stones, bones, groans, moans

Answer 8

Low [Mg+2] - tetany, arrhythmias High [Mg+2] - decreased DTRs, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia

Answer 9

Winter's formula: | PCO2= 1.5 (HCO3-) + 8 +/-2

Answer 10

Check with metabolic acidosis: Na+ - (Cl- + HCO3-) ``` Increased: MUDPILES - Methanol - Uremia - Diabetic ketoacidosis - Propylene glycol - Iron tablets/INH - Lactic acidosis - Ethylene glycol - Salicylates ``` ``` Normal: HARDASS - Hyperalimentation - Addison's disease - Renal tubular acidosis - Diarrhea - Acetazolamide - Spironolactone - Saline infusion ```

Answer 11

Type 1 Renal Tubular Acidosis: Failure of distal alpha intercalated cells to excrete H+ Leads to: - Elevated blood H+ - Inability to acidify urine (pH > 5.3)--> increased risk of calcium phosphate stones - Elevated Chloride - Hypokalemia - Bone reabsorption (Rickets in kids, osteomalacia in adults) Hyperchloremic non-anion gap acidosis

Answer 12

Type 2 Renal Tubular Acidosis Failure of proximal tubular cells to reabsorb bicarb Leads to: - Elevated blood H+ - CAN acidify urine (excrete H+)- ph < 5.3 - Hypokalemia - Increased rick for hyposphatemic rickets Seen in Fanconi's anemia

Answer 13

Type 4 RTA Collecting tubule not responsive to aldosterone or hypoaldeosteronism --> HYPERkalamia--> impaired ammoniagensis in PCT - Decreased buffering, decreased urine pH

Answer 14

Type IV collagen defect - type IV collagen= basement membrane, basal lamina of kidneys, ears, eyes X-linked recessive (boys) Symptoms: - Progressive nephritis - Deafness - Ocular disturbances

Answer 15

Calcium oxalate= due to hypercalciuria - Acidic urine (low pH) - Calcium oxalate stones are hard and dark - Presentation: hypercalciuria and normocalcemia - Urinalysis: calcium oxalate crystals are colorless tetrahedra (envelope shape), oval or dumbbell shapes; polarizable * * seen in ethylene glycol poisoning (antifreeze), Vitamin C overuse, Crohn's disease (low calcium reabsorption--> oxalate crystal formation) Calcium phosphate: due to hypercalciuria - increased pH causes precipitation Prevention: thiazides, citrate

Answer 16

Magnesium ammonium phosphate (15% of stones) - Due to urea-splitting bacteria (Proteus, Staphylococcus, Providencia) - Alkaline urine (high pH) - Triple phosphate crystals in urinalysis are colorless, rectangles or coffin lids shaped - Staghorn calculi (nidus for UTIs)

Answer 17

Due to hyperuricemia (6% of stones) - precipitate in collecting duct @ low pH - RadiolUcent: can see on CT, ultrasound - Acidic urine (low pH) - Rhomboid crystals Hyperuricemia also seen in high cell turnover states (leukemia) Tx: alkalinize urine

Answer 18

Due to genetic defects in cystine transport - Autosomal recessive - Yellow-brown radiopaque stones - acidic urine (low pH) - Hexagonal crystals ** Sodium nitroprusside testing--> urine turns purple after 2-10 minutes Tx: alkalinize urine

Answer 19

Sloughing renal papillae: - Presentation: gross hematuria, acute, colicky flank pain (ureteral obstruction from sloughed papillae), proteinuria; recent infection/immune stimulus - Associated with: DM, acute pyelonephritis, chronic phenacetin use (acetaminophen), NSAID use, sickle cell anemia/trait Histo: coagulative infarct necrosis with preserved tubule outline - Scars develop on cortical surface (fibrous depressions replace inflammatory foci)

Answer 20

Elevated nitrogen levels in blood NOT due to kidney damage - Renal blood flow decreased--> decreased GFR--> decreased clearance of metabolites - Kidney is intact and cells are not damaged - Kidney avidly reabsorbs salt and water to try and preserve intravascular blood volume and renal blood flow. Features: - History of volume depletion - Exam consistent with volume depletion - Fractional Excretion of Na (FENa) < 1 % - Urine Na < 20 mEq/L (low if kidney is Na avid, tubules intact) - Urine Osm > 500 mOsm/L - Increased BUN/Creatinine Ratio - Bland urinalysis - Ultimate Test: Give Fluid - If immediate improvement, then it’s pre-renal

Answer 21

Causes: - Acute tubular necrosis - Ischemia/toxins - Acute glomerulonephritis (RPGN); rarer Pathogenesis: 1. Patchy necrosis--> debris obstructs tubule 2. fluid backflow--> decreased GFR Urine sediment: - epithelial/granular casts on urinalysis - Casts= mucoprotein secreted by renal tubule cells - -> decreased GFR--> increased accumulation of casts Urine lytes: - Na > 40 mEq/L or FENa > 2% - Serum BUN/Cr < 15

Answer 22

``` In patients with two functioning kidneys, both need to be effected to produce significant renal failure Causes: - Urethral obstruction – most common - Obstruction of a solitary kidney - Bilateral ureteral obstruction ``` Causes: - Urethral obstruction - Bladder neck obstruction (prostatic hypertrophy, bladder carcinoma, bladder infecion) - Bilateral ureter obstruction: 1. Intraureteral: - Sulfonamide, uric acid crystals, blood clots/stones 2. Extraureteral: - tumor (cervix, prostate, endometriosis) - Retroperitoneal fibrosis - Ureteral ligation/edema due to pelvic operation Features: - low urine osmolality - high urine Na+ - FENa > 2% - Serum BUN/creatinine > 15

Answer 23

Can't make urine (oliguria) or excrete nitrogenous waste Acute loss of kidney function - Typically connotes acute drop in GFR Multiple definitions of this, typically based on changes in: - Serum Creatinine - Oliguria: <50cc UOP/day - Azotemia: elevated blood urea nitrogen (BUN ) without symptoms of uremia - Uremia: buildup of toxins that are cleared by the kidney. Most of these toxins are unknown. (Nausea, anorexia, pericarditis, asterixis, encephalopathy, platelet dysfunction) * * An elevated Urea level alone is NOT sufficient to diagnose uremia - Na/H2O retention (CHF, pulmonary edema, HTN) - Hyperkalemia - Metabolic acidosis - Anemia (failure of interstitial cells to synthesize EPO) - Renal osteodystrophy - Dyslipidemia (increased TG) - Growth retardation, developmental delay in children

Answer 24

- High PTH due to: hypocalcemia, hyperphosphetemia, low calcitriol level, - Low calcium due to low calcitriol level - High phosphate due to decreased GFR - Result of increased PTH: too rapid bone turnover, abnormal bone (woven vs. trabecular)

Answer 25

Osmotic diuretic Not reabsorbed, causing water to be retained initially, then diuresis Site of action: - Proximal tubule: decreased Na reabsorption by osmotic gradient--> increased urine volume - Descending loop of Henle: increased medullary blood flow, inhibit reabsorption of water - Collecting duct: opposes action of ADH Clinical: - Prevents acute renal failure after severe trauma, complicated surgical procedures (hemolysis, rhabdomyolysis) - Drug overdose: Toxin excretion - Reduces intracranial, intraocular pressure--> fluid (not Na) leaves cells - Does not increase Na excretion (only water) - Must be given IV (only effects colon if given orally) AEs: - PULMONARY EDEMA (contraindicated in anuria, CHF) - Rapidly distributes to ECF--> extracts water from cells - Causes acute increase in ECF/hyponatremia (can't use in CHF, pulmonary edema) - N/V, headache - Severe dehydration, hypernatremia - Hyperkalemia

Answer 26

Carbonic anhydrase inhibitor Site of action: proximal tubule MOA: - Inhibits carbonic anhydrase - Decreases sodium bicarbonate reabsorption - Cause bicarbonate diuresis (up to 85%) that may lead to metabolic acidosis - Over time (several days), effectiveness decreases--> soon increase Na reabsorption (thus reversing diuresis) Use: metabolic alkalosis (alkalinizes urine) - Induces hyperchloremic metabolic acidosis after excessive use of other diuretics - Prophylax acute mountain sickness (decreases CSF formation, pH--> increase minute ventilation--> decrease symptoms) - Glaucoma (decreases rate of aqueous humor formation--> decreased IOP) - Pseudotumor cerebri AEs: - Metabolic acidosis (decreased bicarb reabsorption) - Phosphaturia, hypercalciuria (can cause calcium stone formation) - Potassium wasting - Toxicity: drowsiness/fatigue (CNS carbonic anhydrase inhibition), parasthesis, avoid in liver disease (increases ammonia--> hepatic encephalopathy)

Answer 27

Furosemide, Bumetanide, Ethacrynic acid Site of action: cortical and medullary TAL of loop of Henle MOA: inhibits Na+-K+-2Cl- transporter Clinical: - Rapid onset of action (first line in pulmonary edema) - Stimulates prostaglandin synthesis in lung, kidneys (NSAIDs--> decreased prostaglandins--> decreased diuresis) - CHF (decrease ECF volume) - Excretion of: K+, Mg+2 and Ca+2 (Ca reabsorbed later in DCT, but can be used in hypercalcemia) - Nephrotic syndrome Side effects: - OTOTOXICITY (esp, with aminoglycosides, salicylates, cisplatin) - hypokalemia, hypomagnesemia - hyperuricemia (gouty attack) - decreased paracellular Ca+2 reabsorption--> hypocalcemia (+ calciuria) - hypochloremic metabolic alkalosis: 1. increased excretion of H+ in low K+ state in Cortical collecting tubule 2. Volume contraction--> ATII increase--> Na/H exchange in PCT--> increased bicarb reabsorption (contraction alkalosis) - Cross-reactivity with sulfonamide allergy - Dehydration - Increased LDL, triglycerides, decreased HDL

Answer 28

Thiazide diuretics Site of action: early distal convoluted tubule MOA: inhibits luminal co-transport of Na, Cl - Contraction of ECF volume--> decrease in CO--> decrease peripheral vascular resistance Clinical use: - Use in HTN, mild CHF - Idiopathic hypercalciuria - Nephrogenic DI - Renal stones (decreases Ca+ excretion) AEs: - Avoid in low GFR - "Ceiling diuretics": increasing dose does not promote further diuresis - hypokalemic metabolic alkalosis - hyponatremia - hypomagnesemia - Hypercalcemia - Hyperuricemia (gouty attack) - Sulfa allergy interaction: photosensitivity, generalized dermatitis (rare) - Hyperglycemia (impair pancreatic insulin release, tissue utilization of glucose) - Hyperlipidemia - Volume depletion

Answer 29

Potassium-sparing diuretic MOA: competitive antagonist of aldosterone receptors on collecting tubule (Na-H exchanger) SIte of action: - Cortical collecting tubule Clinical: - Most effective in primary/secondary hyperaldosteronism (Conn syndrome) - prevents binding of aldosterone to its receptor - Secondary hyperaldosteronism seen in: CHF, hepatic cirrhosis, nephrotic syndrome - Ascites - HTN - Loop/thiazide-induced hypokalemia AEs: - Hyperkalemia (if not on another diuretic)--> can lead to acidosis (body cells exchange K+ for H+) - Hyperchloremic metabolic acidosis= blocks collecting duct Na-H exchange (aldosterone receptor)--> can't excrete H+ - Endocrine abnormalities: gynecomastia, hirsutism, impotence, benign prostatic hyperplasia, menstrual irregularities

Answer 30

Postassium-sparing diuretic MOA: interferes with Na+ influx thru epithelial Na ion channels in luminal membrane (Na-H exchanger in collecting duct) - K+ secretion coupled with Na+ entry (therefore spare K+ secretion by blocking Na entry) Clinical use: - HTN - Loop/thiazide-induced hypokalemia AEs: - Hyperkalemia (if not on another diuretic)--> can lead to acidosis - Hyperchloremic metabolic acidosis= blocks collecting duct Na-H exchange (aldosterone receptor)--> can't excrete H+

Answer 31

Captopril, enalapril, lisinopril MOA: inhibits ACE--> decreased angiotensin II--> decreased GFR (prevent constriction of efferent arterioles) - Increased bradykinin= vasodilator * Renin increased due to lack of feeback inhibition * ARBs work similarly but do not increase bradykinin Use: - HTN - CHF - Proteinuria, diabetic renal disease - Prevents heart remodeling due to chronic HTN Tox: - Cough - Angioedema - Teratogen (fetal renal malformations) - Creatinine kinase (deceased GFR) - Hyperkalemia - Hypotension * * avoid in bilateral renal artery stenosis--> further deceased GFR--> renal failure * Stop thiazides before initiating ACE-I due to 1st dose hypotension (avoid non-selective beta-blocker with ACE-I--> increased K+)

Answer 32

-sartans MOA: - Bind AT-1 receptors (site of angiotensin II binding)--> decreased aldosterone - Increased renin, angiotensin I and II (no negative feeback) Use: - HTN - CHF - Proteinuria, diabetic renal disease - Prevents heart remodeling due to chronic HTN Tox: - Teratogen (fetal renal malformations) - Creatinine kinase (deceased GFR) - Hyperkalemia - Hypotension * * avoid in bilateral renal artery stenosis--> further deceased GFR--> renal failure * Stop thiazides before initiating ARB due to 1st dose hypotension (avoid non-selective beta-blocker with ARB--> increased K+)

Answer 33

- Microalbuminuria = 30-300 mg albumin daily - Overt nephropathy > 300mg/day - nephrotic syndrome approximately 3,000 mg/day (3g/day) * * Routine urinalysis can’t detect microalbuminuria * * Microalbunuria portends nephropathy

Answer 34

Prolonged analgesic use (NSAIDs) - Patchy interstitial inflammation--> fibrosis, necrosis, scarring of papillae, distorted calices architecture, tubular atrophy

Answer 35

1. Loss of H+ ions from body: vomiting, NG suction--> decreased serum Cl- --> decreased urinary Cl- 2. Thiazide/loop diuretics--> Na+ loss--> Cl- follows Na+--> contraction alkalosis (Cl- responsive) - Corrected by saline administration 3. Hyperaldosteronism (Conn Syndrome): Increases Na+ reabsorption--> K, Cl, H+ losses--> increased HCO3- (metabolic alkalosis) - Increased urine Cl- - Adinistration of saline does NOT correct condition

Answer 36

RBC: glomerulonephritis, ischemia, malignant HTN WBC: Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection Fatty casts (oval fat bodies): nephrotic syndrome - Microalbuminuria= < 300 mg/day - Overt nephropathy= > 300 mg/day - Nephrotic syndrome= 3+ g/day * * Nephrotic syndrome= hyperlipidemia, fatty casts, edema; associated with thromboembolism d/t ATIII loss in urine, infections d/t Ig loss Granular casts (muddy brown)= acute tubular necrosis Eosinophils in urine= acute interstitial nephritis (due to meds) Waxy casts= advanced renal disease/chronic renal failure Hyaline casts= normal, may be seen in low flow rates d/t Tamm-Horsfall glycoprotein accumulation Cholesterol crystals in arterioles (not urine)= atherosclerotic embolization (following angioplasty)--> renal arterial damage

Renal Flashcards

(60 cards)