Kidney Liver

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Kidney Liver
2014-05-05 12:29:21
kidney liver
Clinical Final
kdney liver flashcards
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  1. 1. How much blood does kidney filter daily? How much is resorbed?

    2. Where does kidney control sodium homeostasis? (3) (1-3, 2-3, 3-2)

    3. What are the drivers of sodium reabsorption?

    4. Which part/transporter is thiazide sensitive?
    1. 1600-1800 L. 90%

    2. Locations:

    1. Proximal tubule (3) contains sodium-glucose co-transporters and sodium-hydrogen (from carbonic anhydrase from CO2, H2O) exchange, and Na/K ATPase

    2. Loop of Henle - PASSIVE sodium reabsorption (mostly thick ascending limb), as well as Na/K/Cl cotransporter, and Na/K ATPase

    3. Distal reasborption from Na/K/Cl channel (thizaide sensitive) and ENaC (epithelium sodium channel)

    3. Basolateral Na+/K+ Atpase --> electrochemical and concentration gradients --> reabsorption
  2. 1. What does glomerulus do?

    2/ What does proximal tubule do? How? What does it secrete into filtrate in terms of acids and bases? (2) What does it require? (2) 

    3. What four functions does proximal tubule specifically do? (4)

    4. What is distal tubule responsible for? (4)

    5. What important channels does distal tubule have? 2

    6. Where is remainder of calcium absorbed?
    1. FILTRATION Receives blood from afferent arteriole and drains into efferent. Undergoes high pressure within glomerulus forcing fluids/soluble materials out of capillaries. Larger proteins remain in capillaries creating hypertonic solution.

    2. Reabsorption - regulates pH of filtrate by exchanging H+ ions of bicarbonate ions in filtrate. Secretes organic acids and bases into filtrate. It requires sodium-glucose cotransporter and sodium-hydrogen antiporter

    3. (1) Acid base homeostasis (reabsorbs bicarbonate via Na-ATPase) (2) electrolyte balance (reabsorbs and filters potassium, sodium) (3) Calcium/phosphate - reabsorbs and filters (4) insulin catabolism - filtration and reabsorption

    4. Responsible for regulation of K, Na, Ca, and pH (bicarbonate but less than pct). PRIMARY SITE FOR HORMONAL REGULATION OF CALCIUM, b

    5. Thiazide sensitive Na-K-2Cl channel and amiloride sensitive ENaC. 

    6. Distal tubule
  3. 1. What connects proximal tubule to distal tubule?

    2. What does this thing create? Where is the high concentration gradient located near?
    3. What does it resorb? (3)

    4. What does collecting duct do? What does it regulate? (5)

    5. What is everything driven by?
    1. Loop of Henle

    2. Concentration gradient vital to medulla of the kidney. The area of high concentration is located near the collecting duct

    3. It resorbs sodium passively, but also requires Na-K-Cl transporter (as well as Na-K ATpase for gradient), electolytes (potassium less), most magnesium through voltage

    4. Connects nephrons to ureter, participates in electrolyte and fluid balance through reabsorption and excretion (regulated by aldosterone and ADH). Regulates Cl, K, H+, Na, H2O, and bicarbonate.

    5. Na gradient created by basolateral (capillary side, not tubule side) Na/K ATPase
  4. 1. Describe renin-angiotensin system. Where is renin released from? 
    2. When is renin released? (3) 
    3. What does angiotensin II do? (3)

    4. What are the four main endocrine functions of the kidney?
    1. Renin is released from juxtaglomerular cells of kidney --> 2. Renin cleaves angiotensin (zymogen) into angiotensin I (active form) ---> 3. Angiotensin-converting enzyme (ACE) from lung converts angiotensin I to angiotensin II

    2. During low BP, sympathetic stimulation, decreased sodium delivery to distal tubule (WHEN BP NEEDS TO BE INCREASED) 

    3. Vasoconstrictor, increases aldosterone release from adrenal gland, increases ADH release from pituitary 

    Basically: Low BP --> activates renin release --> activates angiotensin II synthesis --> increase in blood volume --> increase in blood pressure.

    4.  (1) renin secretion (2) synthesis of erythropoietin (3) Hydroxylation of 25 OH vit D (4) Catabolism of insulin
  5. 1. Where is erythropoietin produced?

    2. What stimulates synthesis of erythropoietin? (3)

    3. What is erythropoietin?

    4. What does it do? How?

    5. What increases hydroxylation of 25OH vitamin D in kidney? (4)
    1. Peritubular cells

    2. Hypoxia, anemia, hypoxemia

    3.  a hormone secreted by the kidneys that increases the rate of production of red blood cells in response to falling levels of oxygen in the tissues.

    4. Increases rate of production of RBCs in bone marrow by binding to receptor in bone marrow

    5. Hypocalcemia/phosphatemia, increased PTH, increased GH
  6. 1. How does kidney affect catabolism of insulin? When insulin binds to distal tubule, what is resorbed? (3)

    2. How does kidney failure affect insulin's actions?

    3. What are the two main types of glomerular disease?
    1. Filters insulin with tubular reabsorption in proximal tubule, binding of insulin to distal tubule stimulates reabsorption of sodium, phosphate, and glucose. 

    2. Leads to prolongation of insulin's actions

    3. Nephritis and nephrotic syndrome
  7. 1. What is nephritis? What are some examples? 

    2. What are the symptoms? 6 (hallmark?)

    3. What may nephritis progress to? What are other complications?

    4. How can nutrition treat nephritis? (4) -2 of these aren't confirmed
    1. Inflammation of the kidney. Post-infectious, form of lupus, berger's disease (IgA), Alport's syndrome (hereditary nephritis)

    2. Acute onset, inflammation in glomerular capillary, urinary casts, hematuria (blood in urine), hypertension, edema

    3. Acute or chronic kidney failure. Most are self-lmited and remits with therapy (steroids)

    4. Volume retention treated by diuretics and salt restriction (2 gm/day), no role for protein restriction, fish oils/IgA nephropathy, flaxseed oil/SLE?
  8. 1. What is nephrosis? What are some examples?

    2. Symptoms? (5) How many do you need?

    3. What are complications? (3)

    4. What nutrition recommendations? (3)
    1. Kidney disease. SLE, focal glomerulosclerosis (FLGS), diabetic neuropathy, amyloidosis - loss of podocyte foot processes (fusion) with subsequent leaking of protein due to loss of filtration barrier

    2. <3.5 gm proteinuria per day, severe - hypoalbuminemia (<1.5 g/dL), hypertension, hyperlipidemia, edema (secondary to low oncotic pressure) - 3

    3. Thrombotic disorder due to loss of antithrombin 2 and other anticlotting factors, hypertension, kidney insufficiency/failure

    4. (1) protein restriction is controversial (0.8-1.0 g/kg vs. supplemented 0.6 g/kg - hyponatremia may develop) (2) fish oils for hyperlipidemia for increased cholesterol synthesis due to loss of albumin - can use statins and fibrates  (3) plant sterols/stanols (1.3 g stanols/3.4 g sterols in 2 meals)
  9. 1. Define acute kidney injury

    2. What is acute tubular necrosis? 

    3. What is the most common form of kidney injury?

    4. What are the primary nutritional issues with these diseases? (6)
    1. AKJ - deterioration of kidney function over hours to days --> accumulation of nitrogenous wastes

    2. Acute tubular necrosis - requires more than one insult (volume depletion + toxin OR sepsis - systemic inflammation caused by severe infection + hypotension)

    3. Acute tubular necrosis

    4. Hypercatabolism (requires increased energy intake), TPN may be required (lipids administered during dialysis decrease protein catabolic rate - not with TPN), kidney replacement therapy is most commonly by dialysis although continous arteriovenous hemofiltration (CAVH, CAVHD, and CVVH) can help with fluid balance and allows for large protein loads, 30-40 kcal/kg BW - excess can lead to increased CO2/acidosis sodium restriction (cannot have unlimited water), oliguric, potassium restriction (hypercatabolism releases K --> severe hyperkalemia)
  10. 1. What is type IV renal tubular acidosis?  and what disease is it associated with?

    2. What are symptoms of the disease? (2)

    3. What should treatment be? (1)

    4. What should be avoided? (2)
    1. Type IV renal tubular acidosis = hyporeninemic hypoadlosteronism (hypoaldosteronism means less Na reabsorption with H+ --> acidosis) Associated with diabetic nephropathy and related renal tubular acidosis 

    2. Hyperkalemia (decreased K secretion by distal tubule), mild acidosis.

    3. Oral bicarbonate

    4. ACE inhibitors and Angiotensin Receptor Blockers
  11. 1. Most common type of kidney stone? Who is more likely to get them?  (3)

    2. How should kidney stones be prevented? (7)

    3. How should kidney stones be treated? (2)

    4. How to prevent hyperoxaluria?  lots of things
    1. Calcium oxalate (1 in 20 people). Men (3:1), whites, older people (40-70 years old)

    2. Prevention: (1)  Avoid dehydration (urine volume = 2-2.5L/day), (2) avoid soda with phosphoric acid, (3) avoid grape fruit juice, (4) limit tea to 2 cups per day because of oxalate, (5)  reduce excessive vitamin C intake,

    (6)avoid hypercalciuria (increased calcium intake, increased absorption, low P, prolonged bed rest, but low Ca diets make stone formation worse. 1200 mg/day is best)

    (7) can also be caused by IBD, gastric surgery, hyperparathyroidism, cysteinuria, hyperoxaluria

    3. Treatment = uric acid stones can be treated by dissolution therapy while all others need to be removed/broken down by lithotripsy (shock wave) before excretion

    4. Limit foods with oxalate (beets, chocolate, strawberries, spinach, nuts, etc), avoid overusing antacids, excess animal protein can inhibit stones by promoting excretion of calcium, urate, oxalate, citrate), should drink lemon juice with water, reduce vitamin C intake, oxalobacter formigenes intestinal colonization reduces recurrence of Ca-oxalate stones (sequesters oxalate)
  12. 1. What are the different forms of hemodialysis ? (3)

    2. What are alternatives? (1 - but 3 types)

    3. Nutritional concerns (5)
    1. Arteriovenous fistula (brachial). Complications - infection, thrombosis, steal syndrome

    • 2. PTFE graft (radial) -  complications - infection, thrombosis, high-output heatlh failure (PTFE
    • 3. Double lumen catheter (tunneled under skin). Complications - infection, thrombosis, recirculation in superior vena cava

    2. (1) Continuous Ambulatory Peritoneal Dialysis (CAPD) - requires catheter to be placed in peritoneal cavity - occurs 4-5x a day, diabetic patients may require insulin with the glucose solution

    - Peritoneal dialysis - can lead to weight/fat gain

    - Continuous cyclical peritoneal dialysis (for children) growth is better than with hemodialysis bc of continuous nature of treatment (no sodium restriction)

    3.  Sodium (2 gm/day restriction), fluid (1 L/d plus urine volume), potassium restriction (2 gm potassium for patients with no urine output), energy requirements - higher for patients with hemodialysis patients (25-40 kcal/kg), increased protein intake (esp for CAPD and hemodialysis)
  13. 1. What are some additional nutritional concerns with patients with chronic renal failure? (3)

    2. What are nutrition considerations for drugs used in renal transplant? (3)

    3. Dietary recommendations for transplant patients? (6)
    1. Altered taste/decreased appetite (predictive of mortality)

    2. Hyperlipidemia/hypertriglyceridemia

    3. Carnitine deficiency (IV carnitine on dialysis)

    2. Commonly there is sodium retention, hypertriglyceridemia and hypercholesterolemia (also glucose intolerance/diabetes sometimes)


    • (1) moderate protein restriction (1 gm/kg) if kidney insufficiency, no restriction if normal
    • (2) if hypertensive - 2gm sodium diet
    • (3) if hyperkalemic - 2 gm potassium diet
    • (4) calcium supplemenation (1200-1500 mg daily)
    • (5) magnesium supplemenation -400-800 mg/day as oxide or chelate
    • (6) limit cholesterol and saturated fat intake
  14. 1. What affects balance of acid/base? (5)

    2. What affects calcium resorption? (2) Where? 

    3. What affects phosphate resorption? (3)

    4. What affects magnesium resorption? (5)

    5. What increases excretion of potassium? (5)
    1. Increased dietary acid, volume contraction, ventilator failure/more PCO2, hypokalemia, increased aldosterone (leading to excretion of kalemia)

    2. PTH and vitamin D - cortical collecting tubule

    3. Diet, FGF23 (predicts mortality), PTH --> modulate NaPO4 cotransporter

    4. Diuresis, drug toxicity, hormones, kidney failure, transplantation

    5. (1) increased distal sodium delivery (2) increased urine flow (3) loop/thiazide diuretics - 2 separate things (4) non-reabsorbable anions (5) aldosterone via hyperkalemia or low BP
  15. 1. What part of kidney secretes potassium?

    2. What is resorbed in proximal tubule? (7)

    3. What is resorbed in Loop of Henle? (5)

    4. What is resorbed in distal tubule (6)

    5. What is resorbed in collecting duct? (3)

    6. Where is Na-K-2Cl cotransporter found? (2)
    1. Cortical collecting duct

    2. Sodium (H+ secreted), glucose, amino acids, potassium, bicarbonate (Na-ATPase), calcium, phosphate

    3. Potassium, sodium, magnesium, chloride, water

    4. Sodium, potassium, chloride (Na-K-2Cl) calcium (affected by thiazide, PTH, vit D), bicarbonate, H2O

    5. Calcium, potassium, H2O

    6. Loop of henle and distal tubule
  16. LIVER
  17. 1. What are the primary functions of the liver? (7)
    1. Biliary (bile secretion/excretion) (2) Infectious (globulins/complement system) (3) Oncotic pressure (albumin/transferrin) (4) Lipid metabolism (digestion/absorption) (5) Glucose metabolism - glycogenesis, glycogenolysis, GNG (6) Coagulation - fibrinogen, clotting factors, vitamin K metabolism (7) Detox (conjugation, degradation, urea cycle)
  18. 1. What do hepatocytes do? - 2 (1-7)

    2. What do hepatic stellate cells do? -2

    3. Sinuosidal epithelial cels? (SEC) -2

    4. Hepatic Kupffer cells? (3)

    5. Bile duct epithelial cells? (3)

    6. What do these cell types do all together? (4)
    1. Hepatocytes - (80%) metabolism of AA, NH3, lipids, carbohydrates, hormones, vitamins, minerals, DETOX of xenobiotics and drugs

    2. Hepatic stellate cells - major storehouse for vitamin A in body; collagen formation

    3. SEC - controlling exchange of materials (nutrients) between blood stream and liver; immune functions (antigenpresenting cells)

    4. Hepatic Kupffer cells - largest reservoir of fixed macrophages in the body, protective role against gut-derived toxins that have escaped portal circulation, major producer of cytokines

    5. Bile duct epithelial cells - major role in transport; express a variety of transporters; have important immne functions. 

    6. They work together to create coordinated response against gut-derived toxins, autoimmune reactions. They also modulate hormonal and nutritional status.
  19. 1. What is the major enzyme for ETOH metabolism?

    What are common clinical presentations of liver failure in a patient's:

    2. History? (4)

    3. Physical exam (5)

    4. Labs (6)
    1. Alcohol dehydrogenase

    2. History - lethargy/confusion, nausea/vomiting, bleeding, jaundice

    3. Physical exam - jaundice - skin/whites of eyes become yellow due to excess bilirubin in the blood, hepatomegaly, bruises, asterixis (hand tremors), clonus (involuntary muscle tremors)

    4. Labs - hyperbilirubinemia, hypoalbuminemia, coagulopathy, raised plasma ammonia, hypoglycemia (glycogenolysis and GNG), elevated AST/ALT 
  20. 1. How does liver insufficiency lead to malnutrition? (5)
    1. Decreased intake of nutrients due to anorexia, nausea, vomiting, dysgeusia (distorted taste)

    2. Early satiety due to ascites (accumulation of fluid in peritoneal cavity)

    3. Hypercatabolic/hypermetabolic state

    4. Increased losses

    5. Malabsorption
  21. How does liver insufficiency lead to metabolic derangements? (3; 1-4, 2-2, 3-1)

    How do you assess nutrition in liver insufficiency? (3) What is common? (6) Difficulties? (3)
    1. Altered protein metabolism - low protein methionine, BCAA; elevated circulating aromatic AAs leading to hepatic encephalopathy; increased protein catabolism; decreased overall synthesis

    2. Altered carb metabolism - (1) more rapid transition of substrate utilization from carbs to fat (2) marked insulin resistance

    3. Hypercatabolic state - increased energy expenditure --> correlates with decreased body cell mass

    • -----
    • 1. Subjective global assessment - nutritional history, physical exam, basic anthropometrics

    2. Common - micronutrient deficiencies - Zn, vitamins A, D, E, K (Fat-sol), and B

    3. Difficulties - common markers of nutritional status - plasma albumin, prothrombin time (most sensitive marker for liver function) and weight are altered independent of nutritional state.
  22. 1. What is the predominant feature of advanced liver disease in terms of  malnutrition?
    2. What else is wrong? (5)
    3. What is the most valuable prognostic indicator in advanced liver disease? (ALD)

    4. What else can you measure to determine nutritional status in advanced liver disease? (5) Are they good or bad?
    • 1. Protein malnutrition
    • 2. Low plasma albumin, low transferrin, decreased creatinine/height index, reduced triceps skinfold thickness, decreased total lymphocyte count

    3 Low plasma albumin

    4. Index of hepatic reserve (MELD); biochemical impedance (not reliable in ascites/edema); nitrogen balance measurements (limitations - can't differentiate impaired synthesis from accelerated breakdown); isotopic dilution (most accurate method of measuring body cell mass, but its experimental); hepatic mitochondrial redox potential (ratio of acetoacetate: B-hydroxybutyrate - experimental, allows grading of disease severity)
  23. 1. What are metabolic effects of chronic liver disease? (8)

    2. What is a possible treatment? Why?
    1. Increased plasma glucagon (increased plasma aromatic AAs, hyperammonemia)

    2. Impaired plasma cortisol and epinephrine - impaired hepatic degradation

    3. Accelerated GNG (hyperglucagonemia)

    • 4. Hyperglycemia
    • 5. Hyperinsulinemia (insulin resistance)
    • 6. Decreased liver/muscle carb stores
    • 7. Hyperammonemia (colonic bacterial degradation of protein)
    • 8. Increased plasma AAA (Phe, Tyr, Tryp - decreased hepatic clearance, increased release into circulation, hypoalbuminemia, hyperbilirubimenmia, decreased protein incorporation)
    • 9. Increase plasma BCAA (leu, iso, val) - supplementation as treatment for encephalopathy  competitively inhibits AA transport at blood brain barrier - hyperinsulinemia, increased motbilization for uptake/utilization as energy source.
  24. 1. What nutrition interventions are used in chronic liver disease? (6)

    2. What is tyrosinemia? What else is it called? What is it caused by?

    3. Clinical presentation? (6)

    4. Treatment (4)
    • 1. Provide adequate calories, protein, nutrients without exacerbating hepatic encephalopathy
    • (2) high carb
    • (3) BCAA formulas
    • (4) Medium chain triglyceride supplements if severe cholestasis (bile can't flow to liver)
    • (5) sodium/free water restriction
    • (6) supplemental vitamin with Ca, Zn, Mg, ADEK

    2. Hepatic tyrosinemia; inborn error of metabolism caused by deficiency of fumarylacetoacetate hydrolase (can't break down tyrosine)

    3. Organ damage from toxic precursors, devleopment of hepatic malignancies (hepatocarcinoma, renal disease), hepatophosphatemic rickets, neurological problems (paralysis, decreased activity), hypoglycemia, hypertrophic cardiomyopathy

    4. Dietary intervention (low tyrosine, phenylalanine, no catabolic state); NTBC slows effects, liver transplantation, support during crisis
  25. 1. When is a liver transplant needed? (1-3, 2-4,1)

    2. What are the benefits of a living donor? (4)

    3. What are disadvantages to donor? (2)

    4. What are metabolic complications after liver transplant?
    1. Loss of function (coagulopathy, encephalopathy (if present, restrict protein), cholestasis). Structural related complications (ascites, portal hypertensive bleeding, hepatorenal syndrome, hepatopulmonary syndrome); cancer

    • 2. Timing of procedure, no graft ischemia (restriction of blood flow), potential long-term immunological advantages, bonding experience

    3. Small risk to donor, reduced size of graft (biliary, vascular problems as a result)

    4. Obesity, hyperglycemia, bone disease, growth failure, minimizing/eliminating steroids
  26. 1. What is the definition of non-alcohol fatty liver disease?

    1.5 What are the 3 types of NAFLD?

    2. How is it diagnosed? (4)

    3. What are the causes and complications? 10
    1. NAFLD = spectrum of disorders that range from simple steatosis w/o inflammation to non-alcohol steatohepatitis (NASH) with fibrosis

    1.5 Macrovescular fat in >5% hepatocytes in absence of (1) significant ethanol, drug, toxin ingestion (2) viral hepatitis (3) inborn metabolic errors (4) cystic fibrosis/wilson's disease

    NAFL - fat without inflammation - steatosis (non-alcoholic) accumulation of fat in the liver, IC fat deposition.

    NASH - fat with inflammation --> fat deposits, inflammation, fibrosis with necrosis. 

    • 2. Diagnosis:
    • - Mostly asymptomatic, primary problem is insulin resistance --> increased lipolysis, TG synthesis, hepatic uptake of FFA, increased hepatic TG

    (1) Physical findings - liver function test elevation, fatigue, malaise, incidental finding/imaging

    (2) Lab findings - ALT/AST 2-5x upper limit of normal, AST/ALT <1, ETOH>2, elevated ferritin, autoimmune markers

    (3) Radiographic findings - cannot diff NAFL from NASH - sonogram, CT scan, MRIs, MR spectroscopy, ultrasound (most common)

    (4) Biopsy - hepatocyte injury, ballooning, dead cells, inflammatory cell infiltration, fibrosis. 

    • 3. CAUSES: metabolic syndrome (central obesity, hypertension, dyslipidemia, insulin resistance/diabetes, accelerated atherosclerotic heart disease)
    • TG accumulation, insulin resistance, hepatocellular injury, antioxidant depletion, increased hepatic iron, decreased production of leptin --> obesity, adiponectin (enhances plasma lipid clearance), resistin (overexpression leads to insulin resistance), intestinal microbes

    4. Complications:
  27. 1. How is NAFLD managed? (5)

    2. Drug therapies for NAFLD? (4)
    • 1.
    • 1. Weight loss (1-2 lbs per week via lifestyle mod or bariatric surgery but rapid weight loss can exacerbate fibrosis)
    • 2. Immunize for Hep A and B
    • 3. Optimize blood glucose in DM
    • 4. Treat hyperlipidemia (statins are good)
    • 5. Avoid all alcohol consumption

    2. Vitamin E (decreases oxidative stress), insulin-sensitizing agents, orlistat (inhibits lipase), omega-3- fatty acids
  28. What are common vitamin deficiencies associated with chronic alcoholisms? What are the causes of these deficiencies?
    1. Zinc - decreased intake, increased urinary excretion

    2. Magnesium- decreased intake, increased urinary excretion

    3. Selenium - correlates with severity of liver disease. 

    • 4. Vitamin B2 - decreased intake, increased urinary excretion, increased utilization, deficient absorption, abnormal metabolism
    • 5. Vitamin A - hepatic stellate cells are activated, lose vitamin stores, and become collagenous --> fibrosis.

    6. Vitamin D - decreased intake, impaired absorption, malabsorption, reduced hepatic production of binding protein, impaired cutaneous production, impaired hepatic hydroxylation

    7. Vitamin E - hepatoprotective - membrane stabilization, reduces cytokine/inflammation, inhibits hepatic stellate cell activation

    8. Vitamin B1 - decreased intake, decreased hepatic storage, impairment of absorption

    9. Methionine/SAM and Folate - decreased intake

    10. BCAA
  29. What are causes of malnutrition in alcoholics? (9)
    • 1. Anorexia
    • 2. Altered taste/smell
    • 3. Gi symptoms - malabsorption
    • 4. Poor food availability/quality
    • 5. Metabolic disturbances (hypermetabolism, hypercatabolism)
    • 6. Cytokine effects
    • 7. Complications of liver disease
    • 8. Unpalatable diets (low sodium, protein)
    • 9. Fasting for procedures