Biochem 4Th Long Exam

Front 1

What is water?

Back 1

a. Essential part of body, and medium in intra/extra cell processes,

Front 2

2) What is water’s biochemical role?

Back 2

a. Universal solvent, high suface tension ,high latent heat vaporization

Front 3

3) Why is water an ideal solvent?

Back 3

a. polar molecule, with a neutral pH. therefore, it will dissolve all ions and provide a medium for cellular reactions to occur, liquid at room temperature

Front 4

4) Why is water an excellent nucleophile?

Back 4

a. The oxygen atom of water has two lone pairs and a - charge (oxygen is more electronegative than hydrogen),

Front 5

5) What are the different functions of water?

Back 5

a. Cushion, transport, solvent, matrix of living things,

Front 6

6) What are the different fluid compartments?

Back 6

a. ICF 2/3 , ECF 1/3 : plasma ¼ ecf, interstitial fluid ¾ ecf

Front 7

7) Is the amount of total body water constant?

Back 7

a. Yes, but tissue content varies

Front 8

8) What is water balance?

Back 8

a. The amount of intake of water is equal to the amount outtake

Front 9

9) What are the specific cations in the ECF?

Back 9

a. Na, Hco3, Cl

Front 10

10) What are the specific cations in ICF?

Back 10

a. K, Mg, Po4

Front 11

11) What is osmotic force?

Back 11

a. Attraction of particles in a solution, osmole = 10 milliosmoles/kg solvent

Front 12

12) 3 important hormones secreted by the kidneys:

Back 12

a. Erythropoietin, rennin, 1, 25- dihydroxy vitamin d3

Front 13

15) What is osmolarity?

Back 13

a. measure of osmotic pressure, total concentration of dissolved particles in a solution

Front 14

16) What is the role of sodium in the human body?

Back 14

a. Major determinant for serum osmolarity, ecf volume, rennin secretion

Front 15

17) What regulates osmolarity?

Back 15

a. CHANGING TOTAL BODY WATER AND NOT BY CHANGING BODY SOLUTE

Front 16

How are water balanced diseases diagnosed?

Back 16

SERUM SODIUM CONCENTRATION BEING A MEASURE OF BODY OSMOLALITY

Front 17

18) What is serum osmolarity?

Back 17

a. Concentration of particles in a kilogram of water

Front 18

19) What does tonicity (Effective osmolality) depend on ?

Back 18

-the size of the solute particle and the permeability of the membrane

Front 19

20) What are the functions of sodium?

Back 19

a. regulate fluids in the body and it also plays an important role in nerve tranmisson and muscle contraction

Front 20

21) What is the role of the kidneys in maintaining a normal acid base balance?

Back 20

regulation h20 balance, regulation na balance and ecf volume (rennin secretion), waste excretion, erythropoietin secretion, regulation ecf electrolyte concentration, secretion of 1, 25-hihydrocy vit d33, regulation ecf hco3 (conc for ph control)

Front 21

What is the role of potassium in the body?

Back 21

* Regulates heart function
* Reduces blood pressure
* Essential for protein and nucleid acid synthesis
* Required for normal fluid balance
* Fundamental for normal nerve and muscle function
* Converts glucose into glycogen (muscle fuel)
* Important role in kidney function
* Helps lungs eliminate carbon dioxide
* Needed to maintain acid/alkali balance

Front 22

23) What is the osmoreceptor regulation?

Back 22

a. ADH feedback mechanism which regulates water output
b. ADH signals for water conservation
c. ADH acts on DCT and collecting duct
(ADH will signal kidneys reabsorb more fluid back  blood diluted  ADH secretion stops)

Front 23

24) What regulates water balance?

Back 23

a. Thirst Mechanism: which regulates water intake, angiotensin 2 involved
b. Osmoreceptor: ADH feedback mechanism which regulates water output

Front 24

25) A decrease in total Body water would lead to the following events

Back 24

a. release of ADH from the pituitary gland

Front 25

What are the fxns of potassium?

Back 25

a. Cell growth
b. DNA and protein synthesis
c. Operation of enzyme systems
d. Control of cell volume
e. Maintenance of normal acid-base balance
f. Maintenance of cell excitability and muscle contraction

Front 26

28) What is the distribution of potassium in the body?

Back 26

29) Body compartment concentration (mmol/L)
- Intracellular – 150
- Extracellular – 4
30) Organs and compartments (mmol)
- Muscle – 2650
- Liver – 250
- Interstitial fluid – 35
- RBC – 35
- Plasma – 15

Front 27

31) What is the renal handling of potassium?

Back 27

a. 100% filtered, 65% reabsorbed pct, 25% loop henle, dpt on body balance

Front 28

32) Role of distal tubule and collecting ducts and potassium?

Back 28

a. Have principle cells, carry K+, secretion altered by aldosterone to meet needs balance

Front 29

33) Role of medullary collecting duct in K+ balance?

Back 29

a. High K, secreted DCT/CCT, high aldoesterone promotes K ecretion, incrase H20 thru DCT allow K secretion

Front 30

34) What is hypokalemia?

Back 30

a. Losses > intake
Urine concentration > 15-20 mEq/L
b. FEK > 10-20%
c. Serum Na/K < 1
d. TTKG > 2

Front 31

What is hyperkalemia?

Back 31

35) What is hyperkalemia?

 Inadequate intake
- Chronic deprivation
 Increase entry of K+ in cells
- Pseudohypokalemia
- Metabolic alkalosis
- Insulin therapy
- Hypokalemia periodic paralysis
 Non-renal K+ loss
- Chronic diarrhea
- Protracted vomiting
- Excessive sweating
 Renal K+ loss
- Increased plasma renin – drugs, increased nephron flow, intrinsic renal defects
- Decreased plasma renin – increased aldosterone

Front 32

37) What is the hormonal regulation of potassium?

Back 32

a. Epinephrine: stimulation of beta 2 adrenergic receptors →decreased [K]
b. Insulin: shifts K into cells (after ingestion of K in a meal)
c. Aldosterone: stimulates urinary K secretion

Front 33

38) What is the treatment of potassium disorders in accordance to etiology?

Back 33

38) What is the treatment of potassium disorders in accordance to etiology?
Are abnormal leukocytes present?

If YES  Pseudohypokalemia, confirm by rapid separation of plasma or stored sample at 4º C.

If NO  Proceed to #2

2. Evidence of elevated aldosterone, present insulin, theophylline or adrenergic agent used?

YES  Redistribution
a. If NO  Proceed to #3
b. 3. Evidence of fluid loss from skin (excessive sweating) or GIT (gastric or stool fluid loss)?
c. If YES  Non-renal potassium loss
d. If NO  Renal Potassium loss if greater than 20mmol/2days in urine

Front 34

39) What is the major site of conservation of nutrients?

Back 34

a. Proximal tubule?

Front 35

40) What is the site of Na filtration?

Back 35

a. Loop of Henle

Front 36

41) What is the major ECF cation?

Back 36

Na

Front 37

What is the major ICF cation?

Back 37

K+

Front 38

43) What does a decrease in TBW lead to?

Back 38

a. Release of ADH from pituitary gland

Front 39

44) What is the most common presentation of hypokalemia?

Back 39

a. Malaise

Front 40

45) What is the most integral membrane transporter involved in hypokalemic weakness?

Back 40

a. K channel

Front 41

46) Which of the following ECG changes is specific for hyperkalemia?

Back 41

a. Decreased amplitude of T wave

Front 42

47) What are the changes in the compartment with diarrhea?

Back 42

a. Isotonic dehydration, no mvmt water, decrease vl ecf, no change osmolarity

Front 43

48) What are the changes in the compartments with hypertonic dehydration?

Back 43

a. Higher osmolairty in ecf than icf, give hypotonic fluids

Front 44

49) What may too mauch water in icf lead to?

Back 44

a. Brain edema

Front 45

Basis of ORS?

Back 45

a. Water moves with sodium and sugar, hypertonic dehydration, higher osmolarity ecf

Front 46

51) What are changes in hypotonic dehydration in the compartments?

Back 46

a. Decrease in vl and osmolarity in ecf, water moves from icf to ecf

Front 47

52) What are disorders of water balance with water depletion?

Back 47

a. Diabetes insipidus-no adh, diabetes mellitus-gluc brings water, vomiting and diarrhea

Front 48

53) Disorders of water balance with water excess?

Back 48

a. Congestive heart failure: decrease CO, decrease gfr, increase aldosterone and na reabsorption and serum osmolarity, increase adh release, increase reabsorption water, excess

Front 49

2) What are the metabolic functions of the liver?

Back 49

a. Central processing and distributing role in metaboilism- distributes appropriate mix nutrients and provides energy

Front 50

What are major fxns of liver?

Back 50

metabolic and excretory fxns

Front 51

3) What are the biosynthesis processes exclusive to the liver?

Back 51

a. Bile/bile acid metab, ethanol metab, fruc/galac metab, gluconeogenesis, ketogenesis, urea cycle

Front 52

4) What are the excretory functions of the liver?

Back 52

a. Inactivation / detox toxic substances, excretion of metabolic products in bile

Front 53

5) What is the central receiving and recycling center for the body?

Back 53

a. Has enzymes to carry out biosynthetic rxns, constant monitoring, recycling, modifying, distributing various compounds for potentially toic subs: brain, rbc, cells renal medulla

Front 54

6) What regulates blood glucose level?

Back 54

a. Glucose entry into hepatocytes via GLUT2 dpt on high glucose in portal vein 10-40mM

Front 55

7) What are characteristics of GLUT2?

Back 55

a. High on glu, not on insulin, high Km glu

Front 56

8) What are characteristics of
glucokinase?

Back 56

a. Specific substrate, high km glucose, not inhibited by glu 6 p,

Front 57

9) What is glucokinase regulated by?

Back 57

a. Regulatory protein RP, low glu, inactive, increase glu- active

Front 58

10) What does insulin release lead to?

Back 58

a. Glycogen synthesis, liver glycolysis, fa syn, tag and cholesterol syn

Front 59

11) What des glucagon relase lead to?

Back 59

a. Increases in glycogenolysis, gluconeogenesis, lipolysis/b-oxidation, liver glycolysis

Front 60

12) Whydoes the liver depend on hmp?

Back 60

a. Has greater requirement for NADPH for FA syn, chol biosyn, detox/eliminate drugs

Front 61

16) What is the urea cycle?

Back 61

a. Conversion of NH3+ to non toxic water soluble urea

Front 62

17) What is ketone body formation?

Back 62

a. Ketogenesis- occurs exclusively in mitochondria of hepatocytes from excess acetyl coa

Front 63

20) What are important derivatives of cholesterol?

Back 63

a. 7 alpha hydroxycholseterol -> cholyl coa chenodeoxychoyl coa –> taurocholic acid & glyocholic acid => deoxycholic acid/litocholic acid (bile acids) and secondary bile acids

Front 64

21) What is the excretion function of the liver?

Back 64

a. Xenobiotic of waste -> phase 1 rns (reduction,oxidation, hydroxylation, hydrolysis) -> primary metabolite (conjugation, sulfation, methylation, glucuronidation)-> secondary metab suitable for excretion

Front 65

22) What is the inactivation of detoxifciation of xenobiotics and metabolites?

Back 65

a. Cyp2e1 + ethanol -> napq1 toxic

Front 66

23) What is cytochrome p450?

Back 66

a. Major enzyme involved in drug metabolism and bioactivation 75% for modification and degradation
b. Also cholesterol, vitamin d, hormone metab

Front 67

24) What are toxic effects of ethanol?

Back 67

a. Increased nadh/nad and acetaldyehyde tonicity

Front 68

1) What is diarrhea?

Back 68

a. Increase in fluidity of stools, increase in frequency, increase in stool weight > 200g, children >20g,

Front 69

4) What is the normal intestinal fluid and electrolyte transport mechanism in GIT for water?

Back 69

a. Largely passive coupled w/ solute mvmt, either paracellular or transcellular

Front 70

6) What are carriers in transport?

Back 70

a. Ion and nutrient across cell mem, dpt on electrochem gradients

Front 71

7) What are channels in transport?

Back 71

a. Ion selective/conductive, eg: CFTR, electrogenic Na channels

Front 72

8) What are channels in transport?

Back 72

a. Energy driven, against a concentration gradient, hydrolysis of high energy compound like Na+/K+ ATPase

Front 73

9) What are the different mechanisms that cause diarrhea?

Back 73

a. Osmotic diarrhea, secretory diarrhea, exudative diarrhea, altered motility

Front 74

10) What is osmotic diarrhea?

Back 74

a. Poorly absorbable, osmotically active solutes (hyposmotic) in intestinal lumen, attracts h20

Front 75

11) What is secretory diarrhea?

Back 75

a. Intestinal ion secretion, enterotoxins increase cGMP

Front 76

12) What is exudative diarrhea?

Back 76

a. Outpouring into bowel lumen of mucus, pus blood and proteins from structural damage of mucosa

Front 77

13) What is altered motility?

Back 77

a. Deranged intestinal motility w/ disordered contact b/w luminal contents and mucosal surface- common in diabetics

Front 78

what causes osmolality disturbance?

Back 78

OSMOLALITY IS REGULATED BY CHANGING TOTAL BODY WATER AND NOT BY CHANGING BODY SOLUTE
a. MEASUREMENT OF OSMOLALITY ( WATER BALANCE ) IN ONE COMPARTMENT WILL REFLECT THE OSMOLALITY IN ALL COMPARTMENTS

Front 79

5) What is the normal intestinal fluid and electrolyte transport mechanism in GIT for electrolyte (Na, Cl, K, HCO3)

Back 79

carriers, channels, pumps

Front 80

23) What is physiologic basis and advantage of oral rehydration therapy? ORT

Back 80

a. Transcellular water transport, h20 channel proteins w/ aquaporins and na+ dpt glucose transport (SGLT1)
b. Sln glucose and salt administered
c. Mvmt na and glucose from intestine across membrane to blood = diff in osmotic pressure, water flows thru cell across basolateral mem by simple diffusion, upatek water needs na and gluc to be present in lumen intestine,

Front 81

6) What is mature milk?

Back 81

a. Bluish color, watery, ph 6.8-7.4, sg 1.026-1.036, higher levels fat, lactose, vit b, lower concentration vitamins, immunoglobulins, minerals, fat soluble vitamin

Front 82

5) What is transitional milk?

Back 82

a. 6-10th day, concentration of fats, lactose, vit b increase, PHOSPHORUS higher than colostrums and mature milk, decrease in number of cells

Front 83

4) Colostrum vs mature milk?

Back 83

a. Lower lactose and fat, higher protein and immunoglobulin, rich vit a d na k, mononuclear cells, mostly macrophages

Front 84

3) What is colostrum?

Back 84

a. First milk, 5 days, deep yellow, alkaline, ph 7.7, sg 1.040, 10-40ml/day

Front 85

1) What is the process of human milk production?

Back 85

a. Ejection reflex- suckling- hypothalamus-ant/post pitituary gland release prolactin and oxytocin, stimulation milk production in alveoli of mammary glands

Front 86

1) What is the difference b/w mature breast milk and cows’ milk?

Back 86

a. Same water, human – higher caloric density, fat, lactose, cow- higher protein, ash, human- protein nitrogen factor lower

Front 87

7) What are the different whey to casein ratios of breast milk and cows’ milk?

Back 87

a. Human milk 60:40, cow milk 18:82

Front 88

8) What are the advantages of breast milk?

Back 88

a. Can never be approximated, immunoglobulins and major nutrients, antibodies, large amts lactoferrin, lysozyme bacteriostatic against enterobacteriacea and staph

Front 89

9) What are the advantages and disadvantages of cow’s milk?

Back 89

a. Higher essential fatty acid, IgA, iGm, IgG and lysozyme, negative: higher essential amino acid so harsher on kidneys

Front 90

10) What are the advantages and disadvantages of evaporated milk?

Back 90

a. Disadvantages: high density, high saturated fattyacids, heavy for digestion and renal solute load

Front 91

11) What are the advantages and

Back 91

disadvantages of condensed milk?
a. Similar caloric yield, higher protein, high carb content out of balance, low vitamin content, nt recommended

Front 92

12) What are the advantages and disadvantages of soy protein or milk free formula?

Back 92

a. Same caloric density, higher protein content, 100% casein, lower fat, so lower carnitine, added

Front 93

1) What is nutritional status?

Back 93

a. Condition of the body as a result of ingestion and utilization of food

Front 94

2) What are the factors that affect nutritional status?

Back 94

a. Intake, outtake, expenditure (physical activity), variety of food/diet,

Front 95

3) What are macronutrients?

Back 95

a. Carbs, lipids, proteins,

Front 96

4) What are micronutrients?

Back 96

a. Vitamins fat soluble: a, d, e, k
b. Vitamins water soluble: b,c
c. Inorganic elements: macrominerals: na, k, cl, mg, fe, p, s, ca
d. Microminerals: cu, zn se,

Front 97

5) What is the minimum daily requirement?

Back 97

a. Smallest exogenous supply of nutrient that must be absorbed to prevent deficiency

Front 98

6) What is the recommended daily allowance?

Back 98

a. Level of dietary intake sufficiently high to meet needs of all healthy individuals of life stage/gender

Front 99

7) What is the dietary reference intake?

Back 99

a. Standards that define amt of energy, nutrients, dietary components, physical activites that support life

Front 100

8) What are the factors affecting RDA?

Back 100

a. Age, sex, body size, work load, physiologic condition

Front 101

9) What is malnutrition?

Back 101

a. Pathologic state resulting form lack or excess of one/more essential nutrients: primary – lack of food or secondary- conditions

Front 102

12) What is respiratory quotient?

Back 102

a. Indirectly determines heat evolved calorie* from oxidation of food or caloric requirements of organicsims, ratio of co2/o2 in oxidation of food

Front 103

13) What is a kilocalories?

Back 103

a. Amt of heat needed to raise temp of 1 kg h2o to 1 degree C

Front 104

14) What is basal metabolic rate?

Back 104

a. Energy needed by awake individual during physical, digestive, and emotional rest
b. Wt x 24 kcal/day

Front 105

15) What is physical activity?

Back 105

a. Can change calorie requirements

Front 106

18) What are the different methods for calculating the total energy requirement?

Back 106

a. Joint consultation – calc BMR then TCR
b. Factorial method: BMR + FA + SDA
c. Krause: DBW x activity factor

Front 107

28) What are unsaturated fats?

Back 107

a. Mono: olive oil, poly: omega 33-fish oil, seafood, omega 6- sunflower oil

Front 108

27) What are saturated fats?

Back 108

a. No double bonds b/w carbon atoms, fully sat, butter, lard, dairy

Front 109

21) What is the AMDR of fat?

Back 109

a. 25-35g or 30% ter

Front 110

20) What are Carbs and fiber? Including AMDR, glycemic index, glycemic load

Back 110

a. Carbs: 50-55% TER, adults: 130g /day, preg 175,latate 210,
b. Amdr: 45-65%
c. Fiber: increase up to 20-30g/day
d. High gi- raidly digested/ absorbed, marked fluctuations in blood sugar levels
e. Low gi: slowly digested and absorbed, gradual rises

Front 111

23) What is biologic value?

Back 111

a. Quantitative measure of extent to which protein satisfies aa requirement for growth/maintenance of total body function, degree usefulness protein

Front 112

22) What are proteins? Biologic value

Back 112

a. Build and repair tissues, syn of enzymes, antibodies, plasma pro, aa syn of hb, creatinine bile salts

Front 113

25) What is nitrogen balance?

Back 113

a. State where amt nitrogen ingested each day balanced by amt excreted, no net change in amt body nitrogen

Front 114

24) Recommended intake protein?

Back 114

a. 0.8g/kg/day, 60gm/day men, Filipino 1.1g/kg/day, infants 2-2.2 g/kg/ dbw

Front 115

What are trans fat?

Back 115

a. Partial hydrogenation of plant oils to reduce rancidity and raise melting pt, double bond in trans, straight shape, raises ldl and risks

Front 116

What is BMI?

Back 116

person's body weight/ divided by their ht squared, statistical measure of healthy weight for height, shows if underweight, normal, overweight

Front 117

29) What nutrients are low in a vegetarian diet?

Back 117

a. Iron, vitamin b12, calcium, eaa- lysine, methionine, threonine, typtophan, zinc

Front 118

30) What are natural toxicants in food?

Back 118

a. Saffole, solamine, nitrates, aflatoxin, potrease inhibitors, hemagluttins, cyanide

Front 119

31) What are Filipinos deficient in?
a. Iron, vitamine A, iodine

Back 119

a. Iron, vitamine A, iodine

Front 120

What are antioxidant nutrients? BCES?

Back 120

free radicals-prevent oxidation of PUFA esp in RBC/lungs

Front 121

What are examples of some antioxidants?

Back 121

beta carotene, vit c, vit e, selenium

Front 122

What is food exchange list 1?

Back 122

vegetable exchange list, 1 cup raw, 1/2 cup cooked

Front 123

What is food exchane list 2?

Back 123

fruit, 40cal, 10g cho

Front 124

What is food exchange list 3?

Back 124

milk exchanges, 1/4 glass

Front 125

What is food exchange list 5?

Back 125

meat exchanges, low fat exchanges, 50 cal, 8g CHON, 2g fat

Front 126

What is food exchange list 4?

Back 126

rice exchange, 100 cal, 23g CHO , 2g CHON

Front 127

What is food exchange list 6?

Back 127

fat exchange, 1 = 45cal, 5g fat

Front 128

What is food exchange list 7?

Back 128

sugar exchanges, 1 = 20 cal, 5gms CHO

Front 129

What is scurvy?

Back 129

ascorbic acid (vit c) deficiency, deefective colagen syn, subcutaneous hemorhages, muscle weakness, swollen gums, loose teeth

Front 130

What does ascorbic acid do?

Back 130

maintain integrity of plasma mem, cofactor for mixed fxn oxidase, antioxdiant, spaces vit a/e

Front 131

What is ascorbic a?

Back 131

deriveative 6 C aldehdye glucose, plant,

Front 132

What are properties of isorenoid vitamins?

Back 132

5-C, apolar hydrophobic molecules, dept on amt of lipids in body, similar in structure

Front 133

What are deficiency effects of thiamin?

Back 133

chronic peripheral neuritis, wernicke's encephalopathy w/ korsakoff psychosis, lactic acidosis

Front 134

What are deficiencies of riboflavin?

Back 134

choelosis, desquamation, inflammation of the tongue, seborrhheic dermatitis

Front 135

What is causedby niacin deficiency?

Back 135

pellagra

Front 136

What is caused by folic acid deficiency?

Back 136

megabolastic anemia

Front 137

What are the various active forms of vitamin a?

Back 137

retinol: steroid, retinal: visual, retinoic acid: steroid

Front 138

What is rickets?

Back 138

continous formation of osteoid matrix and cartilage that are improperly materialized - soft bones

Front 139

What are deficiencies of vit d?

Back 139

rickets, osteomalacia, metastatic calficifcation

Front 140

what is osteomalacia

Back 140

demineralization of pre-existing bone causing bone to become softer

Front 141

what is metastatic calcification?

Back 141

enhanced calcium absorption and bone resoprtion cause hypercalcemia

Front 142

What are vitamin a deficiencies?

Back 142

anemia, follicular hyperkeratosis, nightblindedness, xeropthalmia

Front 143

what is follicular hyperkeratosis

Back 143

rough keratinized skin- goosebumps

Front 144

what is xeropthalmia?

Back 144

keratinization of cornea- eye hemorrhaging, loss vision

Front 145

What are effects of toxicity vitamin a intake?

Back 145

increase rbp, bone pain, exposed to unbound retinol, scaly dermatitis, hepatosplenomegaly, nausea, diarrhea

Front 146

what is vitamin d?

Back 146

1, 25 dihydroxycholecalciferol, incerased by PTH, decreased serum ca increased pth

Front 147

What is vitamin E?

Back 147

lipid soluble antioxidant, maintain fluidity cell membranes, cell signaling

Front 148

Luminal Flow Rate

Back 148

 Increase tubular flow → increase secretion in DT-CCD
 As potassium is secreted into tubular fluid there is an increase in tubular potassium concentration
– If tubular fluid flow is increased the secreted potassium is swept downstream, thus driving force for K to move out of the cell is maintained
– If however the tubular fluid flow slows down, the effective driving force is decreased due to the rise in K secreted into “stagnant” tubular fluid.
 Because diuretic drugs increase tubular fluid in DT/CCD, these drugs also enhance K excretion via increased tubular fluid flow.

Front 149

Blocks Na-Cl channel

Back 149

 Hypokalemia
 Glitelman’s syndrome
 Metabolic alkalosis
 Increase renin-aldosterone
 Hypocalciuria
 Hypomagsenemia
 Age at diognosis > 6 years
 Mid growth retardation

Front 150

Blocks Na-K-2Cl channel

Back 150

 Bartter’s syndrome
 Hypokalemia
 Metabolic alkalosis
 Increase urinary PGE
 Increase renin-aldosterone
 Hypocalciuria
 Nephrocarcinosis
 Age at diagnosis – infancy
 Premature birth/growth retardation

Front 151

Regulation of Potassium Secretion

Back 151

 Luminal flow rate
 Aldosterone
 Extracellular potassium
 Extracellular pH

Front 152

 Reabsorption of sodium

Back 152

Freely filtered
- Sodium reabsorption in different parts of nephron:
-Proximal convoluted tubule: 60% is absorbed in this area
-Loop of Henle: 25%
-Distal Convoluted tubule: 5-7%
-Collecting duct: 3-5%

Front 153

Sodium depletion disorder

Back 153

GIT losses: vomiting, diarrhea
- Burns: excessive water and sodium loss

Front 154

Sodium Excess disorders

Back 154

- Cirrhosis: decreased albumin, nothing to put all the fluid inside
- Nephrotic syndrome: putting out all the albumin so the water is not inside the cell but outside the cell
- CHF: same as water

Front 155

what hormones increase sodium reasoprtion

Back 155

- cortisol, estrogen, growth hormone, insulin

Front 156

what hormones decrease sodium reasoprtion

Back 156

- glucagon, progesterone, parathyroid hormone

Front 157

What is the equation for serum osmolarity?

Back 157

2[na] + [glucose]/18 + [bun]/2.8

Front 158

What is the krause method?

Back 158

for work places, etc..easy
dbw X p.a

Front 159

How do you calculate anion gap?

Back 159

[na] - ([cl] + [hco3])

Front 160

what is the norm anion gap?

Back 160

12meq/L

Front 161

how to calculate tannhauser ideal body weight?

Back 161

[ht(cm) -100] x .9

Front 162

how to calculate tcr?

Back 162

bmr + p.a + sda

Front 163

what is normal serum osmolarity of Na?

Back 163

135-145

Front 164

what is normal serum osmolarity of K

Back 164

3.5-4.5

Front 165

what is normal serum osmolarity of cl-?

Back 165

98-108

Front 166

what is normal serum osmolarity of Creatinine?

Back 166

0.5-1

Front 167

what is normal abg of glucose??

Back 167

70-105

Front 168

what is normal bun?

Back 168

8-25

Front 169

what is normal hc03- abg?

Back 169

21-28

Front 170

what is normal co2 Abg?

Back 170

35-45

Front 171

what is normal po2 abg

Back 171

80-100

Front 172

what is normal ph?

Back 172

7.35-7.45

Front 173

what 3 systems does acid base homeostasis depend on?

Back 173

Liver -metabolizes proteins that produce H+ ions
2. Lungs -removes CO2
-H2 reflecting the bicarbonate (HCO3
-) role as an extracellular buffer
3. Kidneys -to generate new HCO3
- to replace the one used in buffering

Front 174

kidneys main purpose acid bbase?

Back 174

-2 main purposes in the regulation of the acid-base balance:
*Regulates plasma HCO3 by reabsorbing filtered HCO3 (recycling)
*Affects H+ excretion thru the formation of titrable acids and ammonium (synthesis)

Front 175

what is h+ secretion?

Back 175

Net retention of CO2 → Hypoventilation → net gain of H+
Net loss → Hyperventilation → net loss of H+

co2+h20->h2c03->h + hco3

Front 176

factor that affects h+ secretion rate?

Back 176

tubular fluid buffer concentration.

Front 177

what is anion gap?

Back 177

means of approximating the total concentrations of anions other than Cl- and HCO3- in the plasma

(na + k) - (cl + hco3)
-sum of the major cations in the plasma minus the sum if the major anions

Front 178

what is pc02 regulated by?

Back 178

respiratory compensation

Front 179

what does chronic acidosis lead to?

Back 179

stimulates ammonium production and excretion, this is an additional compensating factor that ameliorates the acidosis.

Front 180

what are factors effect hco3 secretion?

Back 180

1. non-bicarbonate buffer concentration in the tubular fluid

-function of buffers like phosphate and the rate of production and secretion of ammonia
-in chronic acidosis, the rate of ammonia production is stimulated and increases the ability of the kidneys to excrete the acid

2. plasma bicarbonate concentration

3. blood pCO2

Front 181

what is h+ secretion proximal tubule?

Back 181

-regulation of the HCO3- recycling is accomplished by the Na+/H+ antiporter which actively transports and reclaims 85% of the filtered load
-it is at the apical membrane while the NaHCO3 transport is at the basolateral membrane
-rate of secretion is gradient limited
-the Na+/H+ exchanger can be blocked by high doses of amiloride (a K+ sparing diuretic)

Front 182

what is h+ secretion distal mechanism?

Back 182

-an active process that is accomplished thru the H+-ATPase and reclaims the remaining 15% of the HCO3-
-it is located at the late sections of the proximal tubule and primarily at the apical membrane of the intercalated cells in the late distal tubule and in the collecting duct
-the HCO3- generated is transported by the Cl-/HCO3- exchanger at the basolateral membrane
-the limiting gradient on the collecting duct is when the tubular fluid is 4.5
-H+-ATPase resides in the alpha intercalated cells
-The beta intercalated cells has the H+-ATPase and Cl-/HCO3- exchanger reverse their positions with the net result in the addition of alkali to the urine and acid in the blood

Front 183

what is ammonium titration?

Back 183

*major precursor of NH3 is the amino acid glutamine which contributes its amide and amino nitrogen in the formation of NH3
*glutamine is extracted from both the blood and tubular cells within the mitochondria, it is deaminated by phosphatedependent glutaminase
*glutamate can be deaminated to alpha ketoglutarate and ammonia by glutamate dehydrogenase in the presence of nicotinamide adenine dinucleotide group
*alanine and glycine may contribute their amino group to alpha ketoglutarate by transamination to form glutamate which again can be deaminated

Front 184

what are the buffer reactions w/ the tubules?

Back 184

1. Bicarbonate titration – predominates in the proximal tubules
2. Phosphate titration – at the distal tubules
3. Ammonium titration – at the distal tubule

Front 185

what causes metabolic acidosis?

Back 185

diarrhea, lactic a, renal faliure, d, sulfur, shock, hypovolemia

Front 186

what causes m. alkalosis?

Back 186

vomit, diuretics

Front 187

what causes r. acidosis?

Back 187

descreased respiration, hypoventilation, affects effective alveolar ventilation

Front 188

what causes r. alkalosis?

Back 188

hyperventilation, cns, drugs, increased respiration

Front 189

what causes hyperkelemia

Back 189

k+ shift out of cells, hypoaldosteronism, K+ sparing diuretics,

Front 190

what causes hypokelemia

Back 190

K+ shift into cells, hyperaldosteroneism, thiamide loop diuretics