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A Nutr 425 > quiz 3 > Flashcards

quiz 3 Flashcards

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1
Q

hematocrit

A

proportion of the blood made up by RBC usually around 45%

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2
Q

MCV

A

mean corpuscule volume- volume of a rbc

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3
Q

Total iron binding capacity:

A

capacity for transferrin to bind iron.

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4
Q

Albumin!!!!

A

most well known measure of visceral prtein status - low to show disease staes- burns. higher when dehydrates
indicates trauma, surgery, inflammation and stress

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5
Q

Transferin!!!!!

A

negative acute phase respondent

transports iron in the blood, higher level indicate low iron stores

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6
Q

prealbumin!!!!!

A

Negative acute phase protein
decreases with illness
responsible for transporting thyroxine and is associated with retinol binding protein- short turnover rate- 2 days

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7
Q

total iron binding capacity

A

capacity for transferin to bind iron

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8
Q

Somatic Protein Assessment
creatine height index

limitations:

A

Correlates daily urine output of creatinine with height
= lean body mass related to muscle
creatinine height index

Uses ratio of 24 hour output to expected output
limitation
-> kidney function
2. Hard to measure all of the irine unless in hospital
3. diet: meat intake or supplements

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9
Q

nitrogen balance

A

In healthy individual, nitrogen excretion should equal nitrogen intake
Requires 24 hour urine collection
take protein intake/6.25 -UUN (urine urea nitrogen)-4

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10
Q

retinol binding protein!!!!!

A

negative acute phase proteins
transports vitamin a, shortess half life!!!! 12 hours. most sensitive protein stauts indicator in non-critically ill
elevated with renal failure, decreased with hyperthyrodism, cystic fibrosis

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11
Q

CRP

A

C- reactive protein is a positive acute phase protein that is released during periodes of inflammation and infection

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12
Q

what are non skeletal protein

rename as acute phase protein

A 
Albumin
Transferrin
Prealbumin/transthyretin
Retinol binding protein (RBP)
Fibronectin (FN)
Insulin like growth hormone (IGF-1)
C-reactive protein (CRP)
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13
Q

TLC

A

TOTAL lymphocyte count

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14
Q

CHEM 7 panel

A 
Bun (Blood urea nitrogen)
Serum chloride
Co2
Creatine
Glucose
serum potassium
Serum Sodium
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15
Q

BUN

A

BLLOD UREA NITROGEN- detects kidney function - in our diet, protein will cause it to go up - if kidney is impaired it will be high

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16
Q

serum cl,k,na

A

electrolytes

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17
Q

glucose

A

high in diabetes and in trauma

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18
Q

co2

A

acid base

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19
Q

Creatinine:

A

detects change in kidney function (increased when kidney is impaired)

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20
Q

ggt and ALP

A

elevated serum of these two can be found in diseases of the biliary tract.
ALP is first test but ggt is used to confirm alp results as alp can also be used seen in bone diseases

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21
Q

feritin

A

storage form of iron

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22
Q

serum ferrition

A

indicator of iron storage in organs, especially in liver

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23
Q

Protoporphryin-C

A

precursor to heme synthesis- it increases in iron deficiency

increase in zinc protoporphyrin because zn substitutes for the iron

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24
Q

Hematological Assessment

A 
Hemoglobin (Hgb)
Hematocrit (Hct)
MCV, MCH, and MCHC
Ferritin, transferrin saturation, protoporphyrin
Serum folate, serum B12

The first two is detecting anemia
The rest are to figure out the cause

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25
Nutrition-Focused Physical Findings (PD) what 4 things to do
Assess for signs and symptoms consistent with malnutrition or nutrient deficiencies/excesses Inspection, palpation, percussion, and auscultation Perform: objective; Ask: subjective Inspect: look Palpation: touching Percussion: listening for sounds Auscultation: stethoscope
26
Functional Assessment
Patient’s perception on Subjective Global Assessment Perception of self-care abilities and environment ADL/ IADLs (activities of daily living(eating, dressing)/ instrumental activities of daily living- child rearing,care pets, See Table 3.11 Handgrip dynamometry Included in proposed criteria for malnutrition diagnosis
27
what are the 3 types of etiology-based malnutrition definition
starvation-related (no inflammtion) chronic disease-related- organ failure, cancer, rheumatoid arthitis acute disease or injury-related malnutrition (injection, burns, trauma)
28
Third spaces: | pathology
Peritoneal, pericardial, and thoracic cavities Joints and bursae Pathology: ascites, anasarca between the body compartments: Peritoneal: abdominal area\pericardia: around the heart
29
Ascites:
fluid in peritoneal cavity (usually very small becaseu organs are jammed together). Usually caused by liver or kidney failure Ascites is a gastroenterological term for an accumulation of fluid in the peritoneal cavity. Almost always is due to liver failure (cirrhosis)
30
Anasarca (same as kwashiorkor-
North American terminology): widespread- swelling in the skin, lots of extracellular fluid space- caused by serosis (liver), renal failure (better example), also in severe malnutrition- lack of protein , low cardiac output (heart failure): decreased blood flow to the kideney- see this as not enough blood flow and retains sodium and thus causing water retention
31
Albumin:
major payer in osmotic pressure
32
hypo and hypertonic values
more solutes or more protein- higher osmolarity- greater than 300mosm/kg Hypotonic: lower than 300mosm/kg
33
Fluid output Sensible losses Insensible losses Starling’s forces-
``` Fluid output Sensible losses Obligatory and facultative urine; feces Insensible losses Respiration Skin by evaporation ``` force that moves liquid between the cells 30-40ml/kg for fluid intake in adults- depends on urine output obligatory is the minimum urine to get rid of the things such as urea. Facultative- excess urine due to drinking, feces, breath, sweat
34
Orthstatic blood pressure
- usually large change in blood pressure on changing posture
35
hypovelemia vs hyper
Hypovolemia (dehydration) Hypervolemia (hyponatremia) dehydration- extra cellular fluid defecit Hypervolemia: hyponatremia- extra celluar fluid excess- Changes in fluid volume alter measured plasma concentrations: e.g. Plasma glucose of 5 mmol/L = numerator/denominator e.g. volume deficit of -10% 5 mmol/0.90 L = 5.6 mmol/L e.g. volume excess of 10% 5 mmol/1.1 L = 4.5 mmol/L
36
natremia
means sodium deficit- this does not always occur in hypervolemia When a patient has patient excess or defecit- this can interfere with biochemical assessment – need to interpret this when doing assessment
37
Calcium: levels
need to examine albumin in the blood- 45% of Ca in the blood stream is bound to albumin. Therefore need to measure both as albumin levels can change. Ionized calcium will not change in the albumin So need to look at the look at adjusted calcium (without the albuin) because if albumin is low it will make it seem as thought calcium is low
38
NSAis- non selective anti inflammatory drug e.g.
aspirin | can lead to more stomac ulcers because impairing protective layer that protects from acid
39
``` Extracellular fluid (ECF) what 2 percentages ```
Interstitial (80%) + Plasma (20%) | Pathology: ↑ fluid in interstitial  edema
40
examples of ild to moderate inflammatory responses
chd,celiac, pancreatitis, diabetes, IBD, obesity ...
41
examples of severe inflammatory response
severe burns, major abdominal surgery, closed head injury
42
what happens with an acute inflammatory response
release of cytokines-> release of acute phase proteins and increase in catabolism and decrease in synthesis- leads to high CRP increase in REE and negative nitrogen balance
43
CRP
Generally CRP is favored measurement of inflammation acute phase protein that works to enhance phagocytosis by targetting bacterial cells for destruction; used as a sserum marker for inflammation
44
what is COX-1 blocked by
stimulate physiological prostaglandins- protect the GI, RENAL and regulate smooth muscle tone blocked by NSAIDS -Non-steroidal Anti-inflammataory Drugs
45
COX-2 | blocked by
pathologic prostaglandins- inflammation, edema,leukocytosis (all are proinflammatory to help with healing blocked by NSAIDS AND cox-2 inbitors N-3 FAs are mostly anti-inflammatory
46
when blood glucose increases and decreases
b-cells are activated to increase insulin production and a cells are inhibited to decrease glucagon when BG decreases: a cells increase to stimulate glucagon and b cells decrease to decrease insulin
47
In stress – Insulin resistant etiology is different
Stress causes release of cytokines and these appear to prevent normal insulin action -- perhaps to keep bl. glucose levels high to support wound healing etc.
48
cortisol, insulin, glucagon and epinephrine is ana or catabolic
insulin: anabolic glucagon and epi: no efect cortisol : catabolic
49
visceral protein assessment
albumin, prealbumin (affected by inflammation
50
acute phase pro
crp, firnectin, serum amyloid a ceruloplasm
51
hematological ass
hemoglobin, hematocrit, platelet count, erythrocyte
52
other lab indices
eletrolytes, glucose, lactate
53
5 ways starvation is adapted | ketone use implied #4
``` energy needs decrease metabolic rate decreases 20-25kcal/kg/d energy from fat stores> 90% of kclas energy from protein <10% of gluconeogenesis (only used for brain protein sore protected ```
54
catabolic insult-induced protein-energy malnutrition (pro and energy production abnormal
no adaptive responses activated increase matabolic rate 35-40kcal/kg increase glucose production in excess of needs increase use of protein for fuel (glucose)
55
stress response
``` This is Response exaggerated in Acute inflammatory response (acts fast); Chronic is slower • Logical = need to fix the problem rather than maintain body stores increase in glucagon, cortisol, BMR,catabolism ... ```
56
stress response7 | vs starvation
``` This is Response exaggerated in Acute inflammatory response (acts fast); Chronic is slower • Logical = need to fix the problem rather than maintain body stores increase in glucagon, cortisol, BMR,catabolism ... ``` starvation: decrease in metabolic rate, decrease in glucose, use lipid as main source, peserve lean body mass
57
Permissive underfeeding: Nelms
“Permissive underfeeding” = undertaken to prevent acute metabolic and respiratory complications in critically ill patients (p. 102) • Overfeeding may result in hyperglycemia, hypertriglyceridemia and hepatic steosis (“fatty liver”) • Table 22.7 – benefits of permissive underfeeding – Lower omega-6 intake = ↓ pro-inflammatory prostaglandins – Lower CHO = less hyperglycemia risk; spare thiamine – Lower oxidation of metabolism – Reduced DNA damage (due to less pro-oxidation) – Decreased hypermetabolism = less CO2 production
58
Nutrients to Reduce Inflammation (p 672)
``` Glutamine – feeds GI; anti-inflammatory; precursor for GSH • 100 mg IV vitamin C every 8 h • 400 mcg selenium /d C and Se: IV 2 days then EN • 1500 IU vitamin E every 12 h for 7 days • Omega 3 FAs (e.g. 2g/L in Peptamen) • Prebiotics (fiber) and probiotics ```
59
Refeeding Syndrome:
Refeeding syndrome = metabolic alterations that may occur during nutritional repletion of starved (malnutrition, prolonged NPO) patients • Body switches from catabolism to anabolism too quickly • Reintroduction of CHO in starvation shifts metabolism from ketones to glucose – Increase need for phosphorus intracellularly – Increased need for Mg and K which are intracellular cations – Increased need for thiamine (may be deficient) • PO4 Mg++ K+ drawn into cells => drop in blood levels
60
consequences of refeeding
hypokalemia  muscle weakness including poor lung muscle action – respiratory distress • hypophosphatemia  encephalopathy and coma (acute); metabolic bone loss (chronic) • hypomagnesemia  similar to low K, low Ca • Cardiac arrhythmias are the most common cause of death from refeeding syndrome, with other significant risks including confusion, coma and convulsions and cardiac failure.
61
Sepsis
• Immunosuppressive response preventing | adequate response to infection
62
Systemic Inflammatory Response System | SIRS
• Sepsis without infection diagnosis criteria: significant edema, hyperglycemia without diabetes, palsma c reactive protein more than 2 SD above normal value
63
– Multi-Organ Distress Syndrome / Multisystem | Organ Failure
Complication of sepsis and SIRS; altered function | in two or more organs
64
Burns – Clinical Manifestations
Clinical manifestations – Signs and symptoms determined by burn depth and body surface area affected • Rule of 9s used to estimate body surface area • Pathophysiology – Hypermetabolism, catabolism, and altered immune and hormonal response – Generation of free radicals; ↑ oxidative stress

A Nutr 425 (6 decks)

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