quiz 3 Flashcards

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
Q

Nutrition-Focused Physical Findings (PD)

what 4 things to do

A

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

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26
Q

Functional Assessment

A

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
Q

what are the 3 types of etiology-based malnutrition definition

A

starvation-related (no inflammtion)

chronic disease-related- organ failure, cancer, rheumatoid arthitis

acute disease or injury-related malnutrition (injection, burns, trauma)

28
Q

Third spaces:

pathology

A

Peritoneal, pericardial, and thoracic cavities
Joints and bursae
Pathology: ascites, anasarca
between the body compartments:
Peritoneal: abdominal area\pericardia: around the heart

29
Q

Ascites:

A

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
Q

Anasarca (same as kwashiorkor-

A

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
Q

Albumin:

A

major payer in osmotic pressure

32
Q

hypo and hypertonic values

A

more solutes or more protein- higher osmolarity- greater than 300mosm/kg
Hypotonic: lower than 300mosm/kg

33
Q

Fluid output
Sensible losses
Insensible losses

Starling’s forces-

A
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
Q

Orthstatic blood pressure

A
  • usually large change in blood pressure on changing posture
35
Q

hypovelemia vs hyper

A

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
Q

natremia

A

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
Q

Calcium: levels

A

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
Q

NSAis- non selective anti inflammatory drug e.g.

A

aspirin

can lead to more stomac ulcers because impairing protective layer that protects from acid

39
Q
Extracellular fluid (ECF)
what 2 percentages
A

Interstitial (80%) + Plasma (20%)

Pathology: ↑ fluid in interstitial  edema

40
Q

examples of ild to moderate inflammatory responses

A

chd,celiac, pancreatitis, diabetes, IBD, obesity …

41
Q

examples of severe inflammatory response

A

severe burns, major abdominal surgery, closed head injury

42
Q

what happens with an acute inflammatory response

A

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
Q

CRP

A

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
Q

what is COX-1

blocked by

A

stimulate physiological prostaglandins- protect the GI, RENAL and regulate smooth muscle tone

blocked by NSAIDS -Non-steroidal Anti-inflammataory Drugs

45
Q

COX-2

blocked by

A

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
Q

when blood glucose increases and decreases

A

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
Q

In stress – Insulin resistant etiology is different

A

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
Q

cortisol, insulin, glucagon and epinephrine is ana or catabolic

A

insulin: anabolic
glucagon and epi: no efect
cortisol : catabolic

49
Q

visceral protein assessment

A

albumin, prealbumin (affected by inflammation

50
Q

acute phase pro

A

crp, firnectin, serum amyloid a ceruloplasm

51
Q

hematological ass

A

hemoglobin, hematocrit, platelet count, erythrocyte

52
Q

other lab indices

A

eletrolytes, glucose, lactate

53
Q

5 ways starvation is adapted

ketone use implied #4

A
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
Q

catabolic insult-induced protein-energy malnutrition (pro and energy production abnormal

A

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
Q

stress response

A
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
Q

stress response7

vs starvation

A
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
Q

Permissive underfeeding: Nelms

A

“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
Q

Nutrients to Reduce Inflammation (p 672)

A
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
Q

Refeeding Syndrome:

A

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
Q

consequences of refeeding

A

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
Q

Sepsis

A

• Immunosuppressive response preventing

adequate response to infection

62
Q

Systemic Inflammatory Response System

SIRS

A

• Sepsis without infection
diagnosis criteria: significant edema, hyperglycemia without diabetes, palsma c reactive protein more than 2 SD above normal value

63
Q

– Multi-Organ Distress Syndrome / Multisystem

Organ Failure

A

Complication of sepsis and SIRS; altered function

in two or more organs

64
Q

Burns – Clinical Manifestations

A

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