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1
Q

Ideal Body Weight Formula

A 
Male = 50 kg + 2.3 kg for each inch >5'
Female = 45.5 + 2.3 kg for each inch >5'
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2
Q

refeeding syndrome

A

complication of aggressive nutrition support after prolonged starvation

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3
Q

Components of TPN

A 
Percentage of calories:
55% from dextrose
25-30% from lipids
20% from AAs
(10-15% from essential AAs)
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4
Q

Calories in TPN

A

1 mL TPN = 1 cal

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5
Q

Essential FAs

A

linolenic, linoleic

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6
Q

most common complication of TPN

A

line infection

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7
Q

Which amino acids cannot act as precursors to gluconeogenesis

A

leonine and lysine

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8
Q

zinc deficiency

A

skin rash, hair loss

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9
Q

selenium deficiency

A

cardiomyopathy

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10
Q

chromium deficiency

A

poor glycemic control

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11
Q

copper deficiency

A

pancytopenia

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12
Q

protein requirements for healthy adults

A

0.8g/kg/day

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13
Q

protein requirements for critically ill surgical patients WITHOUT renal or hepatic disease

A

1.5-2.0g/kg/day

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14
Q

Kwashiorkor

A

edema, anasarca, anorexia: “protein defecit”

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15
Q

Marasmus

A

no edema. severe muscle wasting, loss of body fat: “total calorie defecit”

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16
Q

In PPN, 50% of calories are from ___

A

lipids

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17
Q

tx for symptomatic or severe hyponatremia (<100 mEq/L)

A

hypertonic saline

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18
Q

presentation of hypercalcemic crisis

A

muscle weakness, fatigue, hypercalcemia

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19
Q

tx of severe hypocalcemia

A

calcium gluconate or calcium chloride

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20
Q

tx of non-severe hypocalcemia

A

PO calcium

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21
Q

1st symptom of hypocalcemia

A

perioral or fingertip numbness

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22
Q

Each __ mEq of potassium will raise serum K by __ mEq/L

A

Each 10 mEq of potassium will raise serum K by 0.1 mEq/L

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23
Q

What is the chemical cause of metabolic alkalosis?

A

Loss of anions (e.g. Cl- from the stomach and albumin from plasma) or increases in cations (rare).

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24
Q

Metabolic derangements in recurrent vomiting

A

hypokalemic, hypochloremic metabolic alkalosis with low urine Cl-

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25
Q

Tx for metabolic derangements of recurrent vomiting

A

Cl- replacement via NS

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26
Q

What causes paradoxical aciduria?

A

It presents in metabolic alkalosis 2/2 recurrent vomiting because of activation of H+/K+ exchanger to conserve K+.

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27
Q

What metabolic effects/derangements are associated with spironolactone?

A

potassium-sparing; hyperchloremic, non-anion gap metabolic acidosis

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28
Q

What are elemental formulas?

A

Easily digestible, low-fat nutrition that uses free amino acids or small chain peptides as protein sources for patients with maldigestion and malabsorption.

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29
Q

Formula for anion gap

A

Na - (Cl + HC03)

cations minus anions

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30
Q

Normal anion gap

A

8 +/- 4

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31
Q

What are the causes of anion gap metabolic acidosis?

A 
MUDPILES, SiR
M: methanol
U: uremia
D: DKA
P: propylene glycol
I: isoniazid
L: lactic acidosis
E: ethylene glycol
S: salicylates
S: sepsis
R: renal failure
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32
Q

What are the causes of non anion gap metabolic acidosis?

A

DR.
D: diarrhea
R: renal tubular acidosis

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33
Q

emergency tx of severe symptomatic hypermagnesemia

A

Calcium gluconate to antagonize the effect of magnesium on neuromuscular function. Can also give IVF and loop diuretics.

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34
Q

What cells rely on glucose as their exclusive fuel source?

A

RBCs
polymorph neutrophils
adrenal medulla

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35
Q

Heart muscles rely on ___ for fuel

A

free fatty acids

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36
Q

Skeletal muscles use ___ for fuel

A

glucose (but can use free fatty acids when stressed)

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37
Q

The brain uses ___ for fuel

A

glucose (but can use ketones in starvation)

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38
Q

What does the pancreas secrete in active forms?

A

amylase
lipase
ribonuclease
deoxyribonuclease

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39
Q

What is the function of pancreatic lipase?

A

It works at the oil/water interface to yield free fatty acids and monoacylglycerols

40
Q

How are medium and short chain fatty acids absorbed? Where are they secreted?

A

by simple diffusion; into the portal venous circulation

41
Q

How are long chain triglycerides metabolized?

A

They must undergo lipolysis into constituent LCFAs and MAGs by pancreatic and gastric lipases before being absorbed by the intestinal epithelium

42
Q

What constitutes the majority of dietary fats?

A

Long chain triglycerides

43
Q

LCFAs, MAGs, cholesterol, and fat soluble vitamins are all absorbed in ____.

44
Q

___ help form micelles, but are not absorbed with them. They are absorbed by ___ in the ___.

A

bile salts; active transport; distal ileum

45
Q

___ is the primary plasma carrier of cholesterol

A

low density lipoprotein

46
Q

Where are bile salts produced? What conjugates them?

A

liver; glycine and taurine

47
Q

What are examples of primary bile acids?

A

cholic acid and chenodeoxycholic acid

48
Q

Where are primary bile acids synthesized?

A

in the liver, from cholesterol precursors

49
Q

What are examples of secondary bile acids?

A

deoxycholic acid and lithocolic acid

50
Q

How are secondary bile acids formed?

A

by deconjugation of primary bile acids by intestinal bacteria

51
Q

half life of albumin

52
Q

Strongest determinant of preoperative poor nutritional status

53
Q

half life of pre-albumin

A

24-48 hours

54
Q

half life of transferrin

55
Q

What is transferrin and how does it change during acute inflammatory conditions?

A

main plasma transport protein of iron; decreases during acute inflammatory conditions

56
Q

___ is the strongest determinant of serum osmolarity

57
Q

Formula for serum osmolarity

A

Osm = 2Na + Glu/18 + Urea/2.8

58
Q

basal energy expenditure (and modification for pregnancy)

A

25 kcal/kg/day (in pregnancy add 300 kcal/day)

59
Q

What is the precursor to urea? What enzyme makes that transition?

A

arginine; arginase

60
Q

Where is urea produced?

61
Q

Where is urea excreted?

62
Q

What is the expected excess weight loss 2 years following sleeve gastrectomy?

A

approximately 60%

63
Q

What is the presentation of ABO incompatibility? How does it progress?

A

tender, erythematous IV site; chest pain; hypotension

can progress to hemoglobinuria and DIC

64
Q

What is the most common blood product to contain a bacterial contaminant? Why?

A

platelets, because they are stored at room temperature

65
Q

What is the most common contaminant of platelets?

A

gram negative rods (most commonly E. coli)

66
Q

Actinic keratosis is a risk factor for ___.

A

squamous cell cancer

67
Q

___ (aka factor ___) cleaves fibrinogen to form fibrin

A

thrombin; IIa

68
Q

What does thrombin activate?

A

factor V, VIII, and platelets

69
Q

What are the components of a platelet plug?

A

platelets and fibrin

70
Q

hemophilia A & B are deficiencies in ___ and ___; and have ___ PT/bleeding time and ___ PTT

A

hemophilia A: deficiency in VIII
hemophilia B: deficiency in IX
normal PT/bleeding time
elevated PTT

71
Q

Acute tx for hemophilia A&B

A

Factor VIII concentrate or cryoprecipitate

72
Q

What is the most common congenital bleeding disorder?

A

von Willibrand disease

73
Q

von Willibrand disease has ___ BT and low ___ and ___

A

prolonged BTT

low vWF and factor VIII

74
Q

What cell types produce von Willibrand factor?

A

endothelial cells and megakaryocytes

75
Q

What is Von Hippel Lindau syndrome?

A 
hemangiomas of CNS and retina
pheochromocytoma
clear cell renal cell cancer
endolymphatic sac tumors
cystadenomas of the epididymis and broad ligament
76
Q

What is the screening for Von Hippel Lindau syndrome? How often does it occur?

A 
annual screening:
urine cytology
ophtho exams
renal ultrasound
24 hr urine for VMA and metanephrine
77
Q

What is caused by the PTEN mutation?

A

Cowden syndrome

78
Q

What is caused by the MLH1 mutation?

A

Lynch syndrome (hereditary nonpolyposis colorectal cancer)

79
Q

What is caused by the MSH2 mutation?

A

Lynch syndrome (hereditary nonpolyposis colorectal cancer)

80
Q

What is caused by the MSH6 mutation?

A

Lynch syndrome (hereditary nonpolyposis colorectal cancer)

81
Q

What is caused by the PMS2 mutation?

A

Lynch syndrome (hereditary nonpolyposis colorectal cancer)

82
Q

What are the most important predictors of poor outcome in melanoma?

A

lymph node involvement and distant mets

83
Q

What procedure must be done before operating on head/neck/trunk melanoma?

A

preop lymphatic mapping of all possible nodal basins

84
Q

What is the most powerful predictor of melanoma prognosis?

A

melanoma depth

85
Q

___ is an FDA approved adjuvant tx following resection of stage IIb-III melanoma.

A

interferon alpha 2b

86
Q

Melanoma: < 1mm

A

T1 melanoma lesions

87
Q

Melanoma: 1.01-2mm

A

T2 melanoma lesions

88
Q

Melanoma: 2.01-4mm

A

T3 melanoma lesions

89
Q

What’s the difference between “a” and “b” in melanoma T staging?

A

“a” is without ulceration
“b” is with ulceration
(b for bad)

90
Q

Melanoma involving 1 lymph node

A

N1 melanoma

91
Q

Melanoma involving 2-3 regional lymph nodes

A

N2 melanoma

92
Q

Melanoma involving 4+ regional lymph nodes

A

N3 melanoma

93
Q

Melanoma without metastasis

A

M0 melanoma

94
Q

Melanoma with mets to skin, subQ, or distant lymph nodes, normal LDH

A

M1a melanoma

95
Q

Melanoma with lung mets, normal LDH

A

M1b melanoma

96
Q

Melanoma with mets to viscera other than lungs with normal LDH or any distant mets + elevated LDH

A

M1c melanoma

97
Q

Thrombotic thrombocytopenic purpura pentad

A 
fever
AMS
hemolytic anemia
renal failure/hematuria
purpura

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