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Pathology > Lec11 Nutritional Pathology > Flashcards

Lec11 Nutritional Pathology Flashcards

1
Q

What is most prevalent nutritional disorder in US

A

obesity

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2
Q

Definition obestity

A

accumulation adipose tissue that imparis health

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3
Q

BMI? Whats normal? overweight? obese?

A

weight [kg]/ (height in meters )^2

normal: 18.5-25
overweight: 25-30
obesity: >30

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4
Q

Is central [visceral] or subcutaneous fat more dangerous?

A

central adipose tissue accumulation associated with higher risk for many diseases

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5
Q

What are main measures of body fat?

A
  • waist and hip circumference ratio
  • skinfold thickness
  • mid-upper arm circumference
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6
Q

What is normal wasit-hip circumference ratio?

A

obesity = >0.8-0.85 for women

= >0.9-1.0 for men

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7
Q

What is steatosis

A

increased fat

- may resolve or may progress to steatohepatitis

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8
Q

What is oil red o stain?

A
  • stain for fat

- use for steatosis

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9
Q

What is steatohepatitis?

A
  • steatosis of liver wtih inflammation
  • leads to: fibrosis, cirrhosis, hepatocellular carcinoma
  • can be due to alcohol or metabolic stuff
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10
Q

What is a mechanical effect of obesity?

A

osteoarthritis

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11
Q

What are 8 major pathologic complications of obesity

A
  • type II diabetes
  • hypertenesion
  • hypertriglycidemia and low HDL
  • non-alcoholic steatoehpatitis
  • osteoarthritis
  • heart disease/atherosclerotsis
  • increased risk of cancer
  • respiratory stuff [sleep apnea, hypoventilation]
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12
Q

Cause of obesity

A

imbalance of caloric intake and energy expenditure complicated by:

  • genetic
  • neural
  • hormonal
  • psychological
  • nutritional
  • environmental
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13
Q

Adipocytes - what do they secrete?

A
  • number of adipocytes set in childhood/adolescence
  • secrete
    • leptin
    • adiponectin
    • TNF, IL6, IL1, IL18
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14
Q

What is leptin? Effect of disruption leptin signalling?

A
  • secreted by adipocytes and go to receptors in brain
  • signals adequacy of fat stores
  • decrease appetite/food intake [anorexigenic effect]
  • downregulates path that increases appetite and upregulates path that increases energy expenditure
  • disruption of signaling –> overeating and weight gain
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15
Q

What is ghrelin?

A
  • produced in stomach
  • increases food intake
  • ghrelin levels rise before eating and fall 1-2 hrs after eating
  • in obese people: grhelin levels always remain high
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16
Q

What is peptide YY [PYY]?

A
  • secreted by endocrine cells in ileum/colon
  • levels of PYY low during fasting and increase during food intake
  • cause reduction in food intake/appetite [anorexigenic]
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17
Q

Adiponectin

A
  • secreted by adipocytes
  • directs fat to muscle and away from liver
  • decreases glucose production in liver
  • lower levels of adiponectin in obese individuals
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18
Q

How is obesity an inflammatory state

A
  • obesity leads to high C reactive protien that is a marker of inflammatory activity
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19
Q

What medications for managing obesity?

A
  • meds that decrease appetite: noradrenergic, serotoninergic

- meds that partition fats, prevent fats being absorbed by GI tract

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20
Q

What surgical methods for managing obesity

A

roux-en-Y: bypass stomach
sleeve gastrectomy: stomach staple to make smaller
gastric banding: make stomach smaller

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21
Q

what is primary vs secondary protein/energy malnutrtion

A

primary: food unavailable
secondary: secondary to coexisting disease

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22
Q

Who does primary protein energy malnutrition effect?

A
  • children in poor countries

- elderly isolated in US with inaccessibility of food

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23
Q

Marasmus

A
  • global starvation
  • wasting appearance: loss of fat/muscle especially in extremities, growth retardation
  • vit and immune deficiency
  • age <1 year
  • normal serum albumin
  • patients are alert
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24
Q

Kwashiorkor

A
  • protein deficiency even though adequate calories
  • occurs when child is switched from milk to predominantly carbohydrate diet
  • edema [low oncotic pressure]
  • fatty liver [low lipoproteins that are needed to transport fat out of liver]
  • skin lesions
  • hair hypopigmentation
  • vit and immune deficiency
  • age > 1 year
  • low serum albumin
  • patients are listless
25
Q

Secondary causes of protein energy malnutrtition

A
  • acute infection [ increases metabolic rate]

- chronic diseases: cancer, HIV, anorexia, bulimia, malabsorption, alcoholism

26
Q

What is cachexia?

A
  • extreme weight loss, fatigue, muscle atrophy, anemia, anorexia
  • in cancer and HIV patients
  • secondary to atrophy of diaphragm and respiratory muscles in cancer patients
27
Q

Which proteins involved in cachexia?

A
  • PIF [proteolysis inducing factor]
  • LMF [lipid-mobilizing factor]
  • cytokines [TNF-a, IL6]
28
Q

What is proteolysis inducing factor [PIF]?

A
  • secreted in urine of patients with pancreatic cancer and cachexia
  • may play role in cachexia
29
Q

What cytokines play a role in cachexia?

A
  • TNF-a or IL-6

- may be secreted by tumor or in response to tumor

30
Q

What is lipid mobilizing factor [LMF]

A
  • increases fatty acid oxidation
  • increases pro-inflammatory cytokines
  • may play role in cachexia
31
Q

What is anorexia nervosa?

A

eating disorder characterized by excessive weight loss, food restriction, distorted body self immage

32
Q

What is anorexia?

A

decreased appetite/food intake, not the same as the eating disorder

33
Q

What is bulimia?

A

bing eating usually followed by induced vommiting

34
Q

What is bulimia nervosa?

A

eating disorder characterized by binge eating followed by induced vomiting

35
Q

Which vitamins are fat soluble?

A
  • vit A, D, E, K
  • can accumulate to toxic levels
  • fat malabsorption syndrome can lead to low levels
36
Q

Which vitamins are water soluble?

A
  • B and C vit

- rarely toxic

37
Q

Are water or fat soluble vit more likely toxic?

A

fat soluble

38
Q

What is vitamin A

A
  • group of related compounds

- retinol, retinal, retinoic acid

39
Q

What are retinoids?

A
  • vitamin A and other compounds with similar structure

- may or may not have vit A effects

40
Q

Sources of vitamin A?

A

caratenoids [B carotene]

    • provitamins that are converted to vit A
    • found in yellow and leafy veggies [carrots]

preformed vit A in animal derived food [eggs, fish, liver, milk, butter]

41
Q

Functions vitamin A

A
  • helps vision, cell differentiation, growth, metabolism, resistance to infection
  • mostly focus on: VISION, CELLULAR DIFFERENTIATION
42
Q

Effects of vitamin A deficiency?

A
  1. blindness
  2. immune deficiency
  3. squamous metaplasia
    - – in lacrimal glands –> get dry eyes and conjunctiva
    - – respiratory tract –> get pulmonary infections more easily
    - – urinary tract –> get kidney and urinary stones
43
Q

Effects of squamous metaplasia in vit A deficiency [3 places]

A

in lacrimal glands –> get dry eyes and conjunctiva

respiratory tract –> get pulmonary infections more easily

urinary tract –> get kidney and urinary stones

44
Q

What is cause and effect of vitamin A toxicity? Acute vs chronic?

A
  • overuse of dietary supplements, or lots of liver in diet [which has lots of vit A]
  • acute toxicity: headache, dizziness, vomitting, blurred vision
  • chronic: weight loss, anorexia, nausea, vomitting, enlarged liver
45
Q

Therapeutic uses of vit A?

A
  • retinoids to treat acne, psoriasis, acute promyelocytic leukemia
  • retinoic acid and preformed vit A are also teratogens
46
Q

What is vitamin C?

A
  • ascorbic acid
  • plays role in biosynthetic paths [COLLAGEN SYNTHESIS
  • antioxidant
  • in citrus fruits, veggies, milk, fish, liver
47
Q

Effect of vitamin C deficiency?

A
  • scurvy, get poorly formed collagen and thus:
  • bleeding [due to weak blood vessel walls]
  • – hemorrhages, swollen and bleeding gums
  • bone pain
  • poor wound healing
48
Q

Why is vitamin C toxic or not toxic?

A

not toxic because:

  • water soluble
  • unstable
  • poorly absorbed in intestine
49
Q

Source of vit D

A
  • 90% from photoconversion of precursor in skin
  • 10% from diet: fish, plants, grains
  • needs to be converted by liver and kidney before active effect
  • acts on osteoclasts/blasts, intestine absorption, kidney itself
50
Q

Function of vit D

A 
CALCIUM REGULATION
- stimulates intestinal Ca reabsorption
- stimulates renal Ca reabsorption
- interacts with parathyroid hormone
- induces mineralization of bone
also [less importantly] regulation of:
- immune system, cell proliferation, cell differentiation, apoptosis, angiogenesis
51
Q

Cause of vit D deficiency

A
  • inadequate vit D in diet
  • fat malabsorption syndrome
  • limited sunlight exposure
  • abnormal conversion to active form [due to liver or kidney disease]
52
Q

3 diseases associated with vit D deficiency

A
  • rickets [ in kids]
  • osteomalacia [in adults]
  • hypocalcemic tetany [muscle problem]
53
Q

what is rickets?

A
  • vit D deficiency in kids
  • inappropriate endochondral bone formation
  • get bowing in legs
54
Q

Effect of vit D toxicity

A
  • get high Ca, Ca deposition in soft tissue [metastatic calcification]
  • bone pain and hypercalcemia
55
Q

General function of B vitamins?

A

usually cofactors

56
Q

General function of vit E?

A

antioxidants

57
Q

General function of vit K?

A

important for clotting factors

58
Q

How to tell marasmus vs kwashiorkor

A

marasmus: 1 yr old, edematous, low serum albumin, patient is listless

Pathology (15 decks)

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