Nutritional pathology Flashcards

1
Q

A child is considered malnourished when

A

weight is <80% of normal

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2
Q

2 protein compartments in body

A

Somatic

Visceral

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3
Q

What makes up the somatic protein compartment

A

Skeletal muscle

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4
Q

What makes up the visceral protein compartment

A

Liver stores

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5
Q

4 examples of Protein Energy Malnutrition

A

Kwashiorkor
Marasmus
Cachexia
Anorexia nervosa

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6
Q

Kwashiorkor predominantly affects

A

Visceral protein - protein deficiency

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7
Q

Marasmus predominantly affects

A

SOMATIC protein

Protein AND energy - caloric deficiency

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8
Q

Marasmus~ starvation characterized by

A
Severe reduction in carloric intake
weight <60% of normal
growth retardation, loss of muscle 
PRESERVE visceral compartment
mobilize subcutaneous fat - decreased leptin
REDUCED BMR - opposite of cachexia
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9
Q

Marasmus may show clinical signs such as

A
  1. emaciation of extremeties
  2. Anemia
  3. Vitamin def
  4. Immune deficiency - T cell mediated - infections
  5. poor wound healing
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10
Q

Kwashiorkor characterized by

A

Greater protein deprivation than reduction in calories

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11
Q

Which PEM is more severe

A

Kwashiorkor IS MORE SERVERE than marasmus

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12
Q

Kwashiorkor may PRESENT as

A

60-80% normal weight
HYPOalbuminemia and EDEMA
FLAKY Paint skin lesions hyperpigmentation and hypo
Loos of color on hair

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13
Q

Clinical presentation of Kwashiorkor

A
1- Liver steatosis 
2- Apathy, listlessnes,anorexia 
3- vitamin deficiencies
4 - immune deficiency and infection
5- poor wound healing
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14
Q

Cachexia characterized by

A
  • loss of fat and muscle
  • INCREASED resting energy and BMR
  • result of TNF, IL-2, IL-6 and proteolysis inducing factor - PIF - tumor secretions
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15
Q

What does proteolysis inducing factor lead to

A

Breakdown of skeletal muscle

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16
Q

Clinical findings of anorexia nervosa are most similar to

A

Marasmus

  • effects on endocrine system
  • dehydration and electrolyte imbalance
  • lethal cardiac arrythmias
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17
Q

Medical complications of bulimia

A
  • electrolyte imbalance- HYPOKALEMIA
  • Pulmonary aspiration
  • Esophageal and gastric cardia tears
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18
Q

What % of adults overweight? and obese?

A

30% … and additional 30% (bmi>30)

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19
Q

Obesity is a disorder of…

A

ENERGY balance

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20
Q

Central processing of food intake/expenditure is through 2 anorexigenic factors

A

POMC

CART

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21
Q

Central processing of food intake/expenditure is through 2 ORExigenic neurons - make you hungry

A

Neuropeptide Y

AgRP

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22
Q

Leptin is secreted by (means thin)

A

Adipocytes

- binds to POMC and CART neurons

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23
Q

Net effect of leptin is TO

A

REDUCE food intake

INCREASE energy expenditure

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24
Q

Loss of function mutations in leptin lead to

A

Early onset severe obesity

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25
Q

Adiponectin is produced by

A

Adipocytes

  • directs FA to muscle for oxidation
  • Decrease INFLUX of FA to liver
  • Decrease glucose production in liver
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26
Q

What is the ONLY known hormone to increase FOOD intake - Orexigenic effect

A

GHRELIN

  • binds to NPY, and AgRP pathway
  • short term initiator of feeding
  • levels rise before meals
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27
Q

Obesity leads to increased expression of

A

IGF-1 - mitogenic and anti-apoptotic
HIF 1 and
VEGF
and leads to conversion of androgens to estrogen

28
Q

Insulin increases

A

Androgen synthesis in adrenals and ovaries

29
Q

Which vitamins can be synthesized endogenously?

A

D
K
Biotin
Niacin

30
Q

Which minerals are needed in large amounts - still micronutrients

A
  • Sodium
  • potassium
  • Calcium
  • phosphorus
31
Q

Which trace minerals are needed

A

Cobalt, Copper
Flourine, Iodine
Iron, Mg
Selenium, Zn

32
Q

Case: Flat occipital bones, Frontal bossing, deformation of chest, Rachitic rosary

A

Vitamin D deficiency

33
Q

Deficiency of vitamin K will cause

A

Bleeding

34
Q

Source of Vitamin D

A

Fish liver, plants, grains

>80% ENDOGENOUS SOURCE

35
Q

Vitamin D on skin synthesized from

A

7-dehydrocholesterol - need UV light

36
Q

What happens to Vitamin D in liver

A

add 25-OH

37
Q

What happens to Vitamin D in kidney

A

1,25 - added 1, from 1a hydroxylase

38
Q

What activates alpha-1-hydroxylase

A
  1. PTH

2. Hypophosphatemia

39
Q

What down regulates alpha-1-hydroxylase

A

High levels of 1,25 OH Vit D

40
Q

What is the function of Vitamin D

A

intestinal absorption of Ca and P
stimulate Ca reasborption from bone and from distal renal tubules via PTH
and for normal mineralization of bone

41
Q

Result of a Vitamin D deficiency

A

HYPOcalcemia - increased PTH production

42
Q

Clinical manifestation of Vit D deficiency

A
  • rickets - inadequatemineralization
  • inadequate calcification and overgrowth of epiphyseal cartilage
  • rachitic costochondral junction
  • in adults leads to osteomalacia
43
Q

Case: Alcohol abuse, bilateral foot drop, sensory loss, retrograde amnesia

A

Vitamin B1 - Thiamin deficiency

44
Q

Source of Vitamin B1 - Thiamin

A
  • in diet, not in polished rice, white flour, white sugar
45
Q

Function of Vitamin B1 -

A

Synthesis ATP- energy production
Cofactor for transketolase
Maintain neural membrane

46
Q

3 causes of thiamine deficiency

A

1- dietary insufficiency
2- Chronic alcoholism
3- excess vomiting diarrhea
- can get subclinical def - if you refeed/give glucose

47
Q

3 main areas affected by thamine deficiency

A
  1. Peripheral nerves - dry beriberi
  2. Heart - wet beriberi
    3- CNA - wernicke-kosrsakoff sybdrome
48
Q

What does dry beriberi result in

A

1 - symmertric polyneuropathy
2- first appears in legs
- toe drop, foot drop, sensory loss with hyporeflexia

49
Q

What does wet beriberi result in

A

1- CVD - peripheral vasodilation
2- rapid AV shunting of blood
3- High output cardiac failure
4- peripheral edema - enlarged heart

50
Q

What is Wernicke-Korsakoff syndrome

A

1- encephalopathy - confusion, opthalmoplegia

2- Korsakoff- retrograde amnesia, confabulation

51
Q

CNS lesions due to thiamine deficiency are found in

A

Mamillary bodies
Periventricular regions of thalams
Floor of 4th ventricle
Anterior cerebellum

52
Q

Case: Partial gastrectomy, megaloblastic anemia -

A

vitamin b12 deficiency

53
Q

Sources of Vitamin B12

A

animal proteins, meat, eggs

54
Q

Excess vitamin B12 stored in

A

Liver

55
Q

What is the function of B12

A

binds to Intrinsic factor (produced by parietal cells)

- forms a complex - dissociates in ileum - binds transcobalamin, delivered to bone liver, marrow, etc.

56
Q

Vitamin B12 deficiency can be due to

A
  • decreased intake
  • Intrinsic factor deficiency - gastrectomy - or pernicious anemia -
  • other malabsorption syndrome
57
Q

How does Vitamin B12 present

A

1- Megaloblastic anemia - (needed for DNA synthesis - and leads to defective erythrocyte maturation)
2- Neurological complications

58
Q

Case: DM, Hepatomegaly, slate-grey skin

A

Iron excess

59
Q

Normal iron absorption is

A

limited - iron efficiently re-utilized in the body

60
Q

Increase absorption of iron with

A

Ascorbic acid

61
Q

Iron excess can result frmo

A

Primary Hereditary Hemochromatosis

Secondary - ineffective erythropoiesis, increased intake, chronic liver diseaes

62
Q

Hereditary Hemochromatosis is a common

A

Autosomal recessive trait
more common in men
HIGH absorption - accummulation of iron in tissues

63
Q

Clinical manifestations of hemochromatosis

A

1 - hepatomegaly, fibrosis
2 -DM - pancreas
3- altered skin pigmentation
- cardiac problems - testicular atrophy

64
Q

how do you treat hemochromatosis?

A

Regular phlembotomy - and supportive treatment

65
Q

What risk has vitamin A shown in lung cancers

A

Increased risk

66
Q

Risk of vitamin A supplementation in head and neck cancers

A

Success in preventing squamous cell carcinomas

67
Q

Lycopene has been shown to have some

A

Antioxidant properties

- tomatoes -