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Multisystems > Path- Nutritional Pathology > Flashcards

Path- Nutritional Pathology Flashcards

1
Q

What are the 4 ways to assess protein-energy malnutrition?

A
  1. Body weight for a given height
    marasmus
  2. Midarm circumference
    - measures somatic protein compartment –>marasmus
  3. Serum proteins [albumin, transferrin]
    - measures visceral protein compartment–> kwashiorkor
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2
Q

What is the difference between primary and secondary energy malnutrition?

A

Primary- they do not have access to nutrition

  1. Marasmus
  2. Kwashiorkor

Secondary- supply of nutrients is adequate but:

  1. malabsorption
  2. impaired use/storage
  3. excess losses [cancer, AIDS]
  4. increased need [huntingtons]
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3
Q

What is marasmus a deficiency in?
What protein compartment is most affected?
What compartments of the body are maintained?
What will the patient look like?
What other problems are associated with the poor nutrition?

A

Deficiency in total calories.
Somatic protein compartment [skeletal muscle] and subcutaneous fat are lost.
Albumin/serum proteins are maintained.

The child will be emaciated [

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4
Q

What is kwashiorkor a deficiency in?
What protein compartment is most affected?
What compartments of the body are maintained?
What will the patient look like?
What other problems are associated with this?

A

Deficiency in protein.
Visceral compartment [serum, liver proteins] are most affected.
Somatic [skeletal] and subcutaneous fat are maintained.

The patient will have low serum albumin and transferrin, so they will have a protruberant belly due to hepatosplenomegaly and ascites. Weight loss is masked by fluid retention.

They will experience:

  1. immune deficiencies
  2. skin lesions -flaky paint, flag sign
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5
Q

Sometimes children with kwashiorkor are still so skinny that it is tough to see edema. Where should you look to see if they are edematous?

A
  1. back of hands/feet

2. around the eyes

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6
Q

What are 4 major causes of secondary protein-energy malnutrition?

A
  1. cachexia
  2. cancer, AIDS
  3. cytokines [IL1/6, TNF, IFNg]
  4. chronic GI disease, elderly, severe trauma, sepsis
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7
Q

What are the 3 main assessments of obesity?

Which one corresponds to central/visceral obesity and is associated with higher risk of obesity-associated diseases?

A
  1. BMI- weight in kg/height in sq meters
  2. Skin fold thickness
  3. Waist:Hip Circumference ratio ** higher the ratio, the more central/visceral obesity and more complications
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8
Q

What percent of adults in the US are overweight?

Obese?

A

50% are overweight and an additional 30% are obese

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9
Q

What are the major health complications associated with obesity?

A
  1. DM
  2. HTN
  3. atherosclerotic coronary artery disease
  4. DVT
  5. metabolic syndrome [insulin resistance, hypertriglyceridemia, low HDL, HTN, CAD]
  6. stroke
  7. NAFLD
  8. hypoventilation/OSA
  9. osteoarthrosis
  10. cancer
  11. dementia
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10
Q

How is the energy balance maintained in the body?

A
  1. Afferent arm [adipose, GI, pancreatic signals]
  2. Central sensor [hypothalamus]
  3. Effector arm [feeding behavior, energy expenditure]
  4. communication via neuropeptides/hormones
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11
Q

Describe the orexigenic arm of energy balance.
What is the effect of grehlin on this pathway?
What is the effect of leptin?

A

Orexigenic neurons –> neuropeptide Y–> melanin-concentrating hormone–> increased food intake, decreased energy expenditure.

Grehlin activates the orexigenic pathway [tells you to eat]
Leptin inhibits the orexigenic pathway [tells you to stop eating]

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12
Q

Describe the anorexigenic arm of energy balance.

What is the effect of grehlin? leptin?

A

Anorexigenic neurons–> MSH, cocaine, amphetamines–>thyrotropin releasing hormone, corticotropin releasing hormone–> decreased food intake, increased energy expenditure.

Grehlin decreases anorexigenic pathway
Leptin stimulates anorexigenic pathway

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13
Q

What mutation is associated with 4-5% of MASSIVELY obeses patients?

A

Melanocortin 4 receptor [target of anorexigenic neurons]

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14
Q

What are the fat soluble vitamins?
What do they need to be absorbed?
Are they stored in the body?
Are they more likely to cause pathology from excess or deficiency?

A

ADEK
They need bile to be absorbed
They are stored in the body
They can cause toxicity in excess [because they are stored so well, they rarely cause deficiency]

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15
Q

What are the water soluble vitamins?
Are they stored in the body?
Are they more likely to cause pathology from excess or deficiency?

A

C and B complexes
They are not stored in the body, except for B12 [cobalamin]
Deficiencies develop faster because they are not stored in the body

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16
Q

What is the storage/transport form of vitamin A?

A

Retinol

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17
Q

What are sources of vitamin A?

A
  1. Liver
  2. green leafy vegetables
  3. dairy
  4. dark orange/yellow fruits
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18
Q

What are the 4 functions of vitamin A?

A
  1. Beta-carotene [pro-vitA] = photo-protective, antioxidant
  2. retinal = visual pigments [rhodospsin, photopsin]
  3. Retinoic acid = cell growth and differentiation
  4. immunity to infections
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19
Q

What are the 5 manifestations of vitamin A deficiency?

A
  1. night blindness [earliest manifestation]
  2. Xerophthalmia [dryness from inability to produce tears]
  3. Squamous metaplasia of respiratory/urothelial mucousa
  4. follicular dermatosis
  5. immune deficiency
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20
Q

Acute toxicity with which vitamin presents like pseudotumor cerebri with headache, irritability, vomiting, stupor and papilledema?

A

vitamin A

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21
Q

Chronic toxicity with which vitamin presents with nausea, vomiting, weight loss, lip dryness, peeling skin, osteoporosis and bone pain, and hepatomegaly with fibrosis?

A

Vitamin A

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22
Q

What is the most severe side effect of isoretinoin/vitamin A toxicity?

A

Teratogen:

  1. cleft palate, small/missing ears
  2. cardio defects
  3. renal defect
  4. limb defects
  5. thymic agenesis
  6. embryonic lethality
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23
Q

What are the 2 forms of vitamin D?
Where does each come from?
Which is the major source of vit D in humans?

A

D2 - ergocalciferol form plant sterols, fish, grains

D3 - cholecalciferol made in skin from 7-dehydrocholesterol on exposure to UVB [animal sterol] *major source in humans

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24
Q

How is ergocalciferol and cholecalciferol processed in the body?

A
  1. 25-hydroxylation in the liver –>25-hydroxyvitaminD

2. 1-hydroxylation in kidneys–>1,25 dihydroxyvitamin D

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25
Q

What are the 4 major sources of vitamin D for humans?

A
  1. sunlight [UVB]
  2. fortified foods [milk,grain]
  3. fatty fish/fish oil
  4. plants, grains
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26
Q

What are the 3 major functions of vitamin D?

A
  1. intestinal absorption of calcium and phosphorus
  2. mobilization of calcium from bone
  3. parathyroid hormone dependent distal renal tubular reabsorption of Ca
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27
Q

What is the effect of vit. D deficiency in children?

Adults?

A

Deficiency causes excess unmineralized osteoid. So you make extra bone, it just doesn’t harden

Children –> rickets

  1. frontal bossing
  2. genu valgus, varus
  3. rachitic rosary
  4. Harrison’s groove [thoracic cage is wierd]
  5. kyphoscoliosis
  6. greenstick fractures
  7. widened wrists, ankles

Adults–> osteomalacia

  1. deranged bone remodeling
  2. gross fractures, microfractures
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28
Q

A patient presents with anorexia, nausea, and vomiting. He has polyuria, polydipsia. He is weak and nervous and itchy.
He has low specific gravity urine, proteinuria, casts and azotemia.
X-ray shows metastatic calcifications.

What vitamin toxicity is likely?

A

Vit D

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29
Q

What is the most active/abundant form of vitamin E?

What is the main function?

A

Alpha-tocopherol is an antioxidant and free radical scavenger

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30
Q

What are sources of vit E?

A
  1. vegetables
  2. grains/fortified cereal
  3. nuts and oils
  4. milk, fish, meat
  5. vitE supplements
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31
Q

What are the 4 major antioxidant nutrients?

A

ACE, selenium

32
Q

What are the 2 major problems associated with the RARE deficiency of vitamin E?

A
  1. neuropathy - posterior column, spinocerebellar degeneration
  2. hemolytic anemia
33
Q

What are 3 problems with the RARE toxicity of vitamin E?

A
  1. muscle weakness, fatigue
  2. nausea, diarrhea
  3. antagonizes vit K and enhances coumadin/anticoagulants
34
Q

What are 3 major sources of vitamin K?

A
  1. intestinal flora
  2. dietary
  3. efficiently recycled
35
Q

What is the main function of vitamin K?

A

It is a cofactor for microsomal g-glutamyl carboxylase that turns glutamine to glutamate to facilitate calcium binding

  1. procoagulant - 2, 7,9,10
  2. anticoagulant - protein C, S, Z
  3. proteins for bone metabolism - osteocalcin, calcification inhibiting matrix
  4. cell growth regulating arrest proteins
36
Q

Vitamin K deficiency is really rare because it is in the diet, gut flora, and is recycled. What 4 scenarios present with vit K deficiency?

A
  1. fat malabsorption, biliary tract disease
  2. broad spectrum antibiotics [destropy gut flora making vit K]
  3. neonates have a small reserve
  4. warfarin anticoagulant blocking Vit K epoxide reductase so it doesn’t get recycled
37
Q

What are the 2 negative effects associated with Vit K deficiency?

A
  1. bleeding diathesis

2. hemorrhagic disease in newborns

38
Q

Of vitamin K1, K2, and K3 which are toxic?

A 
K1 = phylloquinine = NOT toxic
K2 = questionable
k3 = toxic, menaquinones [precursors]
39
Q

An infant has anemia, hyperbilirubinemia, and kernicterus. What vitamin toxicity is associated with this?

A

Vit K [menaquinones]

40
Q

What are the sources of vitamin C?

A

Ascorbic acid in citrus fruit, liver, milk

41
Q

What are the 4 functions of vit C?

A
  1. activate prolyl and lysyl hydroxylase which is important for cross-linking and collagen stability
  2. antioxidant [scavenge free radicals, regenerate vit E]
  3. synthesize dopamine, NE, Epi
  4. synthesize carnitine
42
Q

A patient presents with various hemorrhages:

  • purpura, eccyhmoses on skin and mucousa
  • subperiosteal hemorrhages
  • retrobulbar, subarachnoid, intracerebral

She also has poorly formed osteoid matrix from cartilegenous overgrowth. Her legs are bowed and she has sternal depression.
There is a perifollicular rash, hyperkeratotic, papular rash ringed by hemorrhage.
Her wounds have impaired healing. What vitamin is deficient?

A

Vit C - Scurvy

43
Q

What is Vit B1?
What are the sources?
What is the function?

A

Thiamine- available in the diet, but deficient in refined foods.
Function:
1. carb/glucose metabolism
2. pentose phosphate pathway
3. maintain neural membranes and nerve conduction

44
Q

Chronic alcoholics are usually deficient in what vitamin?

A

B1 - Thiamine

45
Q

What are the 5 syndromes associated with deficient thiamine [B1]?

A
  1. dry beriberi
  2. wet beriberi
  3. wernicke encephalopathy
  4. korsokoff psychosis
  5. megaloblastic anemia, DM, sensineural deafness
46
Q

A patient presents with symmetric peripheral neuropathy. They have mixed motor and sensory symptoms. On exam they demonstrate food drop, toe drop and wrist drop.
What is this called?
What vitamin are they deficient in?

A

Dry beriberi and they are deficient in thiamine [B1]

47
Q

A patient presents with heart failure and peripheral edema. She has a cariomyopathy, and the heart is enlarged, globular, with 4 chamber dilation and thin ventricle walls. What is this presentation? What vitamin is she deficient in?

A

Wet beriberi–> B1 thiamine deficiency

48
Q

An alcoholic sustaining his diet with refined foods presents with opthalmoplegia, nystagmus, ataxia, and global confusion, apathy and disorientation. On imaging you see focal hemorrhage and necrosis of the mamillary bodies [as well as some periventricular thalamus, floor of 4th ventricle, anterior cerebellum].

What disorder does he have?
What vitamin is he deficient in?
Is this problem reversible or irreversible?

A

Wernicke’s encephalopathy

  • thiamine deficiency [B1]
  • REVERSIBLE
49
Q

An alcoholic sustaining diet with refined foods presents with retrograde amnesia with confabulation as well as anterograde amnesia [can’t learn new info].
Imaging shows lesion in the medial dorsal nucleus of the thalamus.

What disorder is this?
What vitamin is he deficient in?
Reversible or irreversible?

A

Korsakoff Psychosis

  • B1/thiamine deficiency
  • IRREVERSIBLE
50
Q

A malnourished alcoholic is in the hospital. The nurses decide to refeed him with IV glucose. What must you make sure they deliver WITH the glucose so as not to exacerbate a deficiency?

A

B1-thiamine

51
Q

What are sources of vitamin B2?

A

B2/riboflavin is found in:

  1. milk
  2. leafy veggies
  3. liver
  4. fortified foods
  5. coloring agents [yellow/orange]
52
Q

What is the main function of riboflavin [B2]?

A

riboflavin is a component of FMN and FAD so it is necessary for oxidation-reduction reactions to produce energy from carbs, fat, protein

53
Q

A patient presents with angular stomatitis [cheilosis], glossitis, interstitial keratitis, and dermatitis of cheeks scrotum and vulva.
What vitamin are they likely deficient in?

A

B2/riboflavin

54
Q

What are the 4 main sources of B3/niacin?

A
  1. meats/coloring
  2. grains, legumes
  3. seed oils
  4. endogenously synthesized from tryptophan [which also synthesizes serotonin, so a niacin def–> depression]
55
Q

What is the main function of niacin/B3?

A

It is a component of NAD and NADP so it is involved in dehydrogenation reactions in energy metabolism

56
Q

What are the 3 signs of a B3 deficiency?

A

Pellagra**

  1. Diarrhea [atrophy/ulcerations]
  2. Dermatitis [photosensitive, glossitis]
  3. Dementia [degeneration of neurons]
57
Q

What 3 naturally occuring substances comprise B6?

What are sources?

A
  1. pyridoxine
  2. pyridoxal
  3. pyridoxamine

Source: widely available in diet, so primary deficiency is rare.

58
Q

Primary deficiency is rare for B6, but what are 3 major causes of secondary deficiency?

A
  1. long term use of pyridoxine antagonists like ISONIAZID, ESTROGEN, PENICILLAMINE
  2. chronic alcoholism
  3. pregnancy
59
Q

What is the function of B6?

A

pyridoxal 5-phosphate participates in transamination, carboxylation and deamination in lipid, AA metabolism

60
Q

A women on long term estrogens begins experiencing the following symptoms:

  1. cheilosis
  2. dermatitis
  3. glossitis
  4. peripheral neuropathy
  5. convulsions.

What vitamin is it likely she is deficient in?

A

B6 [estrogens, penecillamine, isoniazid]

61
Q

What 5 things cause secondary deficiency of B9/folic acid?

A
  1. OCP, anticonvulsant, ethanol
  2. cigarettes
  3. malabsorption
  4. chemo [methotrexate–I DHFR]
  5. B12 deficiency [needed to convert methylTHF to THF]
62
Q

What is the main function of folic acid/B9?

A

synthesis of nucleic acids

63
Q

Deficiencies in which 2 vitamins leads to megaloblastic anemia?

A

B9 and B12

[huge cells, immature nuclei with 6 or more lobes]

64
Q

What are the 3 major problems associated with B9 deficiency?

A
  1. megaloblastic anemia
  2. GI problems
    - sore tongue/taste bud atrophy
    - small bowel villous/crypt atrophy
    - diarrhea
  3. Fetal neural tube defects
65
Q

A woman gives birth to a baby that has anencephaly, meningocele, spina bifida.
What was she deficient in?

A

folate / vitamin B9

66
Q

What is the only water-soluble vitamin to be stored in the human body?
What are sources?

A

B12-cobalamin [cobalt atom in a heme ring]

Meat
Fortified foods

67
Q

Describe the absorption of B12.

A
  1. digestion in stomack releases B12
  2. B12 binds salivary biding proteins [R-binders]
  3. Pancreatic protease releases B12-R in duodenum
  4. B12 binds IF secreted from gastric parietal cells
  5. IF-B12 attaches to receptors in distal ileum and is absorbed into enterocytes
68
Q

What is pernicious anemia?

A

Ab :

  1. attack parietal cells
  2. block attachment of IF to B12
  3. prevent binding of B12-IF in the distal ileum
69
Q

What is the function of B12?

A

Cofactor in the folic acid pathways

70
Q

What are the 4 major presentations of B12 deficiency?

A
  1. megaloblastic anemia
  2. GI symptoms
    - sore tongue/taste bud atrophy
    - small intestine crypt/villous atrophy
    - diarrhea
  3. neural tube defects [anencephaly, meningocele]
  4. Subacute Combined Degeneration of the spinal cord [dorsal column & corticospinal tracts]
71
Q

A patient presents with a hypochromatic, microcytic anemia. What trace element are they deficient in?

A

Iron:

  1. blood loss [chronic]
  2. inadequate diet
72
Q

A patient presents with a goiter and hypothyroidism. What trace element are they deficient in?

A

Iodine

73
Q

A patient presents with muscle weakness, neurological symptoms and abnormal collagen cross-linking. What trace element may they be deficient in?

A

Cu

74
Q

A patient presents with dental caries. What trace element might they be deficient in?

A

Fluoride

75
Q

A patient presents with myopathy and cardiomyopathy. What element might they be deficient in?

A

Selenium [antioxidant with vit E]

Multisystems (29 decks)

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