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5 NUTRITIONAL DISORDERS Flashcards

1
Q

The name “Vita” meaning, life was given by who?

A

Kazimerz Funk (polish biochemist)

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2
Q

Who discovered the first vitamin?

A

Japanese Dr. Umestro zuzuki (the B vitamin) around 1910

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3
Q

Why are vitamins important?

A

Because they are cofactors essential for enzyme activity in biochemical reactions

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4
Q

What are the 2 types of vitamins?

A

water soluble (Bs and Cs) and Fat soluble (A, D, E, K)

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5
Q

What is Vitamin B1?

A

Thiamin

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6
Q

What does Thiamin (B1) do?

A

Maintains neural membranes and good nerve conduction, especially in peripheral nerves.

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7
Q

What will a deficiency in Thiamine (B1) cause?

A

Impairments in neuronal conduction

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8
Q

What are the most important sources of B1 (Thiamine)?

A

Husks of grains (unpolished grains)

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9
Q

Why is it important to only eat unpolished grains when getting a B1 Thiamine source?

A

Refined grains like white rice LOSE B1, which may lead to a deficiency of the vitamin. China has many deficiencies in their diet when they eat more white than brown rice.

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10
Q

What does B1 prevent the development of?

A

Cancer

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11
Q

What is the disease associated with deficiency of B1?

A

BERI BERI

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12
Q

Where is BERI BERI predominantly seen? (In what patients)

A
  • Alcoholics
  • 1st trimester pregnancy
  • Faster growing teens
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13
Q

Why do alcoholics develop B1 deficiencies?

A

Alcohol competes with B1 in neural functions and in biochemical reactions

(They are also more likely to spend money on alcohol than food)

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14
Q

Why are pregnant women more likely to be B1 deficient?

A

The 1st trimester of pregnancy causes morning sickness. Vomiting causes the pregnant women to lose the vitamins and nutrition needed.

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15
Q

Why are fast growing teens likely to have a Thiamine deficiency?

A

They are using up all their nutrients and vitamins faster. They need replacement

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16
Q

What is Vitamin B1 (Thiamine) deficiency?

A

Beriberi

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17
Q

Who discovered Beriberi?

A

Christiaan Eijkman (food consumption vs deficiency)

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18
Q

What is Beriberi?

A

Severe nervous system disorder, and it has 3 types

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19
Q

What are the 3 types of Beriberi, and what are the typical stages?

A

1) Dry
2) Wet
3) Wernicke Encephalopathy

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20
Q

What does Dry Beriberi predominantly affect?

A

The nervous system

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21
Q

What is Dry Beriberi categorized by?

A

It is characterized by a symmetrical peripheral polyneuropathy with MYELIN DEGENERATION and disruption of all 3 neurological arcs:

Sensory, Motor, and Reflex arcs

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22
Q

What are the manifestations or clinical signs of Dry Beriberi?

A

Wrist drop, Foot drop, and big toe drop

Paresthesia, numbness, and loss of reflexes

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23
Q

What does Wet Beriberi predominantly affect?

A

The Heart

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24
Q

What is Wet Beriberi characterized by?

A

Damage to the cardiovascular system, and it is called “Wet” because it is found in the BLOOD

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25
Q

What are the physical manifestations of Wet Beriberi?

A

Enlargement of the heart with thinning of the heart (muscle) wall = WEAK HEART

FLABBY MYOCARDIUM

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26
Q

What happens peripherally in Wet Beriberi?

A

Causes peripheral vasodilation peripheral edema (pitting edema)

  • Occasionally Cardiac Failure
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27
Q

What is the most common thing seen with Wet Beriberi?

A

Dilated Cardiomyopathy

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28
Q

In what form of Beriberi would you see Dyspnea and Othropnea ?

A

WET BERIBERI

“Shortness of breath”

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29
Q

What are the 2 things associated with Wernicke Korsakoff?

A

Wernicke Encepalopathy and Korsakoff’s Psychosis

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30
Q

What does Wernicke Encephalopathy affect?

A

The mammillary bodies in the brain - Atrophy

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31
Q

What is Wernicke Encephalopathy characterized by?

A

Psychological problems

  • Global confusion
  • Apathy
  • Listlessness (not caring about anything)
  • Disorientation
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32
Q

What is the most dangerous symptom of Wernicke Encephalopathy?

A

Opthalmoplegia:

It is a paralysis of one or more eye muscles causing a non symmetrical eye movement

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33
Q

What can happen as a result of Opthalmoplegia (Wernicke Encephalopathy)

A
  • Deep damage of CNS
  • Results in irregular eye movements, not simultaneous
  • Patient is close to death when this is seen
  • Confusion, death, and coma
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34
Q

What are the 3 manifestations of Korsakoff’s Psychosis?

A

1) Anterograde amnesia
2) Retrograde amnesia
3) Confabulation

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35
Q

What is Confabulation (associated with Korsakoff’s Psychosis)?

A

Unawareness of telling invented stories and memories (unconcious lying)

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36
Q

What is Vitamin B2?

A

Riboflavin

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37
Q

When is Vitamin B2 (Riboflavin) usually seen?

A

Usually seen in people with long term chronic debilitating diseases (cancer or renal diseases)

  • This is called Arriboflavinosis
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38
Q

What is Riboflavin required for?

A

The proper development and function of the skin, lining of the digestive tract, blood cells, and many other parts of the body

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39
Q

What are the 4 major symptoms of Vitamin B2 (Riboflavin) deficiency?

A

1) Cheilosis
2) Glossitis
3) Superficial Interstitial Keratitis
4) Dermatitis

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40
Q

What is Cheilosis?

A

(Non-inflammatory)

Cracks in the corner of the mouth, and if infection occurs then it becomes CHEILITIS

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41
Q

What is Cheilitis?

A

A secondary infection of Cheilosis

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42
Q

What is Glossitis?

A

Inflamed tongue, may lead to atrophy of tissue and loss of taste

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43
Q

What is Superficial Interstitial Keratitis?

A

Hardening of the cornea.

  • Some structures do not have blood supply like cartilage, 2/3 of the IVD and the cornea. The cornea relies on intraocular fluid and tears to get nutrients and to eliminate waste material
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44
Q

What happens to the cornea with a deficiency in Riboflavin (B2)?

A

A capillary net forms around and it penetrates into the cornea resulting in inflammation and damage to the cornea (ULCERATION)

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45
Q

What is an Ulceration associated with a Riboflavin deficiency?

A

Painful due to nociceptors in the cornea. As the cornea begins to heal > fibrosis and loss of vision develops

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46
Q

What is Dermatitis? (Associated with B2 deficiency)

A

Inflammation seen in 3 main parts: Especially nasolabial folds, behind the ears, and groin

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47
Q

Does B2 affect the nervous system?

A

NO

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48
Q

What is Vitamin B3?

A

Niacin (nicotinic acid, nicotinamide)

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49
Q

What is Niacin used as?

A

Medicine for its vasodilation ability (nitroglycerine treatment)

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50
Q

How is Niacin produced?

A

Via normal gut flora from tryptophan, but major source is via diet

  • In corn, B3 is bound and cannot be absorbed when eaten
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51
Q

What is the main health function of B3 (niacin)?

A

Leads to decreased production of lipoproteins (LDLs) = Prevention of arteriosclerosis

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52
Q

What does the Deficiency of Niacin (B3) result in?

A

4 D’s!

1) Dermatitis
2) Diarrhea
3) Dementia
4) Death

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53
Q

What does Dermatitis cause in Vitamin B3 Niacin deficiency?

A

It develops on skin exposed to sun

  • Casal’s necklace
  • Glove and stocking lesions
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54
Q

Why do patients have Diarrhea with Niacin deficiency ?

A

Atrophy of epithelial cells of intestinal mucosa with involvement of submucosal layer

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55
Q

Why does dementia occur in Niacin deficiency?

A

Degeneration of cortical neurons in the white matter

  • Loss of Neurological function
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56
Q

What is Vitamin B6?

A

Pyridoxine

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57
Q

What is the distinct characteristic of Vit B6 (Pyridoxine)?

A

It is Thermolabile (a small amount of heat will destroy it)

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58
Q

What can cause a deficiency in B6 (Pyridoxine)?

A

Some drugs and treatments compete with B6 in biochemical reactions and may lead to deficiency

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59
Q

What are the 3 drugs that may lead to a deficiency in B6 Pyridoxine?

A

1) Izoniazid
2) Estrogens
3) D-Penicillamine

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60
Q

What is Izoniazid?

A

Anti-tuberculosis medication, not used as often today

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61
Q

What are Estrogens (associated with Pyridoxine deficiency)?

A

High production of estrogens or hormone treatments can cause B6 deficiency

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62
Q

What do estrogens have?

A

Hyperplastic activity > promotes replication of cells especially in endometrium, which could lead to cancer

  • Predisposes to breast and uterine cancers
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63
Q

What is D-Penicillamine used for?

A

For treatment of Wilson’s disease and systemic sclerosis (scleroderma)

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64
Q

What is Wilson’s Disease?

A

Aka Hepatolenticular Degeneration

  • An autosomal recessive genetic disorder in which copper accumulates in tissues; this manifests as neurological or psychiatric symptoms and liver disease. It is related with medication that reduces copper absorption or removes the excess copper from the body, but occasionally a liver transplant is required.
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65
Q

What deficiency is related to increased sloughing of epithelial cells?

A

Vitamin B6 (Pyridoxine)

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66
Q

What is the characteristic of epithelial cells?

A

They have decreased life span, rapid turnover

B6 Pyridoxine

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67
Q

What type of dermatitis is associated with B6 Pyridoxine deficiency?

A

Seborrheic dermatitis

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68
Q

What is Seborrheic Dermatitis?

A

Sloughing of the skin, dermatitis that usually affects the scalp (hair cells)

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69
Q

What can Seborrheic Dermatitis cause?

A

Dandruff (caspa): shedding of dead skin from the scalp

  • Scaly and greasy squamous epithelial cells
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70
Q

What Vitamin is a Nidus categorized with?

A

Vitamin B6 Pyridoxine

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71
Q

What is a nidus?

A

Stones formation in urinary tract

  • Nidus is the organic core, the site of origin of something. In this case, a clump of epithelial cells that form inside the bladder‘ It can grow larger to form STONES in urinary tract
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72
Q

What can B6 Pyridoxine deficiency lead to?

A
  • Cheilosis/cheilitis
  • Glossitis
  • Peripheral Polyneuropathy
  • Convulsions: Especially in infants and children
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73
Q

What is Vitamin B12?

A

(cyan) cobalamin (AKA extrinsic factor of Castle)

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74
Q

What is a distinct characteristic of B12?

A

It cannot be absorbed by the GI tract

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75
Q

What is B12’s main role?

A

In the normal function of the NS and in formation of RBC’s (erythropoiesis). It is used by every cell for normal metabolism function

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76
Q

Can B12 be directly absorbed?

A

NO, it requires assistance via proteins

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77
Q

What is the process of B12 as soon as it touches your tongue?

A

Salivary glands secrete R-binder protein. R-Binder binds to B12 and carries it from the stomach to the duodenum where they dissociate. B12 becomes free again

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78
Q

What do stomach parietal cells produce?

A

They produce and secrete Intrinsic Factor aka (Intrinsic factor of Castle) which then moves into the duodenum

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79
Q

Once R-Binder protein (bound to B12) and Intrinsic Factor move to the duodenum what happens?

A

Once they are both in the duodenum, intrinsic factor and extrinsic factor (B12) bind and move together into the ileum

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80
Q

What is special about the ileum in regard to B12?

A

The ileum has special receptors only for the intrinsic factor, When both get to the ileum wall, extrinsic factor binds and leaves intrinsic factor free again so that it can flow into the blood circulation and be recycled

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81
Q

Is intrinsic factor essential for B12 resorption?

A

YES

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82
Q

What would cause B12 deficiency beside not enough meat intake?

A

Surgical removal of stomach or ileum, and alcoholism.

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83
Q

What are 2 disorders that affect the ileum?

A

Celiac disease and Crohn’s disease

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84
Q

What medications can lead to B12 deficiency?

A
  • Ranitidine
  • Metformin
  • Both of these are used in Diabetes Mellitus
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85
Q

What causes Pernicious Anemia?

A

B12 Deficiency

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86
Q

Pernicious Anemia aka

A

Malignant Anemia (leads to death)

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87
Q

What is Pernicious Anemia?

A

Autoimmune disease that can lead to B12 deficiency

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88
Q

What would you see in Pernicious Anemia?

A

Decreased RBCs, decreased hemoglobin in RBCs or both

89
Q

In what ways can Pernicious Anemia be autoimmune?

A

1) Blocking Antibodies (Type 1)
2) Binding Antibodies (Type 2)
3) Parietal Canalicular Antibodies (Type 3) - Autoimmune Chronic Gastritis

90
Q

What is “Blocking Antibodies” associated with Pernicious Anemia?

A

Bind to intrinsic factor, blocking the receptor for B12. B12 cannot bind to the intrinsic factor.

91
Q

What is “Binding Antibodies” (Type 2) in regard to Pernicious Anemia?

A

Bind to receptors for intrinsic factor in the ileum.

Intrinsic factor (bound to extrinsic factor) cannot pass through to the GI wall and enter the blood circulation

92
Q

What is “Parietal Canalicular Antibodies” (Type 3) - Autoimmune Chronic Gastritis associated with Pernicious Anemia?

A
  • Immune system produces parietal canalicular antibodies (Type III) which destroy parietal cells in the stomach. This results in no production of intrinsic factor and B12 CANNOT be absorbed
93
Q

Megaloblastic Anemia’s are caused by what 2 factors?

A

1) Vitamin B12 deficient anemia (pernicious anemia)

2) Folic Acid deficient anemia

94
Q

What are the 2 things that provide the normal process of erythropoiesis?

A
  • Folic acid donates a carbon to DNA in blood cells

- B12 activates tetrahydrafolate which promotes the process

95
Q

What is the biochemical pathway when folic acid is eaten?

A

It’s converted to Monoglutamate in blood circulation. Then into Tetrahydrofolate (active form) by reductase enzyme. Then Tetrahydrofolate donates a carbon unit to the DNA in blood cells, and Tetrahydrofolate is now in its inactive form due to loss of C unit (inactive form means that it cant attach to anything). Then Vitamin B12 converts the inactive Tetrahydrofolate into active Tetrahydrofolate so that it can now donate more carbon units for the normal formation of RBC’s.

96
Q

How many times is the biochemical pathway performed in Megaloblastic Anemia?

A

Cycle from active to inactive continues 10-12 times before Tetrahydrofolate is discarded.

  • Reusing material allows for a higher speed of production (hematopoeisis) rather than using Tetrahydrofolate only once.
97
Q

What occurs in Megaloblastic Anemia?

A

There is inhibition of DNA synthesis during RBC production. Cells keep growing, but without division which causes ENLARGED cells.

98
Q

Why does adding folic acid help in a Vit B12 deficiency?

A

This gives the patient carbon to make DNA, and the Tetrahydrofolate could only be used once.

  • Process will depend on FOLATE RECYCLING
99
Q

Does adding B12 help in a folic acid deficiency?

A

NO, if a patient is showing anemia due to folic acid deficiency, this means there is no Tetrahydrofolate. Adding the “Activator” (B12) does nothing if there is no tetrahydrofolate

100
Q

Either deficiency of B12 or Folic acid results in what?

A

Big/Large blood cells (RBCs, WBCs, and Platelets) called Macrocytes (Macrocytosis)

101
Q

What are the blood cells affected by Megaloblastic Anemia?

A

RBC’s, Neutrophils, and Platelets

102
Q

What is the appearance of the RBC’s during Megaloblastic anemias?

A

They are found in a blastic form, aka immature form

103
Q

What is the function of RBCs during Megaloblastic anemias?

A

Immature and dysfunctional RBC’s (Megaloblasts) normally found in the red bone marrow or in very small amounts in blood circulation

104
Q

What is an example of RBC’s in a blastic form aka immature form?

A

Pernicious anemia (type of megaloblastic):

RBC’s are too big to fit in the capillary pores and get to the tissue > folding occurs > their membrane is rigid > decreased O2/nutrient exchange > decreased supply to tissue > DEATH

105
Q

What do Neutrophils look like in Megaloblastic anemia?

A

They are hypersegmented: Nuclear lobes >5 (normal 2-4) is an ABSOLUTE SIGN OF MEGALOBLASTIC ANEMIA

  • They appear in the peripheral blood circulation
106
Q

What is Pancytopenia associated with?

A

Megaloblastic Anemia

107
Q

What is Pancytopenia?

A

Total decrease in the number of blood cells (RBC’s, WBC’s, and Platelets)

  • Anemia = Decreased RBCs
  • Leucopenia = Decreased WBCs
  • Thrombocytopenia = Decreased Platelets
108
Q

What signs and physical symptoms will you see with Folic acid deficiency?

A

Cheilosis/Cheilitis and Glossitis are associated in early stages of folic acid deficiency (not in B12)

  • B12 supplementation DOES NOT HELP
109
Q

Does Folic acid deficiency affect the nervous system?

A

NO (except for the developing fetus), but B12 does

110
Q

What is the main drug used in the treatment of Leukemia?

A

Methotrexate

Works against reductase enzyme

111
Q

What does Methotrexate do?

A

Inhibits reductase > No tetrahydrofolate reactivation > Thereby interfering with hematopoeisis

112
Q

What is the purpose of Methotrexate?

A

Prevent cellular replication (hematopoiesis) of cancer cells

113
Q

What is the consequence of Methotrexate?

A

Suppressed immune system function - DECREASED WBCs

114
Q

What nervous system function can B12 deficiency lead to?

A

Demyelination

  • Myelin degeneration = Decreased rate of conduction
115
Q

What specific parts of the body are affected by Demyelination (B12 deficiency)?

A

Posterior and Lateral column tracts of the spinal cord, peripheral nerves, and DRG

116
Q

What does demyelination from B12 deficiency result in?

A
  • NUMBNESS and TINGLING in hands/feet
  • ATAXIA: Abnormal gait because of spinocerebellar tract involvement
  • PARAPLEGIA: Subacute combined degeneration of the spinal cord
    > Affects PNS
    > May affect CNS = “Megaloblastic Madness”, cognitive dysfunction
117
Q

Are nervous system changes associated with B12 deficiency reversible?

A

NO they are IRREVERSIBLE

118
Q

What is the correlation between severity of pernicious anemia and severity of Demyelination in B12 deficiency ?

A

There is NO correlation

119
Q

Giving _______ to people with B12 nervous system pathology may _______ nervous system problems

A
  • Folic acid

- Exacerbate

120
Q

What are the main functions of Vitamin C?

A
  • Hydroxylation of pro collagen
  • Synthesis of Collagen Peptides
  • Free radical Scavenger
121
Q

What is “Hydroxylation of Procollagen” under Vit C functions?

A
  • Procollagen is full of proline, and proline is Hydroxylated by Vitamin C to become hydroxyproline
122
Q

What is the function of Hydroxyproline?

A

Makes connective tissues, strong and increases tensile strength

123
Q

Procollagen is not hydroxylated, what happens?

A

Proline is weak - collagen is weak (especially blood vessels - bleeding)

124
Q

In what way is Vitamin C a free-radical scavenger?

A

Powerful antioxidant, works with Vitamin E (secures cell membranes from disruption - with selenium)

125
Q

What does vitamin C reduce?

A

Reduces oxidation of LDLs (Theoretically decreasing atherosclerosis condition)

126
Q

What 3 diseases is Scurvy associated with?

A

1) Bleeding Diathesis
2) Skeletal Changes
3) Wound Healing

127
Q

What is the Bleeding Diathesis associated with Scurvy?

A

Development of Petechiae rash and ecchymosis

  • Bleeding of gums and tooth loss
128
Q

What 2 types of tumors are associated with Scurvy (Bleeding Diathesis)?

A

Subperiosteal Heamatomas and Retrobulbar Hematomas

129
Q

What is a subperiosteal hematoma?

A

Hematoma between periosteum and bone

130
Q

What can a subperiosteal hematoma lead to?

A

Bleeding into the joint space - Iron is deposited from the heme group and destroys the articular cartilage leading to hemarthrosis

  • SECONDARY OA (BOWING)
131
Q

What is a retrobulbar hematoma?

A

Blood behind eyeball

  • Increased pressure pushes the eye forward (loss of vision)
132
Q

What gets disturbed in skeletal changes regarding Scurvy?

A

Osteoid Matrix (stroma)

133
Q

What is the Osteoid Matrix?

A

When bones are developing, it starts with connective tissue, stroma (outline) which is embedded with calcium salts for the osteoblasts to make strong bone

  • Bone growth in children, there is cartilage that will become mineralized by the osteoblasts and make it bone
134
Q

What happens to the osteoid matrix in Scurvy?

A

With scurvy, connective tissue is of poor quality and the osteoid matrix, the outline, is weak/delayed (in kids) - provisional calcification occurs > Weak soft bones = bowing legs

135
Q

What major sign will you see in kids with Scurvy?

A

Rickets (bowing of legs) and Protrusion of ribs and sternum

“PIGEON CHEST”

136
Q

In what way is wound healing tampered with in Scurvy?

A

It is delayed, this is due to weak stroma. (Long periods of healing)

  • Repair by fibrosis
137
Q

In what way could Hypervitaminosis of VIT C be bad?

A

It is usually used to fight common cold, however, there can be a relapse because too much Vit C could result in elimination of Vit C.

  • It can also lead to Hemorrhagic strokes
138
Q

Who and when discovered Vitamin A?

A

Professor McCollum June 1913

139
Q

What are the forms of Vitamin A?

A
  • Retinol (Vit A)
  • Retinal (Provitamin A)
  • Retinoic Acid
140
Q

What is Retinol (Vitamin A)?

A

Storage and Transport form; 90% stored in the LIVER and the amount kept in storage is enough to supply the body for 6 months

141
Q

What is Retinal (Porvitamin A)?

A

Maintains normal vision in dim light

142
Q

What is Retinoic Acid?

A

Important in determining life span of epithelial cells

143
Q

What are the 2 types of things found in Vitamin A?

A

Carotenoids and Retinoids

144
Q

What is better for you, Carotenoids or Retinoids?

A

Carotenoids are the natural precursor for retinal aka provitamin A (beta carotene)

  • Retinoids are synthetic/artificial (teratogenic affect)
145
Q

What is the function of Retinal (provitamin A)?

A
  • Maintains normal vision in reduced light

- Important in the production of visual pigments in photoreceptors: Rods - rhodopsin, cones - iodopsin

146
Q

What would deficiency in Retinal do?

A

Result in night blindness aka chicken disease/blindness

147
Q

What does Retinoic acid do?

A

Potentiation and differentiation of specialized epithelial cells, mainly mucous - secreting cells

  • Accounts for the normal life span of epithelial cells (ducts of glands, GI tract, and skin)
148
Q

Deficiency of Retinoic Acid would cause what:

A
  • Xeropthalmia
  • Xerosis
  • Squamous Metaplasia
149
Q

What is Xeropthalmia (associated with deficiency in Retinoic Acid)?

A

Dry Eyes - Due to obstruction of ducts of lacrimal gland; because epithelial cells have a decreased life span, increased sloughing of cells, clump together and block ducts.

150
Q

What is Xerosis associated with Retinoic Acid (Vit A def.)?

A

Dryness pathology - Accumulation of sloughed epithelial cells of conjunctiva in the cornea forming plaques close to cornea = BITOT’S SPOTS

151
Q

What do BITOT’S SPOTS lead to ?

A

Keratomalacia (softening of the cornea > loss of blood vessels > corneal ulcer > loss of transparency of the cornea results in blindness

152
Q

Where would you find Squamous Metaplasia?

A

Deficiency of Retinoic Acid (Vit A deficiency)

  • This is keratinizing squamous cells epithelium and Metaplasia can lead to cancer
153
Q

Follicular and Papullar dermatosis, and Pulmonary infection is associated with what deficiency?

A

Vitamin A (Retinoic Acid)

154
Q

What can happen in the GI tract if there is a deficiency of Vit A (Retinoic Acid)?

A

Nidus formation (organic core stones > urinary tract obstruction)

155
Q

What are the 3 main functions of Vit A?

A

1) Maintains normal vision in reduced light
2) Potentiation and differentiation of specialized epithelial cells, mainly mucous-secreting cells
3) Enhancement of Immunity

156
Q

What is Enhancement of Immunity in regard to Vitamin A function?

A

Infections, particularly in children

  • 30% decrease in mortality rate due to measles, pneumonia, and infection diarrhea with Vit A treatment
157
Q

What are the signs and symptoms of acute Hypervitaminosis A ?

A

Similar to that of a brain tumor or intracranial pressure

  • Increased intracranial pressure > headache, nausea/vomiting, papilledema (swelling of optic disc)
158
Q

What signs and symptoms will you see with Chronic Hypervitaminosis A?

A
  • weight loss
  • nausea, vomitting
  • Dryness of mucosa of lips
  • Bone and joint pain
159
Q

What is a major symptom associated with Chronic Hypervitaminosis A?

A

Heptaomegaly

  • Liver is storing excess (stored as retinol ester) resulting in mechanical pressure on the hepatocytes
160
Q

What disease may be seen as a result of Chronic Hypervitaminosis A?

A

Liver fibrosis (increased pressure causes atrophy, fibrosis)

161
Q

What is the worst disease associated with Chronic Hypervitaminosis A?

A

Hyperostosis (aka DISH aka Forestier’s Disease)

  • Ossification of the ligaments specially the ALL (And/or rarely PLL), overgrowth of bones beyond its boundaries > FUSION

** DISH = Diffuse Idiopathic Skeletal Hyperostosis

162
Q

What is a collective name of Vitamin E?

A

4 tocopherols and 4 tocotrienols

163
Q

What is the main function of Vitamin E?

A

Antioxidant. Antioxidants neutralize free radicals > free radicals destroy lipids > cell membranes > cellular death

164
Q

What would cause a deficiency of Vitamin E?

A

Damage of neuron membranes, damage to RBC membrane

165
Q

What does Vitamin E function in?

A

In cell membrane maintenance - protects/repairs damage from free radicals > antioxidant in concert w/vitamin C and selenium

166
Q

What are the 2 types of cell membrane most susceptible to Vitamin E deficiency?

A

RBCs and Neurons

167
Q

What would deficiency in Vitamin E result in?

A

Nervous system pathology and RBC pathology

168
Q

In what way is there a Nervous system pathology with Vit E deficiency?

A
  • Degeneration of axons in the POSTERIOR columns of spinal cord
  • Loss of nerve cells in the DRG
  • Myelin degeneration of sensory axons in the peripheral neurons
169
Q

What degenerative changes in the spinocerebellar tract occur due to Vit E deficiency?

A
  • Absent tendon reflexes
  • Ataxia - lost balance
  • Dysarthria
  • Loss of Position and vibration sense
  • Loss of Pain sensation (DRG)
170
Q

Describe what RBC pathology means to Vitamin E deficiency?

A

RBC pathology (most damaged cells)

  • Usually does not result in anemia EXCEPT in premature infants whose RBCs are more susceptible to destruction
171
Q

What is the result of Hypervitaminosis E?

A

Decreased coagulative ability of blood due to interference with Vit K > Decreased production of clotting factors

(Impairs normal function of Vit E)

172
Q

What does Vit E inhibit?

A

Atheroma formation in atherosclerosis (through reducing oxidation of LDLs)

173
Q

What is the main role of Vitamin K?

A

Coagulation of blood, without it, clotting cannot occur

174
Q

What is Vit K produced by?

A

Gut Flor, and any food usually animal product

175
Q

What are the clotting factors that Vit K plays a role in the production of?

A

(Produced in the liver)

  • CF2 Prothrombin
  • CF7 Proconvertin
  • CF9 Christmas Factor
  • CF10 Stuart Prower Factor
176
Q

What is Vitamin K used in (besides the production of clotting factors)?

A

Production of proteins

177
Q

What is the hormone that is indirectly stimulated through Vit K?

A

Osteocalcin

178
Q

What is Osteocalcin?

A

A hormone that promotes calcification/mineralization of bones; mineralization of bones (indirectly prevents osteoporosis)

> INDIRECTLY participates in promoting bone calcification

179
Q

What does Deficiency of Vitamin K produce?

A

Hemorrhagic disease of newborns > could result in Intracranial Hemorrhage (stroke) of a baby

180
Q

Why could a baby develop Bleeding Diathesis (hemorrhagic disease)?

A

Baby’s normal gut flora is not yet established = No vitamin K

181
Q

What is recommended of pregnant mothers to do (Vit K)?

A

2-4 weeks prior to delivery, take a Vit K supplement according to OB/GYN direction

(Especially if the mom is taking anti TB or anticonvulsants)

182
Q

What is the biggest symptom of Vit K deficiency ?

A

Malena = Black stool (usually the term used for any hemorrhage, bleeding from the GI tract, stomach)

183
Q

What is PEM?

A

Protein Energy Malnutrition

184
Q

What does PEM refer to?

A

A range of clinical syndromes characterized by an inadequate dietary intake of proteins and calories to meet the body’s needs. Usually seen in children

*LACK OF PROTEIN, CALORIES, OR BOTH

185
Q

What are the 2 protein compartments that we have?

A

Somatic and Visceral

186
Q

What is the Somatic Protein Compartment involved in?

A

Accumulation of protein in the skeletal muscle, and it is a reserve protein source (take from there only if needed)

187
Q

What is the Visceral Protein Compartment that we have?

A

Accumulation of protein in the Viscera

  • Predominantly in the liver
188
Q

What protein compartment is used to check for blood protein level?

A

Visceral Protein Compartment

  • Determines if this compartment is used by checking blood protein level (specifically albumin - look for hyperalbuminemia)
189
Q

Malnourished:

A

< 80% of normal weight

190
Q

Kwashiorkor :

A

60-80% of normal weight

191
Q

What is Marasmus?

A

Lack of energy (calories) and protein. Imparement of somatic protein compartment used resulting in EMACIATED EXTREMITIES

192
Q

What portion of the body protein is affected in Marasmus?

A

Visceral protein is untouched, therefore blood (serum) albumin level is close to NORMAL

193
Q

What are the symptoms of Marasmus?

A
  • Growth retardation
  • Extremities emancipated (key for diagnosis) > bone fractures
  • Head is larger than body
  • Anemia: lack of nutrient (hypoalbulinemia is not related)
  • Multivitamin deficiency
  • Decreased immune function - very vulnerable to infection
194
Q

Is there any decrease in the visceral protein compartment of Marasmus?

A

NO

195
Q

Kwashiorkor aka

A

“First-Second”, because this occurs most often during the first or second month of birth; in 3rd world countries where a breast feeding infant is displaced by the birth of the mother’s 2nd child)

196
Q

What is the actual food problem with Kwashiorkor?

A

Enough energy (calories), not enough protein - only eating carbs

197
Q

Which is worse, Kwashiorkor or Marasmus?

A

Kwashiorkor is WORSE because it leads to IRREVERSIBLE CHANGES

198
Q

What is depleted in Kwashiorkor?

A

Visceral protein compartment =

  • Blood albumin level is low > HYPOALBUMINEMIA
  1. Albumin
  2. Globulin
  3. Fibrinologin
199
Q

Explain why there is generalized edema** with Kwashiorkor:

A

Albumin is responsible for maintaining normal capillary oncotic pressure

Normally keeps serum in the vessels (keeps blood within blood vessels), but when albumin is low, serum moves into the tissues - GENERALIZED EDEMA**

200
Q

What are the symptoms of Kwashiorkor?

A
  • Generalized edema
  • Hair changes
  • Skin lesions
  • Fatty liver (steatosis)
  • Hepatomegaly
201
Q

What happens to the skin during Kwashiorkor?

A

Skin ruptures due to excessive edema, stress on the skin

  • There is generalized edema in SC tissue and cavities
202
Q

What are the Hair Changes that occur in Kwashiorkor?

A
  • Loss of color (turns gray), alternating band of pale and darker hair
  • Straightening
203
Q

What are the skin lesions that occur during Kwashiorkor?

A
  • Zones of hyperpigmentation
  • Areas of desquamousation
  • Hypopigmentation = “Flakey Paint” appearance of skin due to decrease in melanocytes
204
Q

What happens to the liver during Kwashiorkor?

A

Fatty liver (steatosis)

  • Hepatomegaly (filled with fat) > LIVER FIBROSIS
205
Q

What are the milder symptoms associated with Kwashiorkor?

A
  • Apathy, listlessness, anorexia (lots of carbs)
  • Decreased immunity (cause need protein for immunity and there is deficiency in protein) > VULNERABLE TO SECONDARY INFECTIONS**
206
Q

Which disease has a HIGHER mortality, Kwashiorkor or Marasmus?

A

Kwashiorkor

207
Q

What is Anorexia Nervosa?

A

Self induced starvation, resulting in marked weight loss

208
Q

What does Anorexia Nervosa cause damage to?

A

To the Endocrine System - especially pituitary and thyroid glands

209
Q

What are the 4 major symptoms associated with Anorexia Nervosa?

A

1) Amenorrhea
2) Hypothyroidism
3) Decreased immune system
4) Hypokalemia

210
Q

What is Amenorrhea, associated with Anorexia Nervosa?

A

Huge decrease in gonadotropin-releasing (GnRH), leutinizing (LH), and follicle stimulating (FSH) hormones from pituitary (abnormal/dysfunction condition)

211
Q

What is the most common cause of death of people with Anorexia Nervosa?

A

Hypokalemia - Resulting in arrhythmia

212
Q

What is a tell all sign in women with Anorexia Nervosa?

A

Low weight, but it does NOT affect breast tissue

213
Q

What is Bulimia?

A

Condition in which the patient binges on food and then induces vomiting

214
Q

What is worse, Bulimia or Anorexia?

A

Anorexia

Bulimia also has Endocrine Pathology

215
Q

Do people with Bulimia have Amenorrhea?

A

YES, 50% do

216
Q

What are the most common causes of death with Bulimia?

A

1) Aspiration Pneumonia
2) Hypokalemia > Cardiac Arrhythmias
3) Esophageal and Heart Rupture

217
Q

What is Aspiration Pneumonia?

A

Inhalation of vomited particles along with digestive enzymes (pepsine) > Digestion and inflammation of lung tissue. May result in strangulation (also a common cause of death for alcohol abusers)

218
Q

What is seen with Esophageal and Heart Rupture?

A

Irritation of esophagus and

  • Mallory Weiss Syndrome: Destruction of the distal esophagus due to repetitive, long term vomiting

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