Quiz 1

(Ref: Harrison 21st ed, p 768; Harrison 20th ed, p 699) The patient is suffering from macrocytic anemia due to folate deficiency. Reasons for selecting folate deficiency:  Folic acid deficiency takes 3-5 months to develop while B12 deficiency takes 3-5 years. Since the patient is having recent onset of symptoms, chances of having folate depletion first will be higher.  Folic acid is present in legumes and green leafy vegetables. So, a diet poor in these will lead to folate deficiency.  B₁₂ deficiency also leads to neurological features due to 12 demyelination of dorsal column which is not present in our case. B₁₂ deficiency is seen in vegans.  Fast food typically has meat, fish, dairy products like cheese being used that have vitamin B12. Most burgers have a slice of cheese to make it more appetizing.

(Ref: Harrison 21st ed, p 766; Park 25th ed, p 677) Vitamin B12 is found in animal products like fish, meat, poultry, eggs, milk and milk products. So, vegans (who eat only vegetables) are likely to develop B12
deficiency. In contrast if a person does not take green leafy vegetables in diet then he/she will develop folic acid deficiency.

(Ref: Harrison 21st ed, p 768; Harrison 20th ed, p 701) Folic acid once supplemented in these patients with macrocytic anemia will consume the remaining precious Vitamin B12 for DNA synthesis and will improve hematological picture but B12 availability for myelination will be further compromised. Vitamin B12 plays a major role in providing cofactors that are required to form myelin Vitamin B12 is required to produce methionine (Precursor for S-adenosyl methionine), which is required for methylation reaction in myelin production.

(Ref: Harrison 20th edition, p 2316-7; Harrison 19th p 96e-1t, 96e-8, 462e-19)
 Vitamin E deficiency causes axonal degeneration of the large myelinated axons and results in posterior column and spino-cerebellar symptoms.
 Peripheral neuropathy is initially characterized by areflexia, with progression to an ataxic gait, and by decreased vibration and position sensations.
 Ophthalmoplegia, skeletal myopathy, and pigmented retinopathy may also be features of vitamin E deficiency.

(Ref: Harrison 20th edition, p 2309; Harrison 19th p 96e-1)
 Due to defective glucose metabolism in setting of thiamine deficiency, lactic acidosis ensues.
 Type A is lactic acidosis occurring in association with clinical evidence of poor tissue perfusion or oxygenation of blood (e.g, hypotension, cyanosis, cool and mottled extremities). It can be caused by the overproduction of lactate or the underutilization of lactate. In cases of overproduction, circulatory, pulmonary, and hemoglobin transfer disorders are commonly responsible.
 In cases of underutilization of lactate, liver disease, gluconeogenesis inhibition, thiamine deficiency, and uncoupled oxidative phosphorylation can be responsible.
 Type B1 actic acidosis occurs when no clinical evidence of poor tissue perfusion or oxygenation exists. However, in many cases of type B lactic acidosis, occult tissue hypoperfusion is now recognized to accompany the primary etiology.
 Type B1 occurs in association with systemic disease, such as renal and hepatic failure, diabetes and malignancy.
 Type B2 is caused by several classes of drugs and toxins, including biguanides, alcohols, iron, isoniazid, zidovudine, and salicylates.
 Type B3 is due to inborn errors of metabolism

(Ref: Harrison 19th p 415e-6, 1612, 1622)
 Obesity-induced hypertension is associated with increased peripheral resistance and cardiac output, increased sympathetic nervous system tone, increased salt sensitivity, and insulin-mediated salt retention; it is often responsive to modest weight loss
 Severe obesity may be associated with obstructive sleep apnea and the "obesity hypoventilation syndrome" with attenuated hypoxic and hypercapnic ventilatory responses. Sleep apnea can be obstructive (most common), central, or mixed and is associated with hypertension.

(Ref: Facial and plastic reconstruction surgery pg. 23: 3rd ed., Ira D Papel, Harrison 19th p 96e-8)
Factors affecting wound healing:
1. Cortisonc/Corticosteroids markedly inhibit capillary budding, fibroblast proliferation, and the rate of epithelialization.
2. Similar to cortisone, vitamin E adversely affects wound healing by slowing collagen production. This effect may be reversed with vitamin A. Additional vitamin A will not improve wound healing in the absence of vitamin E or cortisone.
3. Excessive zinc delays wound healing by inhibiting macrophage function.
4. Radiation is detrimental to wound healing. Given 7 days before wound creation, healing is impaired.
5. Hypo-proteinemia
6. Uremia
7. Diabetes mellitus
8. Obesity contributes to poor wound healing, primarily as a consequence of poor suture holding in the subcutaneous fat layers
9. Cytotoxic drugs may also delay wound healing.
10. Alkylating agents (e.g, cyclophosphamide, melphalan) slow wound healing by blocking DNA synthesis.