ACUTE REAL FAILURE (ARF).[1]

Acute renal failure is defined as an abrupt decline in renal function with increased creatinine and blood urea nitrogen levels (BUN) over a period of several days. There are three main categories of ARF:

1)    Pre-renal azotemia :decreased renal perfusion causes a decreased glomerular filtration rate. In response, the kidney acts to retain salt and water in an attempt to increase blood pressure and perfusion.

2)    Intrinsic renal failure: generally due to acute tubular necrosis, which leads to obstruction of renal tubules with necrotic debris and subsequent fluid backflow with decreased GFR. In this setting the damages renal tubules are unable to retain salt and water.

3)    Post-renal azotemia: caused by outflow obstruction and can only occurs when such obstruction is bilateral. In this setting there is also backflow to fluid with decreased GFR.

Variable	Prerenal	Renal	Postrenal
Urine osmolality	>500	<350	<350
Urine Na	<10	>20	>40
FE Na	<1%	>2%	>4%
BUN/Cr Ratio	>20	<15	>15

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[1] (Le, Bhushan, Tolles, & Hofmann, 2011)

HYDATIDIFORM MOLE[1]:

A hydatidiform mole is a noninvasive tumor caused by aberrant fertilization , leading to cystic swelling of chorionic villi and proliferation of the trophoblast. It result in a mass that can look like a “cluster of grapes”. Hydatidiform Mole can be complete or partial. The genotype of a complete moles is usually 46,XX, completely consisting of paternal DNA. It result when two sperm fertilize an empty egg. There is no associated fetus despite the eleveted levels of β-human chorionic gonadotropin.

The genotype 46,XX, maternal would not cause a hydatidiform mole. Mole are derived from empty ova that are then fertilized by sperm. 46,XX maternal and paternal describe a genotype of a normal fetus, receiving one set of chromosomes from each parent.

69, XXX; 69 XXY or 69 XYY, maternal and paternal describe another posible DNA make up of a partial mole. A partial mole contains more than two set of chromosomes thet usually consist of two paternal and one maternal, or consist of  both paternal and maternal set, resulting in triploidy or tetraploidy. Partial moles may present with a similar grape like mass and are associated with fetal parts.

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[1] (Le, Bhushan, Tolles, & Hofmann, 2011)

BIOCHEMISTRY: METABOLIC DISORDERS.

Pyruvate dehydrogenase deficiency	Congenital or acquiered (as in alcoholic due to B1 deficiency)		Neurologic defect, Lactic acidosis	Increase intake of ketogenic nutrients (high fat content or ↑ lysine/leucine)
Gkucose-6-phosphate dehydregenase deficiency	X-linked recessive	Most common human enzyme deficiency,more prevalent among black, ↑malarial resistance	↓NADPH in RBCs leads to hemolytic anemia. Heinz bodies, Bite cells
NADPH oxidase deficiency	Chronic granulomatous disease	Defect in microbicidal activity of neutrophils	Marked susceptibility to opportunistic infections	Diagnosis with negative nitroblue tetrazolium dye reduction test
Fructokinase deficiency	Essential fructosuria Autosomal recessive	Bening-milder symptoms than analogous disorder of galactose metabolism	Fructose appear in blood and urine
Aldolase B deficieny	Fructose intolerance Autosomal recessive	Fructose-1-phosphate accumulated. Inhibits glucogenolysis and gluconeogenesis	Hypoglycemia Jaundice Cirrhosis Vomitnig	↓intake of fructose and sucrose (glucose +fructose)
Galactokinase deficiency	Autosomal recessive	Galactitol accumulate if galactosa is present in diet	Galactose appear in bood/urine Infantile cataracts Failure to track obj./develop social smile
Galatose-1-phosphate uridyl transferase	Autosomal recessive	Accumulation of toxic substances (galactitol)	Failure to thrive Jaundice Hepatomegaly Infantile cataracts Mental retardation	Exclude galactose and lactose ( galactose  + glucose) from diet
Lactose deficiency	Age dependent or hereditary	Loss of brush border enzyme, also fallow to gastroenteritis	Bloating Cramps Osmotic diarrhea	Avoid dairy product or add lactose pills to diet

DEFICIENCIA DE TIAMINA (VITAMINA B1).

Funciona como cofactor, pirofosfato de tiamina, para múltiples enzimas:

1)    Piruvato deshidrogenasa  (glicolisis)

2)    α-ketoglucorato deshidrogenasa

3)    Trasketolasa

4)    Deshidrogenasa para AA de cadena ramificada.

La tiamina es una vitamina soluble en agua que se absorbe a nivel del yeyuno por medio de dos procesos, un transporte portal activo cuando los niveles de tiamina en el intestino delgado están bajos; y un proceso pasivo a nivel de la mucosa cuando la concentración de tiamina es alta. En el intestino delgado es donde se produce la fosforilizacion de la tiamina (Wooley, 2008).

Alimentos ricos en tiamina según Wooley (2008).

.Los alimentos con granos enteros.

 • La carne / pescado / pollo / huevos

 • Leche y productos lácteos

 • Verduras (hojas verdes, remolacha, patatas)

 • Legumbres (lentejas, soja, nueces, semillas)

 • Jugos de naranja y tomate

Su deficiencia produce una alteración en la degradación de la glucosa que trae consigo una depleción de ATP, los tejidos altamente aeróbicos como el cerebro y el corazón, son los primeros dañados. Se puede ver en estados de malnutrición como el alcoholismo, otras causas de malnutrición y malabsorción. (Le, Bhushan, Tolles, & Hofmann, 2011).

Wernicke-Korsakoff: Confusión, oftalmoplegia, ataxia unido a confabulación, cambios de personalidad y perdida de la memoria (permanente); producto de un daño en el núcleo dorso-medial del  tálamo, cuerpos mamilares (Le, 2011). El uso elevado y  prolongado del alcohol es la más común asociación con la aparición del síndrome de Wernicke-Korsakoff (Xiong, 2011).

Beriberi seco: forma que afecta al sistema neuromuscular presentándose como polineuritis con perdida de la musculatura  de forma simétrica (Le, 2011).

Beriberi húmedo: forma que afecta al sistema cardiovascular , se divide en aguda y crónica: en la forma aguda también conocida como Shoshin beriberi, la lesión predominante es en el corazón por la incapacidad para mantener su función; la forma crónica se caracteriza por un fallo cardiovascular con gasto cardiaco elevado (cardiomiopatía dilatada), edemas. (Radinowitz, 2009).

Conducta:

En los casos en que se sospeche la deficiencia de tiamina, esta indicada su administración parenteral a dosis de 50 mg durante varios días, dependiendo de la intensidad de los síntomas, manteniendo un tratamiento hasta que los síntomas hayan desaparecido. Se recomienda una dosis de mantenimiento de 2.5-5 mg por día, vía oral (descartando la presencia de síndrome de malabsorción) (Nguyen-Khoa, 2011).

La encefalopatía de Wernicke, es considerada una emergencia médica, su pronto reconocimiento es crucial para establecer  su tratamiento adecuado: Tiamina 100 mg por vía parenteral es el tratamiento de elección, su comienzo temprano puede revertir la oftalmoplegia, la ataxia, la confusión mental en sus primeros estadios, así como prevenir un futuro estado amnésico, según nos expone Xiong (2011).

Bibliography

Le, T., Bhushan, V., Tolles, J., & Hofmann, J. (2011). First AID for the USMLE step 1. usa: McGraw Hill.

Nguyen-Khoa, D.-T. (2011, dec 13). medscape.com. Retrieved feb 14, 2012, from Beriberi (thiamine deficiency) treatment & management: http://emedicine.medscape.com/article/116930-treatment

Radinowitz, S. S. (2009, sep 18). Medscape.com. Retrieved Feb 14, 2012, from Pediatric beriberi clinical presentation: http://emedicine.medscape.com/article/984721-clinical

Wooley, J. A. (2008). Characteristic of Thiamine and its relevance to the management of heart failure. Nutr Clin Pract.Oct-Nov , 23:487-93.

Xiong, G. L. (2011, sep 15). Medscape.com. Retrieved feb 14, 2012, from Wernicke-Korsakoff syndrome: http://emedicine.medscape.com/article/288379-overview#aw2aab6b2b2

 

LUNG CANCER:

Divided in two main categories: Small cell lung carcinoma and non-small cell carcinoma (NSCLC), the latter is divided further into adenocarcinoma, squamous cell carcinoma, and large cell carcionama according to its histological characteristics.

Small cel carcinoma (oat cell): central location, undifferenciated, exhibits aggressive behavior, with rapid growth, early spread to distant sites, exquisite sensitivity to chemotherapy and radiation, and frequent associated with distint paraneoplastic syndromes (Tan, 2011). May lead to Lambert-Eaton syndrome. It is considered inoperable (Le, Bhushan, Tolles, & Hofmann, 2011) surgery usually plays no role in its management except in rare situactions (Schreiber, Rinner, & Vongtama, 2008).

Histology: neoplasm of neuroendocrine Kulchitsy cells (small dark blue cells).

Squamous cell carcinoma: located central, hiliar mass arising from brochus, cavitation; tendency to spread to regional lymph nodes and has clearly linked to smoking (Navarro & Arroyo, 2007) (Le at el, 2011)Parathyroid-like activities(PTHrP).

Histology:Keratin pearls and intracellular bridges.

Adenocarcinoma: arise from the mucus glands or from any epithelial cell within  or distal to the terminal bronchioles, usually present as peripheral nodules or masses (Tierney, McPhee, & Papadakis, 2005), 2 types:

1)    Bronchial: develop in site prior pulmonary inflammation or injuty; most common lung cancer in Nonsmoker and female.

2)    Broncho-alveolar: Not linked to smoking, grows along airway, can present like pneumonia, can results in hypertrophic osteoarthropathy.

Histology: (both) Clara cell---type II pneumocytes.

Large cell carcinoma: peripheral location, highly anaplastic undifferenciated tumor with rapid doubling time and aggressive clinical course (Tierney at el, 2005), poor prognosis, less responsive to chemotherapy but it is removed surgically (Le al el, 2011).

Histology: pleomorphic giant cell with leukocytes fragments in cytoplasm.

Carcinoid tumor: secrets serotonin can cause carcinoid syndrome, fibrous deposit in right heart valve may lead to tricuspid insufficiency, pulmonary stenosis, and right heart failure.

Mesothelioma: pleural location, malignancy of the pleura associated with asbestosis, but not all cases are associated with asbesto exposure (Hodgson & Darnton, 2000) according Winston W Tan, MD.  Results in hemorrhage pleural effusion, and pleural thinckening (Le at el, 2011). Mesothelioma is most common in males, and occurs most commonly in the fifth-seventh decades of life (Tan, 2011).

Histology: Psammoma bodies.

Lung cancer complications:

1)    Superior Vena Cava syndrome

2)    Pancoast’s tumor

3)    Horner’s syndrome

4)    Paraneoplastic endocrine manifestation

5)    Recurrent Laryngeal simptoms (hoarseness)

6)    Pleural and pericardial effusions.

Metastases to lung is most common, often from breast, colon, prostate,

and bladder cancer.

         Sites of metastases: adrenal, brain, bone, and liver.

Bibliography

Hodgson, J., & Darnton, A. (2000). The quantitative risk of mesothelioma and lung cancer in relation to asbestos exposure. Ann Occup Hyg. Dec , 44 (8):565-601.

Le, T., Bhushan, V., Tolles, J., & Hofmann, J. (2011). First AID for the USMLE step 1. usa: McGraw Hill.

Navarro, F., & Arroyo, M. (2007). Cancer de Pulmon. In Cliniguia actualizacion de diagnostico y tratamiento (pp. 861-867). Spain: EviScience publicaciones.

Schreiber, D., Rinner, J., & Vongtama, D. (2008). Surgery for limited-stage small cell lung cancer, should the paradigm shift? A SEER-based analysis. J Clin Oncol (Sppl) , 26:403s.

Tan, W. W. (2011, Nov 16). Medscape.com. Retrieved Feb 3, 2012, from small cell lung cancer: http://emedicine.medscape.com/article/280104-overview

Tierney, L. M., McPhee, S. J., & Papadakis, M. A. (2005). CURRENT medical diagnosis & treatment. usa: McGraw Hill.