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Blood brain barriers
Blood-brain barriers (BBB) are unique structural features of capillaries found in the brain that are responsible for making it difficult the diffusion of substances from the capillary blood into the brain compared to similar capillary diffusion elsewhere in the body (Nag, 2003). The BBB have tighter barrier between their endothelial cells lining brain capillaries in comparison to those lining capillaries elsewhere in the body. The capillary endothelium of the BBB has thicker basement membrane relative to other capillaries in other body parts. Unlike other capillaries, the BBB are also shielded by astrocytes. Blood brain barriers thus play a crucial role in maintaining homeostasis in the brain. The endothelial cells serve the function of restricting diffusion of microscopic materials such as bacteria and hydrophilic or large molecules into the cerebrospinal fluid (CSF) on the one hand, while permitting passage of micro hydrophobic molecules e.g. carbon dioxide, oxygen, alcohols, steroids (Nag, 2003). Diffusion of water-soluble molecules such as chloride ions, potassium, and sodium through the BBB is facilitated by special carrier molecules.
Lesch-Nyhan syndrome
Lesch-Nyhan syndrome, also referred to as Kelley-Seegmiller syndrome or HPRT deficiency refers to a rare genetic disorder caused by the deficiency of hypoxanthine-guanine phosphoribosyltransferase (HGPRT) enzyme, which is produced through mutations in the HPRT gene found on the X chromosome. HPRT gene serves to catalyze the reaction needed to check the buildup of uric acid (which is a nitrogenous waste product ordinarily excreted from the body via the kidneys) (Gillberg, 2003). When the HPRT gene severely mutates, there is lack of HPRT enzyme action which results in heightened uric acid levels in the blood (a condition known as hyperuricemia) as a result of massive oversynthesis of purine de novo. The apparent lack of the HPRT enzyme action alters the chemistry of some parts of the brain, e.g. basal ganglia, which in turn compromises the normal activity of neurotransmitters, acids, as well as other chemicals resulting in changes in the nervous system(Gillberg, 2003). Males affected by Lesch-Nyhan syndrome have athetosis (uncontrollable writhing movements) as well as spasticity (muscle stiffness). Patients are also affected by self-mutilative biting behavior which includes biting of own tongue, lips, finger tips, together with head banging.
Congestive heart failure (CHF) and dilated cardiomyopathy
Congestive heart failure (CHF) refers to a condition where the heart is unable to effectively pump blood to other parts of the body. CHF is a common type of heart failure that results in congestion in the lungs, as well as fluid retention and swelling in ankles and legs (Medifocus.com Inc., 2011). CHF results from myocardial dysfunction together with progressive cardiac remodeling (which refers to alteration of function and structure of the heart). In the event that the heart is unable to effectively pump sufficient blood for metabolic requirements to the tissues, the movement of blood through the heart and the entire body is stepped down, leading to increased pressure in the heart. In response, compensatory mechanisms are effected in order to sustain cardiac function, e.g. sympathetic nervous system and the rennin-angiotensin-aldosterone system. Over time, the compensatory mechanisms can be destructive to the heart as well as circulation via a remodeling process that causes enlargement of the heart, thickening or thinning of the cardiac walls, and further inability of the heart to undertake its pumping function (Parker, 2003). The weakening of the heart and declining pumping capacity leads a symptomatic heart failure. The pressure build-up in the heart and lungs adversely affects the kidneys leading to retention of fluid in the body. The continued buildup of fluid in the such body parts as the legs, feet, organs and lungs makes the body to become “congested” with fluid; thus the name “congestive heart failure” (Medifocus.com Inc., 2011).
Dilated cardiomyopathy
Dilated cardiomyopathy, (traditionally known as idiopathic dilated cardiomyopathy, IDC), refers to a progressive heart muscle disease characterized by enlargement of the ventricular chamber and contractive dysfunction of the left ventricular wall thickness. It results from gross damage of the myocardial muscle fibres, which affects with the myocardial metabolism of the heart resulting in extensive dilation of all four chambers of the heart into a globular shape and appearance. The hearts pumps less blood than normal, with the large volumes of blood remaining in the left ventricle. Unchecked ventricular enlargement along with dysfunction often leads to progressive heart failure characterized by further drop of the left ventricle to contract as needed. Failure of compensatory mechanisms to sustain cardiac output at optimum left ventricle filling pressures, results in chronic heart failure.
Generally, compensatory mechanisms are relied on to maintain sufficient cardiac output during a heart failure. They include (1) tachycardia along with increased contractility via sympathetic nervous system activation; (2) the Frank-Starling mechanism, in which there is an increase in stroke volume following an increase in preload; (3) vasoconstriction (shunts blood from other nonessential organs to the heart and brain during reduced cardiac output); and (4) ventricular hypertrophy & remodeling (reduces myocardial wall stress).

Disseminated intravascular coagulation (DIC)
Disseminated intravascular coagulation (DIC) is a disorder in which protections responsible for blood clotting become abnormally active. In treatment, the goal is always to establish and treat the cause of DIC. There is consensus on the ultimate treatment of DIC given its many possible causes. Transfusions of blood cells along with other blood products may be done to replace blood lost through bleeding and replacement of clotting factors that have been used up by the body (Labelle & Kitchens, 2005). Some cases may require heparin (a blood thinner) to shut down the triggers of the body overusing its blood clotting elements.
Surgical bleeding is treated by instantenous management of the source of bleeding through surgical or radiological interventions. Blood-sourced products and hemostatic agents (e.g. aprotinin, DDAVP, tranexamic acid) are used to improve the hemostatic balance in a bleeding patient. Where conventional therapy fails, Recombinant activated factor VII (rFVIIa) is used (Marrietta et al, 2006).
Cheyne-stokes respiration and heart failure
Cheyne-stokes respiration refers to a disorder with characteristic recurrent central apneas and hypopneas that alternate with periods of hyperventilation, giving a waxing wanning pattern of tidal volume. Hyperventilation associates with pulmonary cingents, recurrent oxygen saturations along with arousals from sleep, with varying oscillations in both the blood pressure & heart rate of the patient, sympathetic activation as well as heightened danger of ventricular tachycardia. The major pathophysiological mechanism that causes Cheyne-Strokes respiration is the hyperventilation together with low arterial CO2 (PaCo2) which trigger a central apnea when it falls below the apneic threshold. Cheyne-Strokes produces poor prognosis which could occur in a vicious cycle, causing further stress to the failing heart (Sicar, 2008).

References:
Sicar, S. (2008). Principles of Medical Physiology. New York: Thieme.
Marietta, M., Facchini, L., Pedrazzi, P., Busani, S., Torelli, G. (2006). Pathophysiology of Bleeding in Surgery. Retrieved from: http://www.niceindia.net/knowledge_base/Surgery/Marietta_2006.pdf
Labelle, A.C., & Kitchens, S. C. (20050. Disseminated intravascular coagulation: Treat the cause, not the lab values. Retrieved from: http://ccjm.org/content/72/5/377.full.pdf
Parker, B. R., Patterson, H., & Johnson, A., J. (2003). Heart Failure. Retrieved from: http://faculty.ksu.edu.sa/NAloudah/Documents/PHCL%20441/HF/HF%20Pharmacotherapy.pdf
Medifocus.com Inc. (2011). Medifocus Guidebook On: Congestive Heart Failure. Maryland: Medifocus.com Inc.
Nag, S. (2003). Blood-Brain Barrier: Biology and Research Protocols. New York: Springer.
Gillberg, C. (2003). Clinical Child Neuropsychiatry. London: Cambridge University Press.