Patho Bridge PDF

### **Week 1** 1. Discuss the definition and the various theories of stress. Walter B. Cannon - Hans Selye - - - - - [Specificity theory] - - [Pattern theory] - - - [Gate control theory] - - - - [Neuromatrix theory] - - - - 2. Examine the...

### **Week 1** 1. Discuss the definition and the various theories of stress. Walter B. Cannon - Hans Selye - - - - - [Specificity theory] - - [Pattern theory] - - - [Gate control theory] - - - - [Neuromatrix theory] - - - - 2. Examine the three stages of Selye's general adaptation syndrome. → The alarm stage - - - - - - - - - - - - → Stage of resistance or adaptation - - - - → Stage of exhaustion - - - - 3. Explain the pathophysiological mechanisms and role of the nervous and endocrine systems in the stress process. In the stress response, the nervous and endocrine systems work closely to help the body manage and adapt to stressors through a series of physiological changes. 1\. Nervous System\'s Role: The nervous system, particularly the autonomic nervous system (ANS), plays a key role in initiating the stress response. The sympathetic nervous system (SNS) is activated when a stressor is perceived, initiating the \"fight or flight\"response. The primary actions include: - - - - - - - 2\. Endocrine System\'s Role: The endocrine system, particularly the hypothalamic-pituitary-adrenal (HPA) axis, is critical for the longer-term, slower stress response. This process is initiated by the hypothalamus and involves hormone release: - - - - - - 3\. Feedback Mechanism: Cortisol also provides a feedback loop to the hypothalamus and pituitary gland, signaling them to reduce CRH and ACTH production once the stressor has passed. This helps the body return to a state of homeostasis. Summary of the Stress Process: - - Both systems collaborate to help the body adapt and cope with the demands of stress. However, prolonged or chronic activation of this stress response, particularly high cortisol levels, can lead to adverse health effects such as immunosuppression, hypertension, and metabolic imbalances 4. Describe the effects of stress on the immune system Chronic stress affects many immune cell functions, including decreased natural killer cell and T-cell cytotoxicity and impaired B-cell function. Importantly, these impairments in the immune system may have negative health consequences for stressed individuals, such as increased risk of infection and some types of cancer. Common pathophysiologic origins relating to chronic inflammatory processes include cardiovascular disease, osteoporosis, arthritis, type 2 diabetes mellitus, chronic obstructive pulmonary disease (COPD), other diseases associated with aging, and some cancers; all are characterized by the prolonged presence of proinflammatory cytokines. 5. Stress response - The concepts of allostasis (stability through change; monitoring the environment for adaptive response) and homeostasis (return to base levels reflecting an unchanging set point) both indicate physiologic responses. Allostatic overload can occur when there is overactivation of adaptive responses that may in turn increase susceptibility to disease. - Chronic dysregulation of the HPA axis, especially abnormal elevated levels of cortisol, has been linked to a wide variety of disorders, including obesity, sleep deprivation, lipid abnormalities, hypertension, diabetes, atherosclerosis, and loss of bone density. - Glucocorticoids from the adrenal cortex, in response to ACTH from the pituitary gland, comprise the major stress hormones along with the catecholamines epinephrine and norepinephrine. - In general, catecholamines of the sympathetic system prepare the body to act; for example, cortisol mobilizes glucose (for energy) and other substances. The parasympathetic system balances or restrains the sympathetic system, resulting in slower heart rates, and anti-inflammatory effects. During prolonged stress (allostatic overload) the parasympathetic system is less effective in opposing the sympathetic system. - Epinephrine exerts its chief effects on the cardiovascular system. Epinephrine increases cardiac output and increases blood flow to the heart, brain, and skeletal muscles by dilating vessels that supply these organs. It also dilates the airways, thereby increasing delivery of oxygen to the bloodstream. - Norepinephrine\'s chief effects complement those of epinephrine. Norepinephrine constricts blood vessels of the viscera and skin; this has the effect of shifting blood flow to the vessels dilated by epinephrine. Norepinephrine also increases mental alertness. - Glucocorticoids reach all tissues, including the brain, easily penetrate cell membranes, and react with numerous intracellular glucocorticoid receptors. Because they spare almost no tissue or organ and influence a large proportion of the human genome, they broadly exert diverse biologic actions. For example, glucocorticoids have an important modulatory role in the CNS. These hormones regulate memory, cognition, mood, and sleep and influence many other body systems. - Cortisol is the primary glucocorticoid produced during stress. - Cortisol\'s chief effects involve metabolic processes. By inhibiting the use of metabolic substances while promoting their formation, cortisol mobilizes glucose, amino acids, lipids, and fatty acids and delivers them to the bloodstream. As an example, anabolic effects of cortisol increase the rate of protein synthesis in the liver, whereas the catabolic effects of cortisol increase levels of amino acids, ultimately depleting protein stores in muscle, bone, skin, and connective tissue. - Cortisol contributes to elevated blood glucose and inhibits glucose uptake by body cells providing energy to combat perceived or anticipated stressors. - Glucocorticoids contribute to the development of metabolic syndrome and the pathogenesis of obesity. They can directly cause insulin resistance and influence genetic variations that predispose to obesity. - Elevated levels of glucocorticoids and catecholamines (epinephrine and norepinephrine), both endogenous and exogenous (synthetic pharmaceuticals), may decrease innate immunity and increase autoimmune responses. However, prolonged effects of cortisol may accentuate inflammation. Overall, stress activates an excessive immune response and, through cortisol and the catecholamines, suppresses Th1 responses while enhancing Th2 responses. - The impact of cortisol on fetal development and subsequent risk of future disease is being considered. - Other hormones, including β-endorphins, growth hormone, prolactin, oxytocin, the steroid sex hormones, and antidiuretic hormone, influence the stress response by their diverse actions. 6. Describe the physiologic effects and management of stress on an individual's health and illness. The stress response is initiated when a stressor is present in the body or perceived by the mind. Psychological stress may cause or worsen several diseases or disorders including anxiety, depression, insomnia, chronic pain and fatigue syndromes, obesity, metabolic syndrome, essential hypertension, type 2 diabetes, atherosclerosis and its cardiovascular consequences, osteoporosis, and autoimmune inflammatory and allergic disorders. A classic example of stress and allostatic overload is sleep alteration and the associated damaging effects of elevated evening cortisol, insulin, and glucose 7. Define pain. Pain is a complex experience. It is composed of dynamic interactions between physical, cognitive, spiritual, emotional, and environmental factors and cannot be characterized as only a response to injury. - "whatever the experiencing person says it is, existing whenever he says it does." - "an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage." Pain (nociception) is a complex, unpleasant sensory experience involving emotion, cognition, and motivation. Pain is protective. 8. Characterize the neural mechanisms of pain and pain modulation. Three portions of the nervous system are responsible for the sensation, perception and response to pain: 1. The afferent pathways, which begin in the peripheral nervous system (PNS), travel to the spinal gate in the dorsal horn and then ascend to higher centers in the central nervous system (CNS). 2. The interpretive centers located in the brain stem, midbrain, diencephalon, and cerebral cortex. 3. The efferent pathways that descend from the CNS back to the dorsal horn of the spinal cord 9. Differentiate between nociceptive, neuropathic, somatic & visceral types of pain. There are two types of nociceptors. **Myelinated Aδ fibers transmit sharp, "fast" pain. Smaller, unmyelinated C fibers more slowly transmit dull, less localized pain.** - Nociceptive Pain: - - - - - - - Neuropathic Pain: - - - - **Acute** - Somatic Pain (a type of nociceptive pain): A- beta fibers - - - - Visceral Pain (a type of nociceptive pain): C fiber - - - - Referred Pain - **Chronic** - Chronic pain is pain lasting well beyond the expected normal healing time and may be intermittent (e.g., low back pain) or persistent (e.g., migraine headaches). In summary, nociceptive pain arises from tissue damage, while neuropathic pain stems from nerve damage. Somatic pain is linked to muscles, bones, and skin, whereas visceral pain comes from the internal organs. 10. Neurotransmitters of pain modulation Excitatory transmitters in tissue injury - - - - Excitatory neurotransmitters in brain and spinal cord - - - - Inhibitory neurotransmitters in spinal cord - - Inhibitory transmitters in medulla and pons - - Inhibitory transmitters in the periphery, spinal cord and brain. Endogenous opioids inhibit pain transmission and include enkephalins, endorphins, dynorphins, and endomorphins. They are produced in the central nervous system. Receptors include Mu, Kappa, and Delta - - - - 11. Explain the physiological dimensions of pain and the pain process. 1. **Transduction** - - 2. **Transmission** - - - - - - - 3. **Perception** - - - - - 4. **Modulation** - - - - - [Summary of the Pain Process] 1. 2. 3. 4. This pain process can be influenced by several factors, including the intensity of the injury, emotional state, and psychological factors, which can either amplify or dampen pain perception. 12. Discuss the physical and psychological effects and the manifestation of unrelieved pain. [Physical Effects of Unrelieved Pain] 1. - - 2. - - 3. - - 4. - - 5. - - 6. - [Psychological Effects of Unrelieved Pain] 1. - - 2. - - 3. - - 4. - - 5. - - [Manifestation of Unrelieved Pain] 1. - - - 2. - - 3. - - 4. - - 13. Explore pharmacological and non-pharmacological methods of pain relief. Pharmacological - - - - - - Non-pharmacological - - - - - - - ### **Week 2** 1. Describe the inflammatory response, including vascular and cellular responses and exudate formation. The inflammatory response - - - - Inflammation will be activated by virtually any injury to vascularized tissues, including infection or tissue necrosis (e.g., ischemia, trauma, physical or chemical injury, foreign bodies, immune reactions). The classic or cardinal signs of acute inflammation are redness, heat, tenderness, and pain. A fifth sign, loss of function. 1. 2. 3. 1. Vascular Response The vascular response is the first stage of inflammation, marked by changes in blood vessel function to increase blood flow to the affected area. Key Steps in the Vascular Response: - - - - - - - - 2. Cellular Response The cellular response involves the migration of immune cells to the site of injury or infection to eliminate harmful agents and promote healing. Key Steps in the Cellular Response: - - - - - - - - - - - 3. Exudate Formation Exudate is the fluid and cells that escape from blood vessels due to increased vascular permeability and accumulate in the affected tissue during inflammation. Types of Exudate: - - - - - - - - Purpose of Exudate: - - - 2. Differentiate between inflammation and infection. **Inflammation** - - - - - - - - - - - - - - - - - **Infection** - - - - - - - - - - - - - - - - - Key Differences According to *Understanding Pathophysiology* **Aspect** **Inflammation** **Infection** -------------------------------- ------------------------------------------------------------------------------------------------------------- ----------------------------------------------------------------------------------------------------- **Definition** The body\'s nonspecific response to tissue injury or harmful stimuli. The invasion and multiplication of microorganisms that cause disease. **Cause** Can be triggered by a wide range of factors (trauma, toxins, allergies, autoimmune diseases, or infection). Always caused by pathogens (bacteria, viruses, fungi, parasites). **Mechanism** Involves vascular and cellular responses to remove harmful stimuli and initiate healing. Involves the proliferation of pathogens, which triggers an immune response, including inflammation. **Purpose** Protect the body from further damage and promote healing. Eliminate the invading microorganisms and prevent their spread. **Presence of Microorganisms** Not always present; inflammation can occur due to non-infectious causes. Always present; infection is caused by microorganisms. **Relationship** Inflammation can occur without infection (e.g., in trauma, allergies). Infection typically leads to inflammation as part of the immune response. **Differences:** - - 3. Discuss and understand Innate and Acquired Immunity. **Innate Immunity (Natural/Native Immunity)** - - - - - - - - - - - - - **Acquired (Adaptive) Immunity** - - - - - - - - - - - - - - - - - 4. Explain local and systemic manifestations of inflammation and their physiologic bases. **Local Manifestations of Inflammation** Local manifestations occur at the site of injury or infection and are due to the vascular and cellular changes triggered by the inflammatory response. The classic local signs of inflammation are often referred to as the five cardinal signs: 1. Redness (Rubor): - - 2. Heat (Calor): - - 3. Swelling (Tumor): - - 4. Pain (Dolor): - - 5. Loss of Function (Functio Laesa): - - **Systemic Manifestations of Inflammation** When inflammation becomes more widespread, or when there is a significant infection or injury, the body exhibits systemic manifestations. These systemic effects are the result of chemical mediators like cytokines entering the bloodstream and affecting various organ systems. 1. Fever (Pyrexia): - - 2. Leukocytosis: - - 3. Acute Phase Reactants: - - 4. Increased Heart Rate and Blood Pressure: - - 5. Malaise, Fatigue, and Anorexia: - - 6. Lymphadenopathy: - - 5. Medication for inflammation - Ibuprofen - Celecoxib - Corticosteroids - Dexamethasone - Prednison 6. Compare and contrast primary, secondary, and tertiary intention healing. **Primary Intention Healing** - - 1. 2. 3. - 4. 5. 6. **Secondary Intention Healing** - - 1. 2. 3. 4. - 5. 6. 7. 8. **Tertiary Intention Healing (Delayed Primary Intention)** - - 1. 2. 3. - 4. 5. 6. Comparison of Healing Types Aspect Primary Intention Secondary Intention Tertiary Intention -------------------- ------------------------------ ------------------------------- ---------------------------------------------- Wound Edges Well-approximated, closed Edges not approximated Initially open, then surgically closed Tissue Loss Minimal Significant Varies, often moderate Healing Time Fast Longer Intermediate (depends on closure time) Granulation Tissue Minimal Extensive Moderate Scar Formation Minimal scar Larger, more noticeable scar Moderate scarring Examples Surgical incision, paper cut Pressure ulcers, severe burns Contaminated wounds, infected surgical sites 7. Identify the factors that delay and enhance wound healing and common complications of wound healing. 1. - 2. - 3. - 4. - 5. - 6. - 7. - 8. - 9. - 10. - 1. - 2. - 3. - 4. - 5. - 6. - 7. - 1. - 2. - 3. - 4. - 5. - 6. - 7. - 8. List the modes and variables involved in the transmission of the human immunodeficiency virus (HIV). Modes of HIV Transmission 1. Sexual Contact: - 2. Blood-to-Blood Contact: - - - - 3. Perinatal Transmission (Mother-to-Child): - 4. Other Body Fluids: - Variables Involved in HIV Transmission 1. Viral Load: - 2. Type of Exposure: - - - - 3. Presence of Other Sexually Transmitted Infections (STIs): - 4. Circumcision: - 5. Genetic Factors: - 6. Health of the Immune System: - 7. Duration and Frequency of Exposure: - 8. Use of Antiretroviral Therapy (ART): - 9. Explain HIV in terms of risk factors for, pathophysiology, clinical manifestations, complications, diagnosis and treatment. 1\. Risk Factors for HIV Infection Certain behaviors and conditions increase the likelihood of acquiring HIV. These include: - - - - - - - - 2\. Pathophysiology of HIV HIV is a retrovirus that primarily targets the immune system, particularly CD4+ T-helper cells (T-cells), which are crucial for immune function. Here's the basic pathophysiology: 1. - - 2. - 3. - 4. - - 5. - 3\. Clinical Manifestations of HIV HIV infection progresses through several stages, each with distinct clinical manifestations: 1. - - - 2. - - - 3. - - 4\. Complications of HIV - - - - - 5\. Diagnosis of HIV HIV is diagnosed through the following methods: - - - - - - - - - 6\. Treatment of HIV HIV is treated with antiretroviral therapy (ART), a combination of drugs that target different stages of the viral replication cycle. The primary goals of ART are to reduce the viral load to undetectable levels and restore immune function. ART significantly improves the quality of life and life expectancy for individuals with HIV. 1. Antiretroviral Therapy (ART): - - - - - - 2. Pre-exposure Prophylaxis (PrEP): - 3. Post-exposure Prophylaxis (PEP): - 4. Treatment of Opportunistic Infections: - 10. Describe antiviral therapy and identify where the drugs work in respect to replication. Antiretroviral Therapy (ART) Goal: - The primary goal of ART is to reduce the viral load to undetectable levels in the blood, thereby improving immune function and preventing progression to AIDS. - ART aims to suppress viral replication to the extent that the immune system can recover and function effectively. Classes of Antiretroviral Drugs and Their Mechanisms of Action 1. - - - - - 2. - - - - - 3. - - - - - 4. - - - - - 5. - - - 6. - - - ### Week 3 1. Describe the process of maintaining normal acid base balance. **Buffer System** is the body's first line of defense against changes in pH. - - - - - - **Respiratory System** is the second line of defense and works within minutes to hours. - - **The Renal System** is the third line of defense and takes hours to days but is the most effective. - - - - - - +-----------------------------------+-----------------------------------+ | pH of Body fluids | Buffer Systems | +===================================+===================================+ | - - - - - - | - - - - - - | +-----------------------------------+-----------------------------------+ 2. Describe the composition of the major body fluid compartments. - **Intracellular** (⅔ of total fluid in the body) - - - - - **Extracellular** - - - - - - - - - - 3. Review the following processes and give examples of: - **Osmosis** is movement of water across a semipermeable membance from low concentration to high concentration of soloute without energy - - **Diffusion** is the movement of solutes from high to lower concentration without the need for energy. - - **Filtration** is the movement of water and solutes through a membrane due to hydrostatic pressure. Fluid is pushed out due to force. - - **Hydrostatic pressure** the pressure againts the walls of capillaries. Pushes water and small solutes out of the vessels into the surrounding tissue. - - **Oncotic pressure or colloid pressure** is created by plasma proteins such as albumin in blood to pull fluids from the intertial to the intravascular. It counteracts hydrostatic pressure. - - **Osmotic pressure** is force generated by water during osmosis - 4. Review the etiology, laboratory diagnostic findings clinical manifestations of the following disorders: - **Water excess** can occur with excessive intake of water, decrease in renal water excretion, SIADH, and use of hypotonic IV fluids. - - - - - - - - **Water deficiency** can occur from dehydration, excessive water loss like diarrhea, vomiting, burns, diabetes insipidus (excessive urination), and diuretics - - - - - - - - **Sodium imbalances (135-145)** - - - - - - - - - - - - - - - - - - - - - - - - **Potassium imbalances (3.5-5.0)** - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - **Albumin** - - - - - - - - - - - - - - - - - - - - - **Calcium imbalances (2.1-2.5)** - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - 5. Discuss the etiology, laboratory diagnostic findings, clinical manifestations, and risk factors of the following acid-base imbalances: (same at theory) **Respiratory acidosis** occurs when there is decreased alveolar ventilation, leading to an accumulation of CO2 in the blood. - Etiology - - - - - - - - - Labs - - - Manifestations - - - - - - - - - Risk factors - **Respiratory alkalosis** occurs when there is excessive alveolar ventilation, leading to a reduction arterial CO2 levels (hypocapnia). - Etiology - - - - Labs - - - - Manifestations - - - - - Risk factors - **Metabolic acidosis** increases in acid production or loss of bicarb. It can occur either quickly as in lactic acidosis due to poor perfusion and hypoxemia, or slowly over time like in renal failure, DKA, and starvation. - Etiology - - - - - - - - - Labs - - - Manifestations - - - - - - Risk factors - **Metabolic alkalosis** occurs when pH of blood is elevated above the normal range due to an excess of bicarb or loss of hydrogen ions. - Etiology - - - - - - - - - Labs - - - Manifestations - - - - - - Risk factors -