FSGV.docx

**[Final Exam Study Guide]** 1. Define Preload **[PRELOAD]** **Definition:** Preload is the volume of blood filling the heart\'s ventricles before contraction. It reflects the \"initial stretch\" of the cardiac muscle fibers at the end of diastole, just before the heart pumps. Preload is directly related to the left ventricular end-diastolic volume (EDV), which is the maximum amount of blood in the ventricle before it contracts. **Analogy:** Think of preload like filling a water balloon. The more water (blood) you add, the more the balloon (ventricle) stretches. The stretch determines how forcefully the balloon can release the water (stroke volume) when you squeeze it. Similarly, in the heart, more blood filling the ventricles leads to a stronger contraction, pumping more blood out, as explained by the Frank-Starling Law. **Key Points:** - Preload is influenced by factors like venous return and ventricular compliance. - Higher preload means a fuller ventricle and stronger subsequent contraction. - Preload plays a crucial role in determining stroke volume, impacting overall cardiac output. **[AFTERLOAD]** **Definition:** Afterload is the resistance that the heart must overcome to eject blood during contraction. Specifically, it refers to the force the left ventricle must generate to open the aortic valve and push blood into the aorta. Afterload is influenced by factors like arterial pressure and vascular resistance; higher afterload means the heart has to work harder, leading to slower and less efficient blood ejection. **Analogy:** Think of afterload like pushing open a heavy door. The heavier (more resistant) the door, the harder and slower you need to push to open it. Similarly, when afterload is high, the heart works harder and ejects less blood with each beat. Lower afterload, like a lighter door, allows the heart to eject blood more easily and quickly. **[Key Points]** - Afterload is directly related to arterial pressure; higher pressure means increased afterload. - It affects the velocity of the heart's contraction, and the amount of blood pumped out (stroke volume). - Changes in afterload can influence preload and overall cardiac function. 2. Modifiable risk factors for hypertension 1. **Diet:** Reducing sodium in your diet can lower the risk of hypertension. Aim for a diet low in processed foods and rich in fruits, vegetables, and whole grains. 2. **Obesity:** Being overweight increases the strain on your heart and arteries, leading to higher blood pressure. Weight loss through diet and exercise is effective in lowering blood pressure. 3. **Physical Inactivity:** A sedentary lifestyle contributes to weight gain and increases the risk of hypertension. Regular physical activity strengthens the heart, improves circulation, and helps maintain a healthy weight. 4. **Smoking:** Smoking damages blood vessels, leading to increased blood pressure. Quitting smoking can significantly reduce the risk of hypertension and improve overall cardiovascular health. 5. **Excessive Alcohol Consumption:** Drinking too much alcohol can raise blood pressure. Limiting alcohol intake to moderate levels (one drink per day for women and two for men) can help manage blood pressure. 6. **Stress:** Chronic stress may contribute to hypertension by prompting unhealthy behaviors such as overeating, poor diet choices, and physical inactivity. Managing stress through relaxation techniques, exercise, and mindfulness can help reduce blood pressure. 7. **High Cholesterol Levels:** Elevated cholesterol, particularly LDL cholesterol, contributes to atherosclerosis, which can increase blood pressure. Diet changes, exercise, and medications can help control cholesterol levels. 8. **Diabetes Management:** - Poorly managed diabetes increases the risk of hypertension. Controlling blood sugar levels through diet, exercise, and medication is crucial in preventing high blood pressure. 9. **Excessive Caffeine Intake:** High caffeine consumption can temporarily raise blood pressure. Reducing caffeine intake, especially in people sensitive to its effects, can be beneficial. 3. Which cells are involved with inflammation? 1. **Neutrophils:** - **Role:** First responders, eat up invaders (phagocytosis). - **Remember:** \"Neutro- = Neutralizes threats quickly.\" 2. **Macrophages:** - **Role:** Clean up crew, engulf debris and activate more immune cells. - **Remember:** \"Macro- = Big eaters.\" 3. **Lymphocytes:** - **Role:** T cells and B cells, target specific invaders and produce antibodies. - **Remember:** \"Lympho- = Long-term memory (adaptive immunity).\" 4. **Mast Cells:** - **Role:** Release histamine, cause swelling and redness. - **Remember:** \"Mast = Massive histamine release.\" 5. **Eosinophils:** - **Role:** Fight parasites and contribute to allergies. - **Remember:** \"Eosin- = Ejects granules.\" 6. **Basophils:** - **Role:** Similar to mast cells, involved in allergic reactions. - **Remember:** \"Baso- = Baseline allergic response.\" 7. **Platelets:** - **Role:** Form clots, also release signals to boost inflammation. - **Remember:** \"Platelets = Plug and protect.\" 8. **Dendritic Cells:** - **Role:** Present antigens to T cells, kickstart immune response. - **Remember:** \"Dendritic = Dispatch to T cells.\" 9. **Endothelial Cells:** - **Role:** Line blood vessels, control immune cell entry. - **Remember:** \"Endo- = Entry control.\" 10. **Fibroblasts:** - **Role:** Repair tissue, build up new structure. - **Remember:** \"Fibro- = Fibers for healing.\" 4. What is the purpose of the inflammatory process? **1. Recognize Harmful Stimuli** - **Cells Involved:** - **Macrophages** and **Dendritic Cells** are among the first to recognize harmful agents through pattern recognition receptors (PRRs), like Toll-like receptors (TLRs). - **Complement System:** - The complement system, a group of proteins in the blood, can be activated directly by pathogens. It helps identify and mark pathogens (opsonization) for destruction by immune cells. **2. Recruit Immune Cells** - **Cells Involved:** - **Neutrophils:** First responders that are rapidly recruited to the site of injury or infection. - **Macrophages:** Arrive after neutrophils and help sustain the inflammatory response. - **Mast Cells:** Release histamine and other mediators that increase blood vessel permeability, allowing immune cells to move more easily to the site of infection. - **Complement System:** - Activated complement proteins (e.g., C3a, C5a) act as chemoattractants, drawing neutrophils and other immune cells to the site of inflammation. **3. Remove Harmful Agents** - **Cells Involved:** - **Neutrophils:** Engulf and digest pathogens through phagocytosis. - **Macrophages:** Continue phagocytosis, clearing away not only pathogens but also dead and dying cells, including neutrophils. - **Complement System:** - The complement system forms membrane attack complexes (MACs) that can directly lyse (break down) bacterial cell walls, aiding in the destruction of pathogens. **4. Regulate the Inflammatory Response** - **Cells Involved:** - **T Cells:** Release cytokines that can either amplify or regulate (suppress) the inflammatory response. - **Macrophages:** Release cytokines like IL-1, TNF-alpha, and IL-6 that regulate the intensity and duration of inflammation. - **Eosinophils and Basophils:** Involved in allergic responses and modulate inflammation through the release of various mediators. - **Complement System:** - Complement proteins, such as C1 inhibitor, regulate the complement cascade to prevent excessive inflammation, ensuring that the response does not damage healthy tissue. **5. Resolve the Inflammation** - **Cells Involved:** - **Macrophages:** Transition to a pro-resolving state, releasing anti-inflammatory cytokines like IL-10 and TGF-beta, which help to suppress inflammation. - **Regulatory T Cells:** Help in shutting down the inflammatory response and promoting tissue healing. - **Complement System:** - As inflammation resolves, the complement system is downregulated to prevent continued activation, which could lead to chronic inflammation. **6. Repair and Heal Tissue** - **Cells Involved:** - **Fibroblasts:** Activated during the later stages to produce collagen and other extracellular matrix components, essential for tissue repair and the formation of scar tissue. - **Macrophages:** Release growth factors that stimulate tissue regeneration and recruit fibroblasts to the site. - **Complement System:** - Although the complement system is primarily involved in the early stages of inflammation, its role diminishes as the process shifts towards resolution and tissue repair. 5. What causes edema in the inflammatory process? **[Steps Leading to Edema]** 1. **Sensitization Phase:** - **Exposure to Allergen:** The first exposure to an allergen (e.g., pollen) leads to the production of IgE antibodies by B cells. - **IgE Binding:** These IgE antibodies bind to receptors on the surface of mast cells and basophils, \"sensitizing\" them to the allergen. 2. **Re-exposure and Activation:** - **Subsequent Exposure:** Upon re-exposure to the same allergen, it binds to the IgE on the sensitized mast cells and basophils. - **Degranulation:** This binding triggers these cells to release pre-formed granules containing histamine, heparin, and other mediators into the surrounding tissues. 3. **Release of Inflammatory Mediators:** - **Histamine:** One of the primary mediators, histamine, increases the permeability of blood vessels (capillaries) by causing the endothelial cells lining the blood vessels to contract and create gaps. - **Prostaglandins and Leukotrienes:** These are synthesized from arachidonic acid after the mast cells are activated. They also contribute to increased vascular permeability and vasodilation. 4. **Vasodilation and Increased Vascular Permeability:** - **Vasodilation:** The blood vessels dilate, increasing blood flow to the area, which raises hydrostatic pressure within the capillaries. - **Increased Permeability:** The gaps between endothelial cells allow fluids, proteins, and immune cells to leak out of the blood vessels and into the surrounding tissue. 5. **Fluid Accumulation (Edema):** - **Fluid Leakage:** As fluids and proteins leak into the interstitial space (the space between cells), they accumulate, leading to the characteristic swelling or edema associated with allergic reactions. - **Result:** This process results in the common signs of an allergic reaction, such as swelling (edema), redness, and itching. **[Key Points]** - **Histamine** is the main mediator that causes blood vessels to become \"leaky,\" leading to fluid accumulation. - **Prostaglandins and Leukotrienes** also play a role in enhancing vascular permeability and maintaining the inflammatory response. - **Edema** in Type I hypersensitivity reactions is a direct consequence of fluid leakage into tissues due to increased vascular permeability and vasodilation. 6. Active versus passive immunity **[Active Immunity]** - **Pathophysiology:** When your body encounters a pathogen (like a virus or bacteria) or is exposed to a vaccine, the immune system triggers a response. B cells produce antibodies specific to the pathogen, and T cells may also be activated to destroy infected cells. Over time, memory B cells and T cells are formed, which \"remember\" the pathogen. If you\'re exposed to the same pathogen again, these memory cells allow your body to mount a faster and stronger immune response. - **Duration:** Long-lasting, often for years or even a lifetime, due to the creation of memory cells. - **Examples:** - **Natural:** Recovering from chickenpox. Your body fights off the virus, creating long-term immunity. - **Artificial:** Getting the flu vaccine. Your immune system produces specific antibodies, protecting you from the flu. - **Mnemonic:** **\"Active = A for Army\"** (Your body builds its own defense). **[Passive Immunity]** - **Pathophysiology:** In passive immunity, antibodies are provided to your body from an external source, rather than being produced by your own immune system. These antibodies can immediately neutralize pathogens, but since your body did not create them, no memory cells are formed. This means your immune system won't remember the pathogen, and the immunity only lasts as long as the antibodies are present in your system. - **Duration:** Short-term, as the protection fades when the externally provided antibodies are eventually broken down and eliminated from the body. - **Examples:** - **Natural:** A newborn receiving antibodies through breast milk, providing temporary immunity against infections. - **Artificial:** Receiving antivenom after a snake bite. The antivenom provides immediate protection by neutralizing the venom, but the effect is temporary since the body does not produce the antibodies itself. - **Mnemonic:** **\"Passive = P for Present\"** (You're given a ready-made gift of antibodies). **[Summary]** - **Active Immunity:** Your body produces its own antibodies and memory cells, offering long-lasting protection. Examples include recovering from an illness or getting vaccinated. - **Passive Immunity:** You receive antibodies from another source, providing immediate but temporary protection. Examples include maternal antibodies passed to a baby or receiving antivenom after a snake bite. 7. Most abundant immunoglobulin - The most abundant immunoglobulin in the human body is **IgG**. This antibody is crucial for long-term immunity and is the most prevalent in the blood and extracellular fluid. IgG plays several important roles in the immune system, including neutralizing pathogens, opsonizing microbes for easier phagocytosis, and activating the complement system, which helps to destroy pathogens. Additionally, IgG is unique among immunoglobulins because it can cross the placenta, providing passive immunity to the fetus during pregnancy 8. Define carcinoma **Carcinoma** is a type of cancer that originates in the epithelial cells, which are the cells that line the inner and outer surfaces of the body. Epithelial cells are found in the skin, as well as in the lining of organs such as the liver, lungs, and breasts. When these cells begin to grow uncontrollably and invade surrounding tissues, they form a carcinoma. There are different types of carcinomas depending on the specific epithelial cells involved: - **Basal Cell Carcinoma:** This type originates from the basal cells in the skin and is the most common type of skin cancer. It typically presents as a pearly papule or nodule and is often found on sun-exposed areas of the body. - **Squamous Cell Carcinoma:** Arises from squamous cells, which are flat cells found on the surface of the skin, in the lining of the esophagus, and other organs. It can cause tumors that are often linked to risk factors like smoking or chronic UV exposure. - **Adenocarcinoma:** A subtype of carcinoma that arises from glandular tissues. It commonly occurs in organs such as the breast, prostate, and lungs. In general, carcinomas are **malignant tumors**, meaning they have the potential to spread (metastasize) to other parts of the body and are often associated with significant morbidity and mortality. 9. Pathology of Alzheimer's disease Alzheimer's disease involves the abnormal build-up of two key proteins in the brain: **beta-amyloid** and **tau**. These proteins disrupt brain cell function and lead to the symptoms of the disease. 1. **Beta-Amyloid Plaques:** - Beta-amyloid is a protein fragment that normally comes from a larger protein called amyloid precursor protein (APP). These fragments clump together to form plaques. - This build up between brain cells (neurons) blocks the signals that neurons send to each other. This disruption in communication is harmful to brain function and leads to the death of neurons. 2. **Tau Protein and Neurofibrillary Tangles:** - Tau usually helps stabilize the structure of neurons by binding to microtubules, which are like tiny tracks inside cells that help transport nutrients and keep the cell\'s structure intact. - In Alzheimer's, tau proteins become abnormal and start sticking together inside neurons, forming twisted structures called neurofibrillary tangles. These tangles mess up the internal structure of neurons, leading to their dysfunction and death. This is another major factor that causes memory loss and cognitive decline in Alzheimer's. **How Beta-Amyloid and Tau Work Together:** - The process usually starts with the buildup of beta-amyloid plaques. - As plaques accumulate, they trigger tau proteins to change and form tangles inside the neurons. - The combination of plaques outside neurons and tangles inside them causes more and more neurons to stop working properly, leading to the progression of Alzheimer's symptoms. 10. Signs and symptoms of multiple sclerosis 1. **Visual Problems:** - **Optic Neuritis:** One of the earliest signs of MS is often optic neuritis, which is inflammation of the optic nerve. This can cause unilateral (one-sided) visual impairment, blurred vision, and pain with eye movement. - **Nystagmus:** Uncontrolled eye movements that can lead to vision problems. - **Double Vision (Diplopia):** Caused by lesions affecting the nerves that control eye movement. 2. **Sensory Disturbances:** - **Lhermitte's Sign:** A shock-like sensation that runs down the spine, often triggered by bending the neck forward. - **Paresthesia:** Tingling, numbness, or \"pins and needles\" sensations, often occurring in the limbs or face. 3. **Motor Symptoms:** - **Muscle Weakness:** Especially in the limbs, which can affect walking and coordination. - **Spasticity:** Increased muscle tone leading to stiffness and involuntary muscle contractions. - **Ataxia:** Loss of full control of bodily movements, resulting in clumsiness or lack of coordination. 4. **Cranial Nerve Signs:** - **Internuclear Ophthalmoplegia (INO):** A specific eye movement disorder caused by lesions in the brainstem, leading to difficulty with lateral gaze (side-to-side eye movements). - **Facial Weakness:** May present similar to Bell's palsy. 5. **Autonomic Symptoms:** - **Bladder and Bowel Dysfunction:** Urinary incontinence, urgency, or retention, and sometimes constipation or bowel incontinence. - **Sexual Dysfunction:** Issues with sexual response and function. 6. **Cognitive and Emotional Changes:** - **Cognitive Impairment:** Problems with memory, attention, and problem-solving. - **Depression and Anxiety:** Common emotional responses, possibly exacerbated by the physical and social challenges of the disease. 7. **Fatigue:** - **Chronic Fatigue:** A common and debilitating symptom, which is often unrelated to physical activity and can be severe enough to interfere with daily activities. 8. **Uhthoff's Phenomenon:** - **Worsening of Symptoms with Heat:** Symptoms may temporarily worsen in hot environments or after exercise due to increased body temperature. 11. Patho of multiple sclerosis 1. **Breakdown of the Blood-Brain Barrier (BBB):** - Normally, the blood-brain barrier protects the CNS by preventing harmful substances and immune cells from entering. In MS, the BBB becomes compromised, allowing immune cells, particularly T lymphocytes, to infiltrate the CNS. 2. **Immune Cell Infiltration:** - **Th1 Cells:** These T lymphocytes cross the compromised BBB and release gamma interferon, which activates macrophages. The activated macrophages then release inflammatory cytokines like tumor necrosis factor-alpha (TNF-α), contributing to inflammation within the CNS. - **Cytotoxic T-Lymphocytes:** These cells are also activated by Th1 cells and directly attack the myelin sheath, leading to its destruction. 3. **Autoantibody Production:** - **Th2 Cells and Astrocytes:** Astrocytes present antigens to Th2 cells, which in turn help B cells differentiate into plasma cells. These plasma cells produce autoantibodies against components of the myelin sheath, such as myelin basic protein, myelin oligodendrocyte glycoprotein, and myelin-associated glycoprotein. - These autoantibodies further contribute to the destruction of the myelin sheath, exacerbating the demyelination process. 4. **Demyelination and Plaque Formation:** - The immune attack on the myelin sheath results in the formation of inflammatory lesions known as plaques. These plaques are most commonly found in the white matter of the CNS, particularly around the lateral ventricles, brainstem, spinal cord, and optic nerves. - **Dawson's Fingers:** Plaques often follow the course of periventricular veins, creating a characteristic pattern known as \"Dawson's fingers\" on MRI scans. 5. **Neuronal Damage:** - The loss of myelin impairs the ability of neurons to transmit signals efficiently, leading to the neurological deficits observed in MS. Over time, this can lead to axonal damage and neurodegeneration, which contribute to the progression of disability in MS patients. **[Summary]** - Breakdown of the blood-brain barrier, allowing immune cells to enter the CNS. - **Immune Attack:** Involves Th1 and cytotoxic T-lymphocytes directly attacking the myelin sheath, and Th2 cells helping B cells produce damaging autoantibodies. - **Demyelination:** Results in plaque formation, primarily in the CNS\'s white matter, leading to impaired neuronal function and progression of the disease. 12. How do you identify Myasthenia Gravis 1. **Muscle Weakness:** - **Fatigable Weakness:** Muscle strength diminishes with repeated use and improves with rest. This is a hallmark of MG. - **Proximal Weakness:** Typically affects muscles closer to the trunk, such as the shoulders and hips, more than distal muscles (hands and feet). 2. **Ocular Symptoms:** - **Ptosis:** Drooping of one or both eyelids, often noticed as the day progresses or with sustained upward gaze. - **Diplopia:** Double vision, which may become more pronounced after reading or other prolonged visual tasks. 3. **Bulbar Symptoms:** - **Dysarthria:** Slurred or slow speech due to weakness in the muscles involved in speech. - **Dysphagia:** Difficulty swallowing, leading to potential choking or aspiration. 4. **Respiratory Symptoms:** - **Dyspnea:** Difficulty breathing due to weakness in the respiratory muscles, which can lead to respiratory failure in severe cases. **[Diagnostic Approach]** 1. **Nerve Conduction Studies (NCS):** - **Decremental Response:** A characteristic finding in MG where repeated nerve stimulation results in a progressively weaker response. 2. **Electromyography (EMG):** - **Increased Jitter:** Single-fiber EMG often shows increased variability in the time it takes for muscle fibers to respond to nerve signals, known as "jitter." 3. **Response to Acetylcholinesterase Inhibitors:** - **Diagnostic Test:** A positive response to medications like pyridostigmine, which increase acetylcholine availability at the neuromuscular junction, supports the diagnosis of MG. 4. **Chest Imaging:** - **Thymic Abnormalities:** A chest X-ray or CT scan may reveal a thymoma or thymic hyperplasia, conditions associated with MG. 13. Signs and symptoms of Meningitis - **Severe Headache:** Most common symptom, often described as diffuse and persistent. - **Neck Stiffness (Meningismus):** Stiff neck with difficulty in flexing the neck forward. - **Fever:** Often high and accompanied by chills. - **Nausea and Vomiting:** Accompany the headache; due to increased intracranial pressure. - **Photophobia:** Sensitivity to light is a common feature, especially in viral meningitis. - **Altered Mental Status:** Confusion, drowsiness, or even coma can occur. - **Seizures:** Particularly in bacterial meningitis, seizures may be a presenting symptom. - **Rash:** In cases of meningococcal meningitis, a petechial or purpuric rash may develop. **[Specific Signs Based on Type of Meningitis]** - **Bacterial Meningitis:** - Rapid onset of symptoms. - **Classic Triad:** Fever, neck stiffness, and altered mental status. - May show positive Kernig\'s and Brudzinski\'s signs (specific physical exam tests indicating meningitis). - **Viral Meningitis:** - Generally milder symptoms compared to bacterial meningitis. - Gradual onset with headache, fever, and neck stiffness. - Normal mental status is more common. - **Fungal Meningitis:** - Typically presents in immunocompromised individuals. - Symptoms are similar to bacterial meningitis but with a more insidious onset. **[Diagnostic Clues]** - **Kernig\'s Sign:** Pain and resistance when extending the knee while the hip is flexed at 90̊ - **Brudzinski\'s Sign:** Involuntary lifting of the legs when lifting a patient\'s head off the examining table. 14. How do you identify Parkinsons 1. **Resting Tremor:** - A common early sign, typically starting in one hand, and may spread to other limbs. The tremor often subsides with intentional movement and worsens at rest. 2. **Bradykinesia:** - Patients experience a noticeable slowing of movement. Activities like walking, dressing, or even writing become slower and more difficult to initiate. 3. **Rigidity:** - There is increased muscle tone/stiffness and resistance to movement in the arms, legs, or neck. Can cause discomfort and limit the range of motion. 4. **Postural Instability:** - As the disease progresses, patients often develop problems with balance, making them more prone to falls. This symptom usually appears later in the disease course. 5. **Shuffling Gait:** - A characteristic shuffling walk with short, hesitant steps and a reduced arm swing. May also have difficulty starting and stopping movement. 6. **Non-Motor Symptoms:** - **Mood Changes:** Depression and anxiety are common. - **Cognitive Decline:** While not present in early stages, some patients may develop cognitive symptoms, including dementia, in advanced stages. - **Sleep Disturbances:** Problems with sleep, including REM sleep behavior disorder, are common. **[Diagnostic Clues]** - **Asymmetry:** Symptoms start on one side of the body and remain more severe on that side. - **Response to Dopaminergic Medication:** A significant improvement in symptoms with medications like levodopa strongly supports the diagnosis. 15. Anorexia nervosa vs. Bulimia **[Anorexia Nervosa]** - **Definition**: Characterized by a limitation of food intake, leading to a body weight less than 85% of the expected weight for age and height. Patients have an intense fear of gaining weight and a distorted perception of their body size and shape, often seeing themselves as overweight despite being underweight. - **Clinical Signs**: - Low BMI (usually below 18) - Orthostatic hypotension - Cachectic appearance (severe thinness) - Bradycardia (slow heart rate) - Hypothermia (low body temperature) - Dry skin and cold extremities - Increased lanugo hair (fine soft hair) - Secondary amenorrhea (loss of menstrual periods) **[Bulimia Nervosa]** - **Definition**: Involves recurrent episodes of binge eating (eating large amounts of food with a sense of loss of control) followed by inappropriate compensatory behaviors, such as self-induced vomiting, laxative use, diuretics, or excessive exercise, to prevent weight gain. These episodes occur at least twice a week for three months. - **Clinical Signs**: - Normal or increased body weight - Orthostatic hypotension - Salivary gland enlargement (from vomiting) - Dental erosions (due to stomach acid from vomiting) - Knuckle calluses (from self-induced vomiting) - Potential electrolyte imbalances like hypokalemia 16. How do you evaluate seizures? **1. History Taking**: - Establish if the seizure is a new occurrence or part of a recurrent pattern. This helps determine if the patient may have epilepsy or if the seizure was provoked by other factors. - For patients with a history of seizures or epilepsy, assess whether they are adhering to their antiepileptic medication regimen. Non-compliance is a common cause of breakthrough seizures. - Identify recent factors that may have triggered the seizure, such as infections, fever, substance use, or withdrawal. These factors are particularly important in identifying febrile seizures or seizures related to metabolic disturbances. - A family history of epilepsy increases the risk of seizure recurrence and the potential development of epilepsy, particularly in children with febrile seizures. - Obtain detailed eyewitness accounts if the seizure was observed by someone else. This helps distinguish between different types of seizures and seizure mimics. **2. Physical Examination**: - **Post-Seizure Findings**: - **Incontinence**: Check for loss of bladder or bowel control, which can occur during or after a seizure, particularly in generalized tonic-clonic seizures. - **Oral Trauma**: Look for evidence of tongue biting or other oral injuries, which are common in convulsive seizures. - **Post-Ictal Confusion**: Assess the patient\'s mental status after the seizure. Confusion or disorientation is characteristic of the post-ictal state following generalized seizures. - **Neurological Examination**: Conduct a thorough neurological exam to identify any focal deficits, which might suggest a structural brain lesion as the cause of the seizure. **3. Differential Diagnosis**: - **Seizure Mimics**: Differentiate true epileptic seizures from conditions that can mimic seizures, such as syncope, migraines, or psychogenic events. **4. Diagnostic Evaluation**: - **Medication Levels**: For patients already on antiepileptic medications, checking drug levels can confirm adherence and therapeutic range. For example, phenytoin or levetiracetam levels might be assessed. - **Laboratory Tests**: Basic labs, including electrolytes, glucose, and possibly a toxicology screen, should be performed to rule out metabolic or toxic causes of the seizure. - **Neuroimaging**: If there is concern for a structural brain abnormality, such as a tumor or hemorrhage, an MRI or CT scan may be indicated. - **Electroencephalogram (EEG)**: Helps diagnose epilepsy and differentiate between seizure types. It can identify abnormal electrical activity in the brain. **5. Management**: - **Airway Management**: Ensure that the patient\'s airway is protected, particularly if they have experienced tongue biting or oral trauma during the seizure. - **Medication Administration**: If the seizure was due to missed doses of antiepileptic drugs, these should be administered promptly. Acute seizures may require benzodiazepines, such as lorazepam, for termination. - **Chronic Management**: Adjust antiepileptic medications, treating any underlying conditions, and possibly referring the patient to a neurologist. 17. What is anti-diuretic hormone, where is it synthesized, where does it act? - **What is ADH?** - ADH, also known as vasopressin, is a hormone that primarily regulates water balance in the body. - **Where is ADH Synthesized?** - ADH is synthesized in the hypothalamus; stored and released by the posterior pituitary gland. - **Where Does ADH Act?** - ADH acts on the kidneys, specifically on the collecting ducts. It increases the permeability of these ducts to water, allowing more water to be reabsorbed back into the bloodstream, thus concentrating the urine and conserving body water. 18. What would you order to evaluate a "lump on the trachea"? 1. **Physical Examination**: - Assess the size, consistency, and mobility of the lump. - Check for associated symptoms like dysphagia (difficulty swallowing), hoarseness, or respiratory distress. 2. **Ultrasound of the Neck**: - **Purpose**: To visualize the lump and determine if it\'s related to the thyroid gland, lymph nodes, or other structures around the trachea. - **Details**: Particularly useful in differentiating between solid and cystic masses, as well as evaluating thyroid nodules or goiter. 3. **Fine Needle Aspiration (FNA) Biopsy**: - **Purpose**: To obtain cells from the lump for cytological examination. - **Details**: Especially indicated if the lump is suspected to be a thyroid nodule, as this can help in distinguishing between benign and malignant nodules. 4. **CT or MRI Scan**: - **Purpose**: To provide detailed imaging of the trachea and surrounding structures. - **Details**: These scans can help in assessing the extent of the lump, its relationship to adjacent structures, and potential invasion into the trachea or other tissues. 5. **Chest X-ray**: - **Purpose**: To evaluate the lungs and mediastinum for any associated abnormalities. - **Details**: Can help in ruling out or identifying related respiratory conditions, such as tracheal deviation or lung masses. 6. **Thyroid Function Tests**: - **Purpose**: To assess thyroid hormone levels if the lump is suspected to be related to the thyroid gland. - **Details**: Includes tests like TSH, Free T4, and possibly thyroid antibodies, depending on the clinical context. 7. **Bronchoscopy** (if indicated): - **Purpose**: Direct visualization of the trachea and bronchi. - **Details**: Useful for examining the internal structure of the trachea, especially if there is suspicion of intraluminal involvement by the lump. 19. Pathogenesis of type 2 DM and risk factors 1. **Insulin Resistance:** - **What Happens:** Cells in muscle, fat, and liver become less responsive to insulin. - **Result:** More insulin is needed to manage glucose, leading to initial hyperinsulinemia but reduced glucose uptake, causing hyperglycemia. 2. **Beta Cell Dysfunction:** - **Early Compensation:** Pancreas increases insulin production to combat resistance. - **Decline:** Over time, beta cells can\'t keep up, leading to decreased insulin output. - **Contributors:** High glucose (glucotoxicity), high fatty acids (lipotoxicity), and inflammation damage beta cells. 3. **Impaired Glucose Homeostasis:** - **Liver:** Keeps making glucose even when not needed (due to insulin resistance). - **Muscle & Fat:** Less glucose is taken up for energy, and more fat is broken down, worsening insulin resistance. 4. **Persistent Hyperglycemia:** - **Outcome:** Chronic high blood sugar leads to complications in blood vessels (eyes, kidneys, nerves, heart). 5. **Incretin Effect:** - **Diminished Response:** Hormones that boost insulin after eating don\'t work well in T2DM, worsening post-meal blood sugar spikes. 20. Goal hemoglobin A1C for diabetic patients - Diabetes mellitus is considered HbA1c ≥ 6.5%Top of Form - Prediabetes is considered HbA1c levels between 5.7% to 6.4% - Aim for levels \ 1. **Increased Estrogen Exposure**: - Factors such as hormone replacement therapy, early menarche, late menopause, and polycystic ovarian syndrome increase estrogen levels, which is associated with a higher risk of breast cancer. 2. **Increased Total Menstrual Cycles**: - A higher number of menstrual cycles correlates with prolonged estrogen exposure, increasing breast cancer risk. 3. **Obesity**: - Obesity contributes to increased estrogen production through the process of aromatization in adipocytes (fat cells), which raises the risk of breast cancer. 4. **Genetic Factors**: - BRCA1 and BRCA2 genes are linked to an increased risk of breast cancer. 22. CD4 count for diagnosis of AIDS **Staging of HIV Infection** - **Stage 1:** **CD4 Count:** \ 500 cells/μL. - **Symptoms:** No visible signs of HIV. - **Stage 2:** **CD4 Count:** 200-499 cells/μL. - **Symptoms:** Still no AIDS-defining illnesses. - **Stage 3 (AIDS):** **CD4 Count:** \< 200 cells/μL. - **Symptoms:** Presence of illnesses that define AIDS. 23. What hormones are involved in **menopause** - **Estrogen**: Levels decrease, leading to symptoms like hot flashes and bone density loss. - **Progesterone**: Also decreases, contributing to the end of menstrual cycles. - **FSH and LH**: Levels **increase** due to the lack of negative feedback from estrogen and progesterone, signaling the ovaries to produce hormones that are no longer effectively produced. 24. How do you treat testicular torsion? - **Orchiopexy**: **Untwist** the spermatic cord and **fixate** the testicle to prevent recurrence. - **Time-sensitive**: Must be treated within 6 hours to prevent irreversible testicular damage. 25. The first sign of puberty for males and females - **Males** testicular enlargement - **Females** breast development (thelarche) 26. Identify a varicocele versus spermatocele versus hydrocele **[Varicocele]** - Enlargement of the veins within the scrotum. More common on the left side. - A \"**bag of worms**\" appearance, typically painless but may cause a dull ache or heaviness. **[Hydrocele]** - Accumulation of fluid around the testicle. Can be congenital, acquired, or associated with underlying infection. - Painless scrotal swelling that transilluminates with light. **[Spermatocele]** - A cyst that forms in the epididymis. Idiopathic; 2/2 blockage in the epididymal ducts. - Painless, cystic mass at the head of the epididymis. Contains milky fluid and sperm. 27. What causes an action potential from the resting state? - An action potential is triggered when a stimulus causes the neuron to become less negative inside, a process called depolarization. Normally, the neuron is at rest with a voltage of about -70 mV. When a stimulus opens sodium (Na⁺) channels, sodium ions rush into the cell, making the inside less negative. If this change reaches a critical level, known as the threshold (around -55 mV), it causes a rapid and large change in voltage, called an action potential. This action potential is the signal that travels down the neuron to communicate with other cells. 28. Where is RNA and DNA stored? **[DNA]** - **Nucleus**: Most of the cell's DNA is located in the nucleus, where it stores genetic information and controls the cell's activities. - **Mitochondria**: A small amount of DNA is also found in the mitochondria, known as mitochondrial DNA (mtDNA), which is involved in energy production for the cell. **[RNA]** - RNA is primarily located in the nucleus (where it\'s made) and the cytoplasm (where it functions). - **Nucleus**: RNA is synthesized in the nucleus during the process of transcription, where DNA is used as a template to create messenger RNA (mRNA). - **Cytoplasm**: Once transcribed, mRNA is transported to the cytoplasm where it is translated into proteins by ribosomes. Transfer RNA (tRNA) and ribosomal RNA (rRNA) are also found in the cytoplasm and play crucial roles in protein synthesis. - **Mitochondria**: Mitochondria have their own RNA, called mitochondrial RNA (mtRNA), which is involved in the production of proteins needed for the mitochondrion\'s functions. - **Ribosomes**: Ribosomes, which are composed of rRNA and proteins, are the sites of protein synthesis where mRNA is translated into proteins. \*Sidenote: If you were thinking that RNA is stored in the rough endoplasmic reticulum, that\'s not the case. The rough ER has ribosomes on its surface that translate mRNA into proteins. These proteins are then either secreted, inserted into the cell membrane, or sent to organelles. Therefore, RNA isn\'t stored in the ER, but it does play a key role in protein synthesis there. 29. Starling's Law - Starling\'s Law states that the more the heart is filled with blood, the stronger it contracts, which increases the amount of blood pumped out. [Read the following for review] Starling\'s Law, also known as the Frank-Starling Law of the Heart, describes how the heart\'s stroke volume increases in response to an increase in the volume of blood filling the heart (the end-diastolic volume or preload). The basic idea is that the more the heart muscle is stretched during filling, the stronger the subsequent contraction will be, leading to a greater stroke volume. - **Preload:** The amount of blood returning to the heart and filling the ventricles before contraction. This \"stretch\" on the heart muscle fibers is what primarily influences the force of the next contraction. - **Stroke Volume:** The amount of blood pumped out of the heart with each beat. According to Starling's Law, as preload increases, stroke volume also increases, up to a certain point. - **Mechanism:** This relationship occurs because cardiac muscle fibers contract more forcefully when stretched, similar to how a rubber band snaps back with more force when stretched further. This process doesn't require extra energy; it's simply due to the nature of muscle fibers. 30. Understand the renin-angiotensin system - - - - - - 31. What is the action of renin? - Renin is an enzyme released by the kidneys that converts angiotensinogen (a protein produced by the liver) into angiotensin I, which is the first step in a series of reactions that ultimately lead to an increase in blood pressure. - **\"Renin Raises Pressure\":** Remember that renin starts the process to raise blood pressure through angiotensin and aldosterone. [Read the following for review] 1\. **Production of Renin:** - **Origin:** Renin is an enzyme produced by specialized cells in the kidneys known as **juxtaglomerular cells**. These cells are located near the glomeruli, which are the tiny filtering units of the kidneys. - **Trigger for Release:** Renin is released into the bloodstream in response to certain conditions, such as: - Low blood pressure. - Decreased blood flow to the kidneys. - Low sodium levels in the blood. 2\. **Action of Renin:** - **Conversion of Angiotensinogen:** Once released into the bloodstream, renin acts on a protein called **angiotensinogen**, produced by the liver and always present in blood. - **Formation of Angiotensin I:** Renin converts angiotensinogen into **angiotensin I**, a relatively inactive precursor hormone. 3\. **Subsequent Steps in the Renin-Angiotensin System:** - **Conversion to Angiotensin II:** Angiotensin I is then converted into **angiotensin II** by an enzyme called **angiotensin-converting enzyme (ACE)**, primarily in the lungs. - **Effects of Angiotensin II:** - **Vasoconstriction:** Angiotensin II causes blood vessels to constrict, which raises blood pressure. - **Aldosterone Release:** Angiotensin II also stimulates the adrenal glands (located on top of the kidneys) to release **aldosterone**, a hormone that prompts the kidneys to retain sodium and water, further increasing blood volume and pressure. - **ADH Release:** Angiotensin II stimulates the release of **antidiuretic hormone (ADH)**, which helps the kidneys retain water, contributing to increased blood volume. **Overall Role in the Body** - **Regulation of Blood Pressure:** The primary role of renin, through its action in the renin-angiotensin system, is to regulate blood pressure. By initiating the cascade that leads to the production of angiotensin II, renin helps the body respond to low blood pressure or low blood flow by raising blood pressure and increasing fluid retention. **Summary** - **Renin:** Enzyme released by the kidneys in response to low blood pressure/low blood flow. - **Action:** Converts angiotensinogen (from the liver) into angiotensin I, which is then converted into angiotensin II. - **Effect:** Angiotensin II raises blood pressure by constricting blood vessels and increasing fluid retention through aldosterone and ADH. 32. Pathogen for pneumonia 1. **Community-Acquired Pneumonia (CAP)**: - **Streptococcus pneumoniae**: Most common cause. - **Mycoplasma pneumoniae**: Associated with atypical pneumonia, especially in younger patients. - **Haemophilus influenzae**: Often seen in patients with chronic lung disease. 2. **Hospital-Acquired Pneumonia (HAP)**: - **Staphylococcus aureus** (including MRSA): Can cause severe pneumonia, especially after surgeries or in patients on ventilators (ventilator-associated pneumonia). 3. **Atypical Pneumonia**: - **Legionella pneumophila**: Often linked to contaminated water sources. - **Chlamydia pneumoniae**: Another cause of atypical pneumonia, typically milder. 33. Identify COPD, and how do you diagnose it? **[Symptoms]** - Breathlessness worsens with exertion. - - - Chronic cough with sputum, often dirty or gray-black. - - Wheezing and occasional blood in sputum. - Chest discomfort from coughing and muscle strain. - Ankle edema due to right heart failure. - Fatigue - Weight loss - High CO2 can lead to morning headaches and drowsiness. - Low FEV1 **[Diagnosing COPD]** - **Spirometry** is the gold standard: - **FEV1 (Forced Expiratory Volume in one second):** Reduced more than FVC (Forced Vital Capacity). - **FEV1/FVC Ratio:** Less than 70% confirms airflow limitation. - **Bronchodilator Response:** Minimal improvement suggests COPD. - **Severity Assessment:** - **FEV1 \< 50%** indicates severe COPD. - **Residual Volume (RV) and Total Lung Capacity (TLC):** Increased due to air trapping, particularly in emphysema. - **Diffusion Capacity of the Lung for Carbon Monoxide (DLCO):** Reduced in emphysema, normal in chronic bronchitis. - **Additional Measures:** - **Peak Expiratory Flow Rate (PEFR):** Reduced due to airflow obstruction. - **Chest X-Ray:** Used to rule out other lung conditions and may show signs of hyperinflation or a flattened diaphragm. 34. UA testing for UTI **Urinalysis (UA):** Used to diagnose urinary tract infections (UTIs) 1. **Appearance:** - **Cloudy Urine:** Can indicate an infection. 2. **Dipstick Test:** - **Leukocyte Esterase:** Positive if there are white blood cells (WBCs) in the urine, indicating infection. - **Nitrites:** Positive if bacteria are present, particularly *E. coli*. 3. **Microscopic Examination:** - **WBCs (Pyuria):** High levels suggest infection. - **Bacteria:** Presence confirms infection. - **RBCs (Hematuria):** Blood in urine can be a sign of UTI. - **Casts:** WBC casts may indicate kidney infection (pyelonephritis). **[How to Interpret]** - **Positive for Leukocyte Esterase and Nitrites** + **Symptoms (e.g., pain during urination):** Likely UTI. - **Microscopic Confirmation:** WBCs and bacteria further confirm the diagnosis. 35. What is the risk of chronic GERD? - **Esophagitis**: Persistent acid reflux can cause inflammation of the esophagus, leading to esophagitis, which can result in pain, bleeding, and difficulty swallowing. - **Barrett's Esophagus**: Chronic GERD can cause changes in the cells lining the lower esophagus, a condition known as Barrett\'s esophagus. This condition increases the risk of developing esophageal adenocarcinoma, a type of esophageal cancer. - **Esophageal Strictures**: Repeated damage from acid can cause scar tissue to form, leading to narrowing of the esophagus (strictures), which can cause swallowing difficulties. - **Esophageal Carcinoma**: Long-term GERD, particularly when it leads to Barrett's esophagus, significantly increases the risk of esophageal adenocarcinoma, a serious and potentially fatal type of cancer. 36. Education recommendations for managing osteoarthritis and gout **[Osteoarthritis (OA) Management]** 1. **Weight Management** - **Importance**: Reducing body weight helps decrease stress on weight-bearing joints, such as the knees and hips. - **Recommendation**: Encourage maintaining a healthy weight through a balanced diet and regular exercise. 2. **Exercise and Physical Therapy** - **Exercise**: Low-impact activities like swimming, walking, and cycling can improve joint mobility and strength without worsening pain. - **Physical Therapy**: A physical therapist can design a personalized exercise program to strengthen muscles around the joints and improve flexibility. 3. **Medications**: - **Pain Relief**: Over-the-counter pain relievers like acetaminophen or NSAIDs (e.g., ibuprofen) are commonly used. - **Topical Treatments**: Creams and gels containing NSAIDs can be applied directly to the affected joints for pain relief. 4. **Joint Protection**: - **Use of Assistive Devices**: Braces, orthotics, and canes can help reduce joint stress and improve mobility. - **Activity Modification**: Avoid repetitive motions or activities that stress the joints. 5. **Lifestyle Adjustments**: - **Heat and Cold Therapy**: Applying heat can ease stiffness, while cold packs can reduce inflammation and numb pain. - **Joint-Friendly Activities**: Encourage hobbies and activities that are gentle on the joints, such as swimming or yoga. 6. **Surgical Options**: - **Indication**: Consider surgery (e.g., joint replacement) for severe OA that does not respond to conservative treatments and significantly impacts quality of life. **[Gout Management]** 1. **Dietary Changes**: - **Avoid Purine-Rich Foods**: Reduce intake of foods high in purines, such as red meat, organ meats, and certain seafood (e.g., shellfish). - **Limit Alcohol**: Especially beer and spirits, as they can increase uric acid levels. - **Hydration**: Encourage drinking plenty of water to help flush uric acid from the body. 2. **Medications**: - **Acute Attacks**: - **NSAIDs**: For pain relief during acute gout attacks. - **Colchicine**: Helps reduce inflammation but should be used carefully due to potential side effects. - **Corticosteroids**: May be prescribed if NSAIDs or colchicine are not suitable. - **Chronic Management**: - **Allopurinol or Febuxostat**: Xanthine oxidase inhibitors to reduce uric acid production. - **Probenecid**: Uricosuric drugs that help the body eliminate uric acid more effectively. 3. **Monitor and Manage Uric Acid Levels**: - **Goal**: Aim to keep uric acid levels below 6 mg/dL to prevent future gout attacks. - **Regular Monitoring**: Blood tests to check uric acid levels and adjust medications as needed. 4. **Lifestyle Modifications**: - **Weight Management**: Achieving and maintaining a healthy weight can reduce the frequency and severity of gout attacks. - **Exercise**: Regular physical activity, with a focus on low-impact exercises, can help maintain joint function and overall health. 37. Understand chickenpox (varicella) and its relation to herpes zoster **Chickenpox (Varicella)** - **Cause:** Varicella-Zoster Virus (VZV). - **Symptoms:** Itchy rash with fluid-filled blisters, fever, fatigue. - **Complications:** More severe in adults, can lead to pneumonia. - **Prevention:** Vaccination reduces severity and incidence. **Shingles (Herpes Zoster)** - **Cause:** Reactivation of the same virus (VZV) that causes chickenpox. - **Symptoms:** Painful, blistering rash along one side of the body (follows a dermatome). - **Risk Factors:** Common in older adults, stress, and weakened immune systems. - **Complications:** Post-herpetic neuralgia (long-lasting pain after the rash heals). - **Treatment:** Antiviral medications (e.g., acyclovir) within 72 hours of rash onset. **Connection Between Chickenpox and Shingles** - **Primary Infection:** Chickenpox occurs first when you get the VZV virus. - **Dormancy:** The virus stays dormant in your nerves after chickenpox clears. - **Reactivation:** Later in life, the virus can reactivate as shingles. 38. What is onychomycosis? - **Fungal** infection of the nails. - Caused mainly by **dermatophytes** (Trichophyton rubrum). - Thick, discolored nails; brittle, crumbling nails; nails may lift off the nail bed (onycholysis). - Treat with topical antifungals for mild cases, and oral antifungals (Terbinafine or Itraconazole) for severe cases or toenail involvement. 39. What is a furuncle? - **Furuncle** (Boil): Single **infected hair follicle**; small, painful, pus-filled. - Treated with: Incision and drainage (I&D) and antibiotics if severe. - Commonly caused by Staphylococcus aureus. 40. Understand atopic dermatitis and scabies - Both cause itchy skin and rashes. - **Atopic Dermatitis:** An inflammatory condition linked to allergies and immune dysfunction. Managed with skin care, topical steroids, and antihistamines. - **Scabies:** Caused by mites burrowing into the skin. Treated with medications like permethrin or ivermectin. 41. What causes thrush? - Thrush is caused by the overgrowth of ***Candida albicans*** (a common yeast) due to factors like weakened immunity, diabetes, poor hygiene, and excessive moisture. It is characterized by white plaques in the mouth and can be confirmed by performing a potassium hydroxide (KOH) preparation, which will show the presence of yeast or pseudohyphae, indicating an overgrowth of *Candida albicans*. Common treatments include topical antifungals like nystatin (often used as a mouthwash for oral thrush) and clotrimazole troches. 42. Identify impetigo - **Honey-Crusted Lesions:** The most distinctive feature of impetigo is the presence of erythematous plaques with honey-colored crusts, often around the mouth and nose. 43. What is the organism associated with impetigo? - **Staphylococcus aureus** (more common) - **Streptococcus pyogenes** (it can lead to post-streptococcal glomerulonephritis, a kidney condition, about four weeks after the skin infection) 44. What would you see on a KOH prep for tinea? - On a KOH (potassium hydroxide) preparation for diagnosing tinea (a fungal infection), you would typically see **septate branching hyphae**. These are long, thread-like structures that are characteristic of dermatophyte fungi, which cause tinea infections. 45. What happens when impaired cellular metabolism? 1. **ATP Depletion:** Without enough ATP, the cell\'s energy-dependent processes start to fail. The Na⁺/K⁺ pump stops working; Na⁺ and water buildup inside the cell, causing swelling. 2. **Shift to Anaerobic Metabolism:** Cells switch to anaerobic glycolysis, producing less ATP. This leads to lactic acid accumulation, lowering the pH and causing acidosis. 3. **Cell and Organelle Damage:** Mitochondria can't produce enough ATP and start producing harmful reactive oxygen species (ROS). This can lead to cell death. Disrupts protein synthesis, affecting the cell\'s ability to repair and maintain itself. 4. **Reversible vs. Irreversible Injury:** If oxygen or nutrients are restored quickly, cells can recover. Prolonged or severe impairment leads to permanent damage; necrosis/ apoptosis. 46. How is bilirubin produced? - Bilirubin is produced by breaking down hemoglobin from old red blood cells. - Red blood cells live about 120 days before breaking down in the spleen, liver, and bone marrow. - Hemoglobin breaks down, and the heme part turns into biliverdin. - Biliverdin changes into unconjugated bilirubin (not water-soluble). - The liver converts unconjugated bilirubin into conjugated bilirubin (water-soluble) by attaching a sugar molecule. - Conjugated bilirubin is released into bile, moves into the intestines, and is excreted in stool (making it brown). - A small amount of conjugated bilirubin is excreted in urine. 47. What is **salivary alpha-amylase**? - An enzyme produced by the salivary glands in the mouth. It breaks down complex **carbohydrates into simpler sugars**, making them easier to digest. 48. What causes physiologic jaundice in a newborn? - Newborns have a high rate of red blood cell turnover. The excess breakdown of these cells releases more hemoglobin, which is then converted into bilirubin. - The newborn\'s immature liver is not fully developed and is less efficient at processing and excreting bilirubin. This leads to an accumulation of unconjugated bilirubin in the blood. - Due to the high turnover of red blood cells, there is an **increased production of bilirubin** that the newborn's immature liver struggles to handle. 49. Where is the vomiting center in the brain? - The vomiting center in the brain is located in the **medulla oblongata**, which is part of the brainstem. 50. What are vaginal changes associated with puberty? - Increased estrogen production during puberty leads to the growth and thickening of the vaginal walls. This prepares the body for future reproductive functions. - Estrogen also causes an increase in vaginal secretions, which help to keep the vaginal environment moist and maintain its health. - Vaginal pH becomes more acidic during puberty. This change helps to protect the vagina from infections by creating an environment that is less hospitable to harmful bacteria. 51. Clinical cause of amenorrhea - **Pregnancy**: The most common cause of amenorrhea in women of reproductive age. - **Hypothalamic dysfunction**: Stress, excessive exercise, or significant weight loss can disrupt the hypothalamic-pituitary-ovarian axis. - **Pituitary disorders**: Prolactinoma or other pituitary tumors can cause elevated prolactin levels, leading to amenorrhea. - **Ovarian disorders**: Polycystic ovary syndrome (PCOS), premature ovarian insufficiency (POI), or menopause. - **Thyroid dysfunction**: Hyperthyroidism and hypothyroidism. - **Uterine abnormalities**: Asherman\'s syndrome (intrauterine adhesions) or congenital absence of the uterus. - **Medications**: Hormonal contraceptives or chemotherapy. - **Chronic diseases**: Diabetes, celiac disease, or chronic kidney disease. 52. What is cryptorchidism? - Undescended testicle(s) 53. Organism for syphilis - Treponema pallidum (bacteria) 54. How does **trichomoniasis** present in males and females? - In males often asymptomatic, but when symptoms do occur, they may include irritation inside the penis, mild discharge, or slight burning after urination or ejaculation. - In females presents with a frothy, yellow-green vaginal discharge with a strong odor. Other symptoms include vaginal itching, irritation, and discomfort during urination or intercourse. The cervix may appear inflamed with a \"strawberry\" appearance due to small red ulcerations. 55. What is DNA transcription? DNA transcription is the process by which a specific segment of DNA is copied into RNA, particularly messenger RNA (mRNA). This is the first step in gene expression, where the genetic information stored in DNA is converted into a format that can be used to produce proteins. 1. **Initiation**: The enzyme RNA polymerase binds to a specific region of the DNA called the promoter. This signals the start of a gene. 2. **Elongation**: RNA polymerase moves along the DNA strand, adding complementary RNA nucleotides to the growing mRNA strand. This RNA strand is a mirror image of the DNA sequence, except that RNA uses uracil (U) instead of thymine (T). 3. **Termination**: When RNA polymerase reaches a termination sequence on the DNA, it releases the newly formed mRNA strand and detaches from the DNA. 4. **Processing**: In eukaryotes, the mRNA undergoes further processing, including the addition of a 5\' cap, a poly-A tail at the 3\' end, and splicing to remove non-coding regions (introns). This mRNA strand then exits the nucleus (in eukaryotic cells) and travels to the ribosome, where it directs the synthesis of proteins during translation. 56. How is an autosomal recessive disorder inherited? - An autosomal recessive disorder is inherited when an individual receives two copies of a mutated gene, one from each parent. 57. Define genotype and phenotype - **Genotype**: The genetic code you inherit (e.g., Bb for eye color). - **Phenotype**: The physical traits you show (e.g., having brown eyes). 58. Define negative feedback for hormonal balance - **Negative feedback** in hormonal balance is a regulatory mechanism where the body reduces the output of a hormone once its effect has reached a certain level. This helps maintain stability and prevents overproduction. - **Example**: When blood sugar rises, the pancreas releases insulin. As insulin lowers blood sugar, the drop signals the pancreas to reduce insulin production. 59. Which electrolyte does insulin transport into the cell? - Insulin transports **potassium (K+)** into the cell. - **Insulin's Effect on Potassium**: Insulin helps move not only glucose but also potassium into cells. Here's how it works: 1. **Cellular Uptake**: Insulin activates a transporter on the cell membrane called the **sodium-potassium ATPase pump**. 2. **Sodium-Potassium ATPase Pump**: This pump moves sodium (Na+) out of cells and potassium (K+) into cells. 3. **Outcome**: When insulin is released (e.g., after eating), it signals the pump to increase its activity, resulting in more potassium being pushed into the cells. **Why This Matters** - **Potassium Levels**: Keeping potassium inside cells is crucial. If too much potassium stays in the blood, it can cause dangerous heart rhythms (hyperkalemia). Insulin helps prevent this by moving potassium into cells. - **Clinical Use**: In medical settings, when someone has dangerously high potassium levels in their blood, insulin (along with glucose to prevent hypoglycemia) is sometimes given to quickly lower the blood potassium by shifting it into cells. 60. What hormone increases with physiologic stress? **Cortisol** is produced by the adrenal glands in response to stress signals from the brain. It helps the body manage stress by: - Increasing blood sugar levels. - Enhancing the brain\'s use of glucose. - Suppressing non-essential bodily functions, like digestion and immune response, to focus on dealing with the stressor. This is part of the \"fight or flight\" response, where the body prepares to either confront or escape from the stressor. 61. Where is epinephrine secreted? - Epinephrine, also known as adrenaline, is secreted by the **adrenal medulla**, which is the inner part of the adrenal glands. The adrenal glands are located on top of each kidney. - When the body experiences stress, the adrenal medulla releases epinephrine **into the bloodstream** as part of the \"fight or flight\" response. This hormone helps prepare the body to react quickly by increasing heart rate, dilating airways, and mobilizing energy reserves. 62. Pathogenesis of Graves' disease Graves\' disease is an autoimmune disorder characterized by the overproduction of thyroid hormones (T3 and T4), leading to hyperthyroidism. The key steps in its pathogenesis are: 1. **Autoimmune Trigger**: - The immune system mistakenly targets the thyroid gland. - The body produces an antibody called **thyroid-stimulating immunoglobulin (TSI)**, which mimics the action of Thyroid-Stimulating Hormone (TSH). 2. **TSI and TSH Receptor Interaction**: - TSI binds to the **TSH receptors** on the surface of thyroid cells. - Normally, TSH would regulate thyroid hormone production, but in Graves\' disease, TSI continuously stimulates the thyroid gland. 3. **Overproduction of Thyroid Hormones**: - This constant stimulation leads to the excessive production and release of thyroid hormones **T3 and T4**. - The high levels of T3 and T4 result in the clinical symptoms of hyperthyroidism. 4. **Type II Hypersensitivity Reaction**: - Graves\' disease involves a type II hypersensitivity reaction, where the immune response is directed against a specific cell surface receptor (TSH receptor). 5. **Genetic Predisposition**: - Certain genetic markers, such as **HLA-DR3 and HLA-B8**, are associated with a higher risk of developing Graves\' disease, indicating a genetic predisposition. 6. **Negative Feedback Suppression of TSH**: - The elevated levels of T3 and T4 suppress the production of TSH from the pituitary gland through negative feedback, which is why TSH levels are typically low in patients with Graves\' disease. **Clinical Manifestations** - **Metabolic Effects**: Increased metabolism leads to symptoms like weight loss, anxiety, and heat intolerance. - **Ophthalmopathy**: Eye symptoms such as exophthalmos (bulging eyes) occur due to inflammation behind the eyes. - **Dermopathy**: Skin changes like pretibial myxedema (thickened skin on the shins). In summary, Graves\' disease results from an autoimmune attack on the thyroid, leading to excessive hormone production and the characteristic symptoms of hyperthyroidism 63. Clinical manifestations of **hypothyroid** - **Fatigue**: Persistent tiredness and low energy levels. - **Weight Gain**: Unexplained weight gain despite a normal or decreased appetite. - **Cold Intolerance**: Sensitivity to cold temperatures. - **Dry Skin and Hair**: Skin may become dry and flaky, hair may be coarse and brittle. - **Constipation**: Slowed digestion leading to infrequent bowel movements. - **Depression**: Low mood, lack of interest in activities, and feelings of sadness. - **Puffy Face and Periorbital Edema**: Swelling around the eyes and face. - **Bradycardia**: Slower than normal heart rate. - **Hoarseness**: Change in voice, often deeper and raspy. - **Myxedema**: Non-pitting edema, particularly in the hands, face, and periorbital area. - **Loss of Lateral Eyebrows**: Thinning of the outer third of the eyebrows. - **Delayed Deep Tendon Reflexes**: Slowed relaxation phase of reflexes. - **Diastolic Hypertension**: Elevated diastolic blood pressure due to increased systemic vascular resistance. - **Decreased Cardiac Output**: Weaker heart function leading to reduced blood circulation. - **Menstrual Irregularities**: Such as amenorrhea (absence of menstruation) or heavy periods. - **Hyperlipidemia**: Increased cholesterol levels, particularly LDL. - **Growth Failure**: In children, it can lead to stunted growth and developmental delays. - **Muscle Weakness and Cramps**: Generalized muscle discomfort and weakness. - **Arthralgias and Myalgias**: Joint and muscle pain. - **Yellow Complexion**: Due to impaired metabolism of carotene. - **Carpal Tunnel Syndrome**: Nerve compression leading to pain, tingling, or numbness in the hands. - **Macroglossia**: Enlarged tongue. 64. Define glomerular filtration rate - **Glomerular Filtration Rate (GFR)**: Measures kidney filtration efficiency. - **Normal Range**: Typically 90 mL/min or higher. - **Key Function**: Indicates how well kidneys filter blood. - **Importance**: Used to diagnose and stage chronic kidney disease (CKD). - **Lower GFR**: Suggests impaired kidney function. 65. Where is CSF produced? - Cerebrospinal fluid (CSF) is produced by the **choroid plexus**, a network of cells located in the ventricles of the brain. Specifically, it is produced in the lateral ventricles, third ventricle, and fourth ventricle. The CSF flows through the ventricular system and around the brain and spinal cord, providing cushioning, nutrient delivery, and waste removal. 66. What is the action of norepinephrine? **Norepinephrine** is a neurotransmitter and hormone primarily involved in the body\'s \"fight or flight\" response. Its actions include: 1. **Vasoconstriction**: Tightens blood vessels, raising blood pressure. 2. **Boosts Heart Activity**: Increases heart rate and makes heartbeats stronger. 3. **Opens Airways**: Slightly relaxes the airways to improve breathing. 4. **Energy Release**: Helps release stored energy (glucose) for quick use. 67. Lab for myocardial damage - **Troponin** (cTnI or cTnT): 1. Best marker for heart muscle damage. 2. Rises within 3-6 hours, peaks at 12-24 hours, stays elevated up to 10 days. 68. Cause of heart failure 1. **Coronary Artery Disease (CAD)**/ **Ischemic Heart Disease**: Reduced blood flow to the heart muscle due to narrowed or blocked coronary arteries. This can lead to heart attacks (myocardial infarctions), which damage the heart muscle. 2. **Hypertension:** Chronically high blood pressure forces the heart to work harder to pump blood, leading to thickening of the heart muscle (left ventricular hypertrophy) and eventually heart failure. 3. **Cardiomyopathy**: Diseases of the heart muscle itself, which can be genetic (hypertrophic cardiomyopathy) or acquired (dilated cardiomyopathy from viral infections, alcohol abuse, etc.). 4. **Valvular Heart Disease**: Malfunction of one or more heart valves (e.g., aortic stenosis, mitral regurgitation) can lead to heart failure by disrupting normal blood flow through the heart. 5. **Arrhythmias**: Irregular heart rhythms, such as atrial fibrillation, can impair the heart's efficiency and lead to heart failure. 6. **Congenital Heart Disease**: Structural heart defects present from birth can cause heart failure later in life if they are severe or untreated. 7. **Myocarditis**: Inflammation of the heart muscle, often due to viral infections, which can weaken the heart and lead to heart failure. 8. **Alcohol and Drug Abuse**: Chronic alcohol abuse or the use of certain drugs (e.g., cocaine, certain chemotherapy agents) can damage the heart muscle. 9. **Diabetes**: Increases the risk of developing heart failure due to associated conditions like coronary artery disease and hypertension. 10. **Chronic Lung Diseases**: Conditions like chronic obstructive pulmonary disease (COPD) can lead to right-sided heart failure (cor pulmonale). 11. **Obesity** 12. **Infections and Toxins** 69. Treatment for cystic fibrosis 1. **Respiratory Therapy**: - Daily physiotherapy to clear mucus from the lungs. - **Medications**: - **Bronchodilators**: Help open airways. - **Nebulized Hypertonic Saline**: Helps thin mucus. - **DNase (Pulmozyme)**: Breaks down mucus, making it easier to clear. - **Prophylactic Antibiotics**: To prevent and treat lung infections, especially against *Pseudomonas aeruginosa*. - **CFTR Modulators**: Drugs like Ivacaftor that improve the function of the defective CFTR protein. - **Lung Transplant**: Considered in severe cases of lung disease. 2. **Nutritional Support**: - **Pancreatic Enzyme Replacement**: To aid digestion and improve nutrient absorption. - **Dietary Supplements**: Including fat-soluble vitamins (A, D, E, K) due to malabsorption. - **Insulin**: For managing CF-related diabetes. - **High-Calorie Diet**: To support growth and weight gain. 3. **Management of Complications**: - **Diabetes Management**: Insulin therapy for CF-related diabetes. - **Bone Health**: Vitamin D supplementation to prevent fractures due to poor bone mineralization. - **Liver Disease Management**: Monitoring for liver complications and treating biliary cirrhosis if necessary. 4. **Infection Control**: - **Regular Monitoring**: For bacterial colonization in the lungs, especially with *Pseudomonas aeruginosa* and *Burkholderia cepacia*. - **Aggressive Treatment**: With antibiotics for any signs of infection. 5. **Allergic Bronchopulmonary Aspergillosis (ABPA)**: - **Treatment**: Includes inhalers, antibacterials, high-dose inhaled steroids, oral prednisolone, and occasionally antifungals for this complication of CF. 70. Risk factors for lung cancer - **Cigarette Smoking** - **Asbestos Exposure**: Linked to mesothelioma. - **Radon Exposure**: A naturally occurring radioactive gas that can accumulate in homes. - **Radiation Exposure**: Previous exposure to radiation therapy, especially in the chest area. - **Family History** - **Chemical Exposures**: Exposure to harmful chemicals like diesel exhaust, arsenic, and certain other industrial compounds. - **Chronic Obstructive Pulmonary Disease (COPD)** 71. Pathogenesis of leukemia 1. **Genetic Mutations**: DNA mutations occur in certain genes, leading to abnormal cell behavior. 2. **Abnormal Cell Growth**: These mutations cause the bone marrow to produce excessive immature white blood cells (blasts). 3. **Crowding Out of Normal Cells**: The excessive blasts crowd out normal blood cells, reducing the production of healthy red blood cells, white blood cells, and platelets. 4. **Bone Marrow Dysfunction**: The bone marrow becomes overwhelmed by the blasts, leading to bone marrow failure. 5. **Organ Infiltration**: The abnormal cells can spread to other organs, such as the liver, spleen, and lymph nodes, causing enlargement and dysfunction of these organs. 72. What are tumor cell markers? 1. **Produced by Cancer Cells**: Tumor markers are often secreted by the tumor itself or by other cells in response to the presence of a tumor. 2. **Used in Diagnosis**: Certain tumor markers can help diagnose specific types of cancer. 3. **Monitoring Treatment**: They can be used to monitor how well a patient is responding to treatment. 4. **Prognosis**: Some tumor markers can provide information about the likely course of the disease (prognosis). **Examples of Tumor Cell Markers** - **PSA (Prostate-Specific Antigen)**: Used in prostate cancer. - **CA-125**: Used in ovarian cancer. - **CEA (Carcinoembryonic Antigen)**: Used in colon, lung, and other cancers. - **AFP (Alpha-Fetoprotein)**: Used in liver cancer and some germ cell tumors. - **HER2**: Used in breast cancer to determine therapy options. 73. Define apoptosis **Apoptosis** is a form of programmed cell death that occurs in an orderly and controlled manner. It's a natural process used by the body to remove unwanted or damaged cells without causing inflammation or damage to surrounding tissues. **Key Features of Apoptosis** - **Cell Shrinkage**: The cell becomes smaller and more condensed. - **Membrane Integrity**: The cell membrane remains intact, but flips a molecule called phosphatidylserine (PS) to the outer surface as an \"eat me\" signal for phagocytes (cells that engulf and digest dead cells). - **DNA Fragmentation**: The cell's DNA is systematically broken down into small fragments in a process known as DNA laddering. - **No Inflammation**: Unlike necrosis (another form of cell death), apoptosis does not trigger an inflammatory response. - **Caspase Activation**: Apoptosis is primarily mediated by a family of enzymes called caspases, which execute the cell death program. 74. Bacterium associated with prolonged antibiotic therapy - The bacterium most commonly associated with prolonged antibiotic therapy is **Clostridioides difficile** (formerly known as *Clostridium difficile* or *C. difficile*). *Clostridioides difficile* is a major cause of hospital-acquired infections, particularly in patients who have been on long-term antibiotic therapy. 75. Where do B cells mature? - B cells mature in the **bone marrow**. 76. What happens with the overcorrection of hyponatremia? Overcorrection of hyponatremia, particularly if done too quickly, can lead to a serious neurological condition known as **osmotic demyelination syndrome (ODS)**, previously called central pontine myelinolysis (CPM). **[What Happens]** 1. **Rapid Sodium Increase**: If sodium levels are increased too rapidly, water shifts out of brain cells, causing them to shrink. 2. **Brain Damage**: This sudden change can lead to damage of the myelin sheath that covers nerve cells, particularly in the pons region of the brain. 3. **Neurological Symptoms**: Symptoms of ODS include difficulty speaking, swallowing, moving, and may lead to locked-in syndrome, where a person is fully conscious but unable to move. 77. How are calcium and phosphate balanced? - **PTH and Vitamin D** raise calcium; **Calcitonin** lowers it. - **Phosphate** is balanced by excretion through the kidneys, mainly controlled by PTH. 78. Is obesity a modifiable risk factor? - Yes, **obesity is a modifiable risk factor**. It can be managed and potentially reduced through lifestyle changes such as a healthy diet, regular physical activity, and weight management strategies. 79. What is Peyronie's disease? - **Penile curvature**, pain during erections, possible erectile dysfunction. - Associated with fibrous plaque formation in the tunica albuginea and may be linked to Dupuytren's contracture (a hand condition). - Treat with oral medications (e.g., pentoxifylline), intralesional injections (e.g., collagenase), or surgical correction in severe cases. 80. Which female hormones are released from the anterior pituitary? - **Follicle-Stimulating Hormone (FSH)**: Stimulates the growth of ovarian follicles and the production of estrogen. - **Luteinizing Hormone (LH)**: Triggers ovulation and stimulates the production of progesterone from the corpus luteum. 81. What happens in the luteal phase of the menstrual cycle? During the luteal phase of the menstrual cycle: 1. **Corpus Luteum Forms**: After ovulation, the follicle becomes the corpus luteum. 2. **Progesterone Production**: The corpus luteum produces progesterone, thickening the uterine lining for potential pregnancy. 3. Outcome: - If pregnancy occurs: The corpus luteum continues hormone production. - If no pregnancy: The corpus luteum breaks down, progesterone drops, and menstruation begins. The luteal phase lasts about 14 days. 82. What is the most common cause of delayed puberty in children? - **Constitutional Delay of Growth and Puberty**: This is just a fancy way of saying that some kids develop later than others. They might hit puberty a bit later than their friends, but they eventually catch up and develop normally. This is the most common reason for delayed puberty and usually doesn't need any treatment. 83. What is painful menstruation called? - Painful menstruation is called **dysmenorrhea**. 84. Risk factors for breast cancer - **Estrogen Exposure:** Higher risk with more estrogen, like in hormone replacement therapy, early periods, late menopause, and polycystic ovarian syndrome. - **Total Menstrual Cycles:** More cycles mean more estrogen exposure. - **Live Birth:** Having children lowers breast cancer risk. - **Obesity:** Extra fat increases estrogen production, raising the risk. - **Inherited genetic mutations:** Mutations in the tumor suppressor genes BRCA1 and BRCA2. 85. Test for anemia to measure iron stores - To measure iron stores when evaluating anemia, the key test is **serum ferritin**. This test measures the amount of stored iron in the body. Low levels of ferritin indicate depleted iron stores, which is often seen in iron deficiency anemia. 86. What is a microcytic hypochromic anemia? **Microcytic Hypochromic Anemia** is a type of anemia characterized by: - **Microcytic**: Red blood cells (RBCs) are smaller than normal. - **Hypochromic**: RBCs have less hemoglobin, making them appear paler than normal. **Common Causes** - **Iron Deficiency Anemia**: The most common cause, usually due to inadequate iron intake, chronic blood loss, or malabsorption. - **Thalassemia**: A genetic disorder that affects hemoglobin production. **Key Characteristics** - Small, pale RBCs due to insufficient hemoglobin production. - Often associated with symptoms like fatigue, weakness, and pallor. This type of anemia typically requires further investigation to determine the underlying cause, such as checking iron levels or genetic testing for conditions like thalassemia 87. What is multiple myeloma? **Multiple myeloma** is a type of cancer that affects plasma cells, which are a type of white blood cell responsible for producing antibodies. In multiple myeloma, abnormal plasma cells accumulate in the bone marrow, where they interfere with the production of normal blood cells and produce abnormal antibodies. This can lead to various complications, including bone damage, kidney dysfunction, and an increased risk of infections. **Key Features of Multiple Myeloma** 1. **Abnormal Plasma Cells**: - The cancerous plasma cells produce large amounts of abnormal antibodies (monoclonal proteins or M proteins), which can be detected in blood and urine. 2. **Bone Damage**: - Multiple myeloma often causes bone pain and fractures because the cancer cells produce substances that break down bone tissue. 3. **Kidney Problems**: - The abnormal proteins can accumulate in the kidneys, leading to kidney dysfunction or failure. 4. **Anemia and Other Blood Issues**: - The overcrowding of the bone marrow by abnormal plasma cells reduces the production of normal blood cells, leading to anemia, increased risk of infections, and bleeding problems. 5. **Hypercalcemia**: - Bone breakdown releases calcium into the bloodstream, leading to high levels of calcium (hypercalcemia), which can cause symptoms like nausea, vomiting, confusion, and kidney issues. 88. Signs and symptoms of PCOS - **Irregular Periods**: - Oligomenorrhea (infrequent menstrual cycles) - **Excess Male Hormones (Hyperandrogenism)**: - Hirsutism (excess hair growth on face, chest, back) - Acne - Male-pattern baldness - **Obesity**: - Often associated with weight gain - **Insulin Resistance**: - Acanthosis nigricans (dark, thick skin patches) - Increased risk of type 2 diabetes - **Fertility Issues**: - Anovulation (lack of ovulation) - **Hormonal Imbalance**: - Elevated LH and testosterone - **Ovarian Cysts**: - Multiple cysts on ovaries (may not always be present) 89. Signs and symptoms of diabetes - **Increased Thirst** (*Polydipsia*) - **Frequent Urination** (*Polyuria*) - **Increased Hunger** (*Polyphagia*) - **Unexplained Weight Loss** - **Fatigue and Weakness** - **Blurred Vision** - **Slow Healing of Wounds** - **Frequent Infections** (e.g., skin, gums, urinary tract) - **Numbness or Tingling in Hands and Feet** (Peripheral Neuropathy) - **Dark Patches on Skin** (Acanthosis Nigricans)

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