FREUC 5 A+P Resit PDF

Question 4: **Key functions of the nervous system.** Feedback (must include)- **revisit your understanding of parasympathetic and sympathetic.** **General Functions of the Nervous System** 1. **Sensory Input**: Detects changes inside and outside the body (e.g., temperature, pain, pressure)....

Question 4: **Key functions of the nervous system.** Feedback (must include)- **revisit your understanding of parasympathetic and sympathetic.** **General Functions of the Nervous System** 1. **Sensory Input**: Detects changes inside and outside the body (e.g., temperature, pain, pressure). 2. **Integration**: Processes and interprets sensory input to determine the appropriate response. 3. **Motor Output**: Activates muscles or glands to respond to stimuli. 4. **Homeostasis**: Maintains a stable internal environment. 5. **Higher Mental Functions**: Includes memory, reasoning, emotions, and learning. **Divisions of the Nervous System** 1. **Central Nervous System (CNS)**: - Brain: Control centre for processing and responses. - Spinal Cord: Pathway for information to and from the brain; reflex actions. 2. **Peripheral Nervous System (PNS)**: - **Somatic Nervous System**: Voluntary control of skeletal muscles. - **Autonomic Nervous System (ANS)**: Involuntary control of vital functions. **Autonomic Nervous System (ANS) Functions** 1. **Sympathetic Nervous System** (Fight or Flight): - Prepares the body for stress or emergency situations. - Key effects include: - Increased heart rate and blood pressure. - Dilated pupils (to improve vision). - Bronchodilation (to enhance airflow to the lungs). - Inhibition of digestion (redirecting energy to essential organs). - Increased glucose release from the liver for energy. 2. **Parasympathetic Nervous System** (Rest and Digest): - Promotes recovery and conserves energy. - Key effects include: - Decreased heart rate and blood pressure. - Constricted pupils. - Bronchoconstriction (normalises airflow). - Stimulation of digestion, salivation, and other metabolic activities. - Encourages energy storage by stimulating insulin release. **Sympathetic vs. Parasympathetic (Key Differences)** ------------------ ------------------------------------------- ----------------------------------- **Function** **Sympathetic (Fight/Flight)** **Parasympathetic (Rest/Digest)** Heart rate Increases Decreases Respiratory rate Increases (bronchodilation) Decreases (bronchoconstriction) Digestion Inhibits Stimulates Pupil size Dilates Constricts Blood vessels Constricts (to prioritise muscles/organs) Relaxes (to restore normal flow) ------------------ ------------------------------------------- ----------------------------------- **Integration of Feedback:** - Emphasise the **specific roles** of the **sympathetic and parasympathetic systems** in maintaining homeostasis. - Use clear examples (e.g., during exercise vs. during sleep) to illustrate how these systems operate in opposition but balance each other. - Include terminology such as \"autonomic balance\" and \"dual innervation\" (most organs are innervated by both systems, providing dynamic control). - Highlight practical relevance for ambulance technicians: - For example, **sympathetic response** during trauma or shock. - **Parasympathetic dominance** in fainting (vasovagal syncope). Question 11: **Physiology of balance and taste.** Feedback (must include)- **more detail required in relation to taste** **Physiology of Balance** **Vestibular System** (Inner Ear): 1. Located in the **semicircular canals** and **vestibule** of the inner ear. **Semicircular Canals**: Detect rotational movements (dynamic equilibrium). **Utricle and Saccule** (within the vestibule): Detect linear acceleration and head position (static equilibrium). Sensory information is provided by **hair cells** in the fluid-filled structures. Movements of the head cause displacement of the **endolymph**, bending the hair cells and generating nerve signals. 6. Vestibular signals are sent via the **vestibulocochlear nerve (cranial nerve VIII)** to the brainstem and cerebellum. These areas process the information and coordinate reflexes (e.g., eye movements) to maintain balance and posture. 8. Vision provides spatial orientation. Proprioceptors in muscles and joints detect body position and movement. The brain integrates input from all systems to maintain balance. **Physiology of Taste (Gustation)** - Found mainly on the **tongue**, but also on the soft palate, pharynx, and epiglottis. - Located within structures called **papillae** (fungiform, circumvallate, and foliate papillae). - Five basic taste modalities: 1. **Sweet**: Indicates energy-rich nutrients (e.g., sugar). **Salty**: Detects sodium ions essential for cellular function. **Sour**: Indicates acidity (e.g., from citrus fruits). **Bitter**: Warns of potentially harmful substances (e.g., toxins). **Umami**: Detects glutamate, indicating protein-rich foods. - Chemical molecules in food dissolve in saliva and bind to receptors on **gustatory cells** within the taste buds. - This triggers electrical signals that travel via cranial nerves: 6. **Facial nerve (cranial nerve VII)** for the anterior two-thirds of the tongue. **Glossopharyngeal nerve (cranial nerve IX)** for the posterior third of the tongue. **Vagus nerve (cranial nerve X)** for areas such as the pharynx and epiglottis. - Signals are processed in the **gustatory cortex** (in the brain) via the **thalamus**. - **Olfaction (Smell)**: Strongly impacts the perception of flavour. - **Texture and Temperature**: Can alter taste sensation (e.g., hot vs. cold food). - **Health Conditions**: Illness, medications, or age can reduce taste sensitivity. **Integration of Feedback:** - **Taste bud anatomy**, including the role of papillae and gustatory cells. - **Cranial nerves** involved in taste signal transmission. - The five basic tastes and their physiological significance. - For example, loss of taste (ageusia) in conditions like stroke, or changes in taste due to medication side effects. Question 13: **Explain acute pyelonephritis.** Feedback (must include)- **a better understanding of pyelonephritis is needed. What happens? Symptoms?** **Definition of Acute Pyelonephritis** **Causes and Pathophysiology** **Common Causes**: - The most common pathogen is **Escherichia coli (E. coli)**, accounting for the majority of cases. - Other causes include **Proteus**, **Klebsiella**, and occasionally **Staphylococcus saprophyticus**. **How it Develops**: - Begins with a **urinary tract infection (UTI)**, typically in the bladder (cystitis). - If untreated or poorly managed, bacteria ascend to the kidneys. - **Inflammatory response** in the kidneys causes tissue damage, including swelling, interstitial inflammation, and, in severe cases, abscess formation. - May lead to systemic infection (**sepsis**) if bacteria enter the bloodstream. **Symptoms of Acute Pyelonephritis** **Localised Symptoms**: - Flank pain or tenderness (typically one-sided, over the affected kidney). - Dysuria (pain or burning during urination). - Increased urinary frequency and urgency. - Haematuria (blood in the urine). - Cloudy or foul-smelling urine. **Systemic Symptoms** (signs of widespread infection): - Fever and chills. - Nausea and vomiting. - Fatigue or general malaise. - Confusion in elderly patients (may be the only symptom). **Risk Factors** - Female sex (shorter urethra increases the risk of ascending infections). - Pregnancy (hormonal changes and pressure on the urinary tract). - Urinary tract obstruction (e.g., kidney stones or enlarged prostate). - Diabetes mellitus (reduced immune function). - Recent urinary catheterisation or instrumentation. **Complications** - Chronic pyelonephritis (if recurrent or untreated). - Acute kidney injury (due to severe infection or obstruction). - Sepsis, potentially leading to multi-organ failure. **Diagnosis and Management** - Urinalysis: Presence of white blood cells (pyuria), bacteria (bacteriuria), and possibly red blood cells. - Urine culture: Identifies the causative organism. - Imaging (e.g., ultrasound or CT): Detects obstructions or complications. - **Antibiotics**: Often broad-spectrum initially, then targeted based on culture results (e.g., ciprofloxacin or ceftriaxone). - Pain relief (e.g., paracetamol). - Hospitalisation for severe cases, especially if complications like sepsis are suspected. **Integration of Feedback:** - Provide a clear **step-by-step explanation** of what happens during pyelonephritis, from initial infection to systemic involvement. - Emphasise the **symptoms**, both localised and systemic, for comprehensive understanding. - Use medical terminology appropriately (e.g., pyuria, dysuria, bacteriuria). - Highlight practical relevance for ambulance technicians: - Recognition of signs of sepsis for prompt intervention. - Awareness of risk factors (e.g., recent UTI in a patient with flank pain and fever). By addressing these points in detail, you'll meet the feedback requirements and provide a thorough answer. Question 14: **Explain peripheral neuropathy.** Feedback (must include)- **this needs more detail, what is it and more causes needed.** **Definition of Peripheral Neuropathy** - **Peripheral neuropathy** is a condition resulting from damage to the peripheral nerves, which transmit signals between the central nervous system (brain and spinal cord) and the rest of the body. - It can affect **sensory nerves**, **motor nerves**, or **autonomic nerves**, leading to a range of symptoms. **Types of Peripheral Neuropathy** 1. **Mononeuropathy**: Damage to a single nerve (e.g., carpal tunnel syndrome). 2. **Polyneuropathy**: Damage to multiple nerves (more common, e.g., in diabetes). 3. **Autonomic Neuropathy**: Affects autonomic nerves, impacting involuntary functions (e.g., blood pressure regulation, digestion). **Causes of Peripheral Neuropathy** 1. **Metabolic and Endocrine Causes**: - **Diabetes mellitus**: The most common cause, leading to diabetic neuropathy due to high blood sugar levels damaging nerve fibres. - Hypothyroidism: Slows nerve signal transmission. 2. **Infections**: - **Shingles (herpes zoster)**: Causes nerve inflammation and postherpetic neuralgia. - HIV/AIDS: Leads to neuropathy due to infection or treatments. - Lyme disease: Bacterial infection affecting the nervous system. 3. **Autoimmune Diseases**: - Guillain-Barré syndrome: Acute neuropathy causing muscle weakness. - Rheumatoid arthritis and lupus: Can cause chronic nerve inflammation. 4. **Toxins**: - Alcohol abuse: Causes alcoholic neuropathy due to direct toxicity and nutritional deficiencies. - Exposure to heavy metals (e.g., lead, arsenic) or chemicals. 5. **Trauma or Compression**: - Nerve injury from accidents or repetitive strain (e.g., carpal tunnel syndrome). - Herniated discs compressing spinal nerves. 6. **Nutritional Deficiencies**: - Vitamin B12 deficiency: Leads to nerve damage and myelin sheath deterioration. - Deficiencies in vitamins B1, B6, and E. 7. **Hereditary Conditions**: - Charcot-Marie-Tooth disease: A genetic condition causing progressive nerve damage. 8. **Other Causes**: - Chemotherapy-induced neuropathy: Resulting from toxic effects of cancer treatments. - Chronic kidney disease: Causes uraemic neuropathy due to toxin accumulation. **Symptoms of Peripheral Neuropathy** - **Sensory Symptoms** (most common): - Numbness, tingling, or \"pins and needles\" sensations. - Burning, stabbing, or shooting pain. - Reduced ability to feel temperature changes or pain, increasing the risk of injuries. - **Motor Symptoms**: - Muscle weakness. - Loss of coordination or balance. - Muscle cramps or twitching. - **Autonomic Symptoms** (if autonomic nerves are affected): - Dizziness or fainting (due to low blood pressure). - Sweating abnormalities. - Bladder, bowel, or digestive issues. **Diagnosis and Management** 1. **Diagnosis**: - Patient history and clinical examination. - Nerve conduction studies or electromyography (EMG). - Blood tests to identify underlying causes (e.g., diabetes, vitamin deficiencies). 2. **Treatment**: - **Address underlying causes** (e.g., controlling blood sugar in diabetes, correcting vitamin deficiencies). - Pain management: Medications such as gabapentin, pregabalin, or amitriptyline. - Physiotherapy: Improves strength and balance. - Lifestyle changes: Alcohol cessation, balanced diet, and regular exercise. **Integration of Feedback:** - Provide a comprehensive explanation of **what peripheral neuropathy is** and how it impacts the body. - Include an expanded list of **causes**, ensuring to mention common, rare, and multifactorial origins. - Emphasise practical relevance for ambulance technicians: - Recognising neuropathic symptoms in conditions like diabetes or trauma. - Awareness of autonomic neuropathy signs such as dizziness or fainting. Question 15: **Explain glaucoma.** Feedback (must include)- **better understanding of this particular disease pathway, not just about fluid pathway, what can cause it and is surgery the only treatment?** **Definition of Glaucoma** - **Glaucoma** is a group of eye conditions that damage the **optic nerve**, usually due to increased **intraocular pressure (IOP)**, although normal-tension glaucoma can occur without elevated pressure. - The damage is progressive and can lead to **irreversible vision loss** if untreated. **Pathophysiology of Glaucoma** 1. **Normal Eye Fluid Pathway**: - Aqueous humour is produced by the **ciliary body** and flows through the **pupil** into the anterior chamber of the eye. - It drains via the **trabecular meshwork** and **Schlemm's canal** into the venous circulation. 2. **What Happens in Glaucoma**: - Impaired drainage of aqueous humour leads to increased IOP. - Elevated IOP damages the **optic nerve fibres** at the back of the eye (optic disc). - Over time, this damage results in loss of peripheral vision (a hallmark symptom) and eventual complete vision loss. 3. **Normal-Tension Glaucoma**: - In some cases, optic nerve damage occurs without elevated IOP. Causes may include reduced blood flow to the optic nerve or vascular issues. **Causes of Glaucoma** 1. **Primary Open-Angle Glaucoma** (most common): - Chronic and slow-progressing, caused by reduced drainage efficiency in the trabecular meshwork. 2. **Angle-Closure Glaucoma**: - Acute and sudden, caused by blockage of the drainage angle (e.g., by the iris). 3. **Secondary Glaucoma**: - Caused by another condition or factor, such as: - **Eye injury** or trauma. - **Inflammation** (e.g., uveitis). - **Medications** (e.g., prolonged use of corticosteroids). 4. **Congenital Glaucoma**: - A rare condition present at birth due to abnormal development of the drainage system. 5. **Risk Factors**: - Age (common in people over 60). - Family history of glaucoma. - Ethnicity (e.g., higher risk in African-Caribbean individuals). - Medical conditions like diabetes or hypertension. **Symptoms of Glaucoma** 1. **Primary Open-Angle Glaucoma**: - Often asymptomatic in early stages. - Gradual loss of peripheral vision (\"tunnel vision\"). 2. **Acute Angle-Closure Glaucoma** (emergency): - Severe eye pain. - Redness of the eye. - Blurred vision or halos around lights. - Nausea and vomiting due to increased IOP. **Treatment Options** 1. **Medications** (first-line treatments): - **Eye drops** to lower IOP by reducing aqueous humour production or increasing drainage: - **Prostaglandin analogues** (e.g., latanoprost). - **Beta-blockers** (e.g., timolol). - **Carbonic anhydrase inhibitors** (e.g., dorzolamide). - **Alpha agonists** (e.g., brimonidine). 2. **Laser Treatments**: - **Laser trabeculoplasty**: Improves drainage in open-angle glaucoma. - **Laser iridotomy**: Creates a hole in the iris for fluid drainage in angle-closure glaucoma. 3. **Surgical Treatments**: - **Trabeculectomy**: Creates a new drainage pathway for aqueous humour. - **Drainage implants**: Tiny devices placed to help fluid escape. 4. **Lifestyle and Monitoring**: - Regular eye checks for at-risk individuals. - Maintaining a healthy lifestyle (e.g., managing blood pressure and diabetes). **Integration of Feedback:** - Provide a **detailed explanation of the disease pathway**, including what happens to the optic nerve and how elevated IOP contributes to damage. - Expand on **causes and risk factors**, ensuring inclusion of both primary and secondary forms of glaucoma. - Address the misconception that surgery is the only treatment; include medications, laser therapy, and monitoring as additional interventions. - Highlight practical relevance for ambulance technicians: - Recognising symptoms of **acute angle-closure glaucoma** as an emergency requiring urgent referral. Question 18: **Describe care pathway for stroke.** Feedback (must include)- **breakdown the assessment more. What are you looking for in each parameter** **Definition of Stroke** - **Stroke** occurs when blood supply to part of the brain is interrupted (ischaemic stroke) or when a blood vessel in the brain bursts (haemorrhagic stroke), leading to brain tissue damage. - **Transient Ischaemic Attack (TIA)**: Often referred to as a \"mini-stroke,\" it involves temporary symptoms with no permanent damage. **Initial Stroke Assessment: FAST** 1. **Face**: - Look for **facial asymmetry**. - Ask the patient to smile or show their teeth. - Assess for drooping on one side of the face. 2. **Arms**: - Check for **arm weakness**. - Ask the patient to raise both arms; one may drift downward or fail to lift. 3. **Speech**: - Look for **speech abnormalities**. - Assess for slurred or incoherent speech and difficulty finding words. 4. **Time**: - Note the **onset time** of symptoms. - Critical for determining eligibility for treatments like thrombolysis. **Expanded Stroke Assessment Parameters** In addition to FAST, consider a more detailed evaluation: 1. **Level of Consciousness**: - Assess alertness and orientation using the **AVPU scale** (Alert, Verbal, Pain, Unresponsive). 2. **Pupil Response**: - Check for unequal pupils, which may indicate increased intracranial pressure or haemorrhagic stroke. 3. **Blood Glucose**: - Rule out hypoglycaemia, as it can mimic stroke symptoms. 4. **Gait and Coordination**: - Look for signs of ataxia or loss of balance (e.g., difficulty walking). 5. **Vision**: - Assess for visual field deficits or double vision. 6. **Neurological Signs**: - Check for unilateral weakness or sensory loss in the limbs. - Examine reflexes if possible. 7. **Blood Pressure**: - Measure blood pressure; elevated levels are common in stroke. 8. **Speech and Cognitive Testing**: - Ask simple questions or give commands to evaluate comprehension and language skills. **Care Pathway for Stroke** 1. **Emergency Recognition and Response**: - Recognise stroke symptoms and call for **immediate transfer to hospital**. 2. **Pre-Hospital Care**: - **Airway, Breathing, Circulation (ABC)**: Ensure airway patency and adequate oxygenation. - Administer supplemental oxygen if SpO₂ \< 94%. - Obtain a thorough history, including: - Onset time of symptoms. - Medical history (e.g., previous strokes, atrial fibrillation). - Current medications (especially anticoagulants). - Perform a **blood glucose test** to rule out hypoglycaemia. - Minimise patient movement to prevent worsening of symptoms. 3. **Hospital-Based Care**: - **Ischaemic Stroke**: - Urgent CT/MRI to confirm diagnosis. - **Thrombolysis** (e.g., with alteplase) within 4.5 hours of symptom onset if appropriate. - Consider **mechanical thrombectomy** for large vessel occlusions. - **Haemorrhagic Stroke**: - Blood pressure management to prevent further bleeding. - Possible surgical intervention to repair or evacuate the haemorrhage. 4. **Post-Acute Care**: - Admission to a **stroke unit** for multidisciplinary care. - Monitor for complications, such as swelling or seizures. - Initiate **rehabilitation**, including physiotherapy, occupational therapy, and speech therapy. **Integration of Feedback** - Provide a **detailed breakdown of assessments**, explaining the purpose of each parameter (e.g., why glucose testing is critical or what pupil changes indicate). - Expand on **FAST** to include additional neurological signs, ensuring a more comprehensive assessment. - Address the full **care pathway**, from pre-hospital to post-acute care, and emphasise time-critical treatments like thrombolysis. - Highlight practical relevance for ambulance technicians: - Importance of early recognition and swift transport to a **stroke centre**. - Accurate documentation of **onset time** to aid hospital decision-making. Question 20: **Management for adult meningitis.** Feedback (must include)- **better description needed. If we are looking at low o2, how low? Specific antibiotic?** **Definition of Meningitis** - **Meningitis** is an acute inflammation of the protective membranes (meninges) surrounding the brain and spinal cord. - It can be caused by bacterial, viral, fungal, or other infections. - **Bacterial meningitis** is a medical emergency due to the risk of rapid deterioration and sepsis. **Causes and Common Pathogens** 1. **Bacterial Meningitis** (most critical): - **Streptococcus pneumoniae**: Common in adults. - **Neisseria meningitidis**: Associated with meningococcal septicaemia. - **Listeria monocytogenes**: More common in immunocompromised or older patients. 2. **Viral Meningitis**: - Often less severe; caused by enteroviruses, herpes simplex virus, or varicella-zoster virus. **Symptoms of Adult Meningitis** 1. **Classic Triad**: - Fever. - Neck stiffness. - Altered mental status. 2. **Other Symptoms**: - Severe headache. - Photophobia (sensitivity to light). - Nausea and vomiting. - Seizures in severe cases. - Non-blanching purpuric rash (in meningococcal septicaemia). **Pre-Hospital Assessment and Recognition** 1. **Vital Signs**: - **Oxygen levels**: SpO₂ \< 94% indicates hypoxia requiring intervention. 2. **Neurological Observations**: - Glasgow Coma Scale (GCS) to assess level of consciousness. - Signs of raised intracranial pressure (e.g., unequal pupils, bradycardia). 3. **Rash Assessment**: - Non-blanching rash indicative of meningococcal septicaemia (perform a glass test). 4. **Other Considerations**: - History of recent illness, infection, or exposure to infected individuals. **Management of Adult Meningitis** 1. **Airway, Breathing, and Circulation (ABC)**: - Ensure airway patency and adequate breathing. - Administer **high-flow oxygen** (15 L/min via non-rebreather mask) if SpO₂ is \< 94%. - Monitor for hypotension and signs of septic shock (tachycardia, poor capillary refill). 2. **Antibiotic Administration**: - Administer **intramuscular benzylpenicillin (1.2 g)** if bacterial meningitis is suspected and hospital transfer will be delayed. - Do not delay transfer for antibiotics unless unavoidable. 3. **Fluid Resuscitation**: - Administer intravenous fluids for hypotension or shock. - Avoid excessive fluids if signs of raised intracranial pressure are present. 4. **Rapid Transfer**: - Time-critical emergency requiring transfer to a hospital with neurological and critical care facilities. - Alert the receiving hospital to suspected bacterial meningitis. **In-Hospital Treatment** 1. **Confirmation of Diagnosis**: - Lumbar puncture and blood cultures to confirm pathogen. - Imaging (CT/MRI) to assess for complications like abscesses or swelling. 2. **Antibiotic Treatment**: - **Empirical therapy**: Intravenous ceftriaxone or cefotaxime, often combined with ampicillin for Listeria coverage. - Tailored therapy based on culture results. 3. **Adjunctive Therapies**: - **Dexamethasone**: Reduces inflammation and improves outcomes in certain bacterial cases. **Integration of Feedback** - Specify **oxygen levels**: Low oxygen is defined as **SpO₂ \< 94%**, which necessitates high-flow oxygen. - Highlight the **specific antibiotic** used pre-hospital: **IM benzylpenicillin**. - Provide a clear step-by-step approach to **ABC management**, antibiotic use, and the importance of rapid transfer. - Emphasise **rash assessment** and the need to distinguish meningitis with septicaemia. Question 22: **Describe recognition features, pathophysiology, screening tools and treatments for septic shock.** Feedback (must include)- **revisit understanding of septic shock, is it sepsis? What defines it, treatment plans etc.** **Definition of Septic Shock** - **Sepsis** is a life-threatening condition caused by the body's extreme response to an infection, leading to organ dysfunction. - **Septic shock** is a subset of sepsis characterised by: - **Persistent hypotension** despite adequate fluid resuscitation. - Elevated serum lactate levels (\>2 mmol/L), indicating impaired tissue perfusion. - Requires vasopressor support to maintain mean arterial pressure (MAP) ≥65 mmHg. **Key Difference**:\ Sepsis involves organ dysfunction, while septic shock adds a severe circulatory and metabolic dysfunction. **Pathophysiology of Septic Shock** 1. **Infection and Immune Response**: - A bacterial, viral, or fungal infection triggers an excessive immune response. - Release of pro-inflammatory cytokines (e.g., IL-1, TNF-alpha) causes widespread inflammation. 2. **Vasodilation and Capillary Leak**: - Inflammatory mediators cause systemic vasodilation and increased capillary permeability, leading to: - **Hypotension**. - Fluid leakage into tissues, causing oedema. 3. **Impaired Tissue Perfusion**: - Reduced oxygen delivery to cells leads to anaerobic metabolism and elevated lactate. 4. **Organ Dysfunction**: - Hypoperfusion and hypoxia result in organ failure (e.g., kidneys, lungs, liver). **Recognition Features of Septic Shock** 1. **Early Symptoms (Sepsis)**: - Fever or hypothermia (\90 bpm). - Tachypnoea (\>20 breaths per minute). - Confusion or altered mental state. 2. **Progression to Septic Shock**: - **Hypotension** (systolic BP \