Additional Flashcards
Hemetemesis
Def :vomiting blood originating from upper gastrointestinal tract
Appearance: blood is typically dark brown or red resembling coffe grounds due to partial digestion by stomach acid
Associated symptoms:abdominal pain ,nausea and signs of gi bleeding like black ,tarry stools
Causes include peptic ulcer ,gastritis esophageal varices,Mallory Weiss tears
Hemoptysis
Coughing up blood from the respiratory tract eg lungs bronchi
Appearance: blood is usualy bright red and frothy (mixed with air and mucus)
Associated symptoms: often associated with coughing chest pain and respiratory symptoms like shortness of breath
Causes-bronchitis tuberculosis,lung cancer pneumonia/pulmonary embolism
Clubbing
Clubbing refers to a physical sign where finger tips becomes enlarged and nail curve around them in bulbous ornrounded way.this can indicate underlying health issues particularly related to lung or heart
Chronic lung desease:eg cystic fibrosis,lung cancer , bronchiectasis or chronic obstructive pulmonary desease
Heart desease:such as congenital heart defect as endocarditis
Gi desease /liver desease
3 organism which causes pneumonia in immunocompromised patient
Staphylococcus aureus
Streptococcus pneumonia
Cmv
Respiratory syncital virus
Klebsiella
GINA guideline
★ Increase awareness of asthma and it’s public health consequences
★promote identification of reasons for the increased prevention of asthma
★promote study of the association between asthma and environment
★reduce asthma morbidity and mortality
★improve management of asthma
Improve availability and accecability of effective asthma therapy
Pectus carinatum
Pectus carinatum, also known as pigeon chest, is a chest wall deformity where the breastbone (sternum) protrudes outward abnormally. It is less common than pectus excavatum (sunken chest) and often develops during adolescence.
Causes
Genetics: May run in families.
Connective tissue disorders: Sometimes associated with Marfan syndrome or other connective tissue conditions.
Growth spurts: Can develop during rapid growth in adolescence due to abnormal growth of the cartilage connecting the ribs to the sternum.
Symptoms
Cosmetic concern: The chest appears to protrude.
Occasionally, symptoms like:
Shortness of breath during exercise.
Chest pain or tenderness.
Reduced endurance.
Diagnosis
Physical examination.
Imaging: Chest X-ray, CT scan, or MRI for structural details.
Pulmonary function tests if breathing issues are suspected.
Treatment Options
- Bracing:
Similar to braces for teeth, a custom-fitted chest brace is worn to gradually reshape the chest wall.
Most effective in children and adolescents.
- Surgical Correction:
Ravitch procedure: Removal or reshaping of cartilage with placement of support bars.
Rarely needed unless severe or causing functional issues.
- Exercise and Physical Therapy:
Helps improve posture and strengthen chest muscles.
- Psychological Support:
Counseling or support groups for body image concern
Pulmonary complications in rheumatoid arthritis
1.* Interstitial Lung Disease (ILD)*
Most common pulmonary manifestation in RA.
Characterized by inflammation and fibrosis of lung parenchyma.
- Pleural Disease
Common in RA, can occur as:
Pleural effusion: Often small, exudative, with low glucose and high LDH.
Pleuritis: Inflammation of pleura causing pleuritic chest pain.
Rheumatoid Nodules
- Airway Disease
Upper airway:
Cricoarytenoid arthritis: Can lead to hoarseness, stridor, or airway obstruction.
Lower airway:
Bronchiectasis: Chronic inflammation leading to airway dilation.
Obliterative bronchiolitis: Rare, presents with obstructive lung disease.
5. Pulmonary Vasculitis
6. Drug-Induced Lung Disease
7. Increased Risk of Infections
Due to RA-related immunosuppression and
Unstable angina
★It can occur at any time,even at risk not necessarily ntriggered but physical exertion
★unpredictablen,new ornchange in severity, frequency or duration
★not easily relieved by rest or medication,often requires emergency treatment
★more dangerous and may signal aeart attack in progress or imminent
usualy due to rupture of plaque in artery leading to reduction in blood flow
Indication of Mv in gbs
- Vital capacity <15–20 mL/kg or rapidly declining.
- Hypoxemia (PaO₂ < 60 mmHg) or hypercapnia (PaCO₂ > 45 mmHg).
- Severe bulbar dysfunction causing aspiration risk.
- Signs of respiratory muscle fatigue (tachypnea, paradoxical breathing).
- Autonomic instability affecting respiration.
Biots breathing
Biot’s Breathing is an abnormal respiratory pattern characterized by groups of quick, shallow breaths followed by periods of apnea (no breathing). This breathing pattern often indicates severe damage to the brain, especially in areas such as the medulla oblongata, which controls involuntary breathing.
Causes of Biot’s Breathing
- Neurological Damage:
Stroke
Traumatic brain injury
Increased intracranial pressure (ICP)
- Infections:
Meningitis
Encephalitis
- Other Causes:
Opioid overdose
Hypoxia (severe oxygen deprivation)
Clinical Presentation
Periods of rapid, deep breathing interspersed with sudden apneic episodes.
Irregular breathing rhythm, unlike Cheyne-Stokes respiration (which has a cyclic pattern).
Management
Treat the Underlying Cause: Address the root condition causing neurological or respiratory dysfunction.
Supportive Care: Oxygen therapy or mechanical ventilation in severe cases.
Monitor Neurological Status: Imaging (CT/MRI) and ICP management may be necessary.
Biot’s breathing is a serious sign of brain dysfunction and requires immediate medical attention.
Hypokalemia
Hypokalemia is a condition where blood potassium levels fall below 3.5 mmol/L. It can be caused by vomiting, diarrhea, diuretics, alkalosis, or poor dietary intake. Symptoms include muscle weakness, cramps, arrhythmias, and fatigue. Treatment involves potassium replacement via diet or supplements and addressing the underlying cause.
Difference between primary and secondary hypertension
The key differences between primary hypertension and secondary hypertension are:
- Primary (Essential) Hypertension
Cause: No identifiable cause; develops over time due to genetics, lifestyle, or aging.
Prevalence: Most common (90-95% of cases).
Treatment: Lifestyle changes and medications.
- Secondary Hypertension
Cause: Caused by an underlying condition (e.g., kidney disease, hormonal disorders).
Prevalence: Less common (5-10% of cases).
Treatment: Treat the underlying condition, along with blood pressure control.
Fever
Fever occurs when your body temperature rises above the normal range (98.6°F or 37°C). It’s usually a sign of an underlying condition, such as an infection or inflammation.
Common Symptoms:
Elevated body temperature
Chills or shivering
Sweating
Headache
Muscle aches
Fatigue
Loss of appetite
Ornganism if HAI
Mrsa
Vrsa
Klebsiella
Ecoli
Hepatitis B
Influenzae
Side effects of corticosteroid therapy
Shortterm effects
Fluid retention
Increased appetite
Insomnia
Increased blood sugar levels
high blood pressure
Long term effect
Osteoporosis
Adrenal suppression
Glaucoma
Skin thinning bruising
Central obesity
Cishings syndrome
Haemothorax
Haemothorax
Haemothorax is the accumulation of blood in the pleural cavity, often resulting from trauma or other medical conditions.
Causes
Trauma (e.g., rib fractures, chest injuries)
Post-surgical complications
Ruptured blood vessels or malignancies
Symptoms
Chest pain
Shortness of breath
Reduced or absent breath sounds on the affected side
Diagnosis
Chest X-ray: Detects fluid in the pleural cavity.
Ultrasound/CT Scan: Confirms the extent of blood accumulation.
Treatment
Small Haemothorax: Observation or drainage if symptomatic.
Large Haemothorax: Chest tube insertion to drain blood.
Manage the underlying cause (e.g., stopping bleeding).
Complications
Infection (e.g., empyema)
Fibrothorax
Respiratory failure if untreated
Snake envenomation
Snake Envenomation
Snake envenomation occurs when venom is injected into a person’s body through a snake bite. It can cause systemic or localized effects depending on the type of snake and the amount of venom delivered.
Types of Snake Venom
- Neurotoxic Venom: Affects the nervous system (e.g., cobras, kraits).
- Hemotoxic Venom: Damages blood vessels and impairs clotting (e.g., vipers).
- Cytotoxic Venom: Causes tissue destruction and local necrosis (e.g., some cobras, pit vipers).
Any three anti arrythmic drugs
Lidocaine
Amiodarone
Metoprolol
Grades of dyspnea
Grade 0-no dyspnea (breathlessness only on straining exersise)
Grade 1 -mild dyspnea (shortness of breath while hurrying or walking hill
Grade 2 -moderate ,walk slower,stops for breath
Grade 3-severe stops for breath after walking 100 m
Grade 4-very severe with breathlessness while dressing also
Name any 3 adrenergic bronchodialator
- Salbutamol (Albuterol)
- Formoterol
- Salmeterol
Central sleep apnea
Central sleep apnea (CSA) is a type of sleep apnea characterized by a temporary cessation of breathing during sleep due to a lack of respiratory effort. Unlike obstructive sleep apnea, where the airway is physically blocked, CSA occurs when the brain fails to send the appropriate signals to the muscles that control breathing.
Causes:
Heart failure: Common in individuals with heart conditions.
Brainstem injury: Damage to the part of the brain that controls breathing.
Medications: Opioids and other sedatives may suppress the respiratory drive.
High altitudes: In some cases, sleep apnea can occur at high altitudes due to lower oxygen levels.
Symptoms:
Pauses in breathing during sleep, often noticed by a partner.
Frequent awakenings during the night.
Shortness of breath, especially when awake.
Daytime sleepiness and fatigue.
Difficulty concentrating.
Treatment:
Adaptive servo-ventilation (ASV) or bi-level positive airway pressure (BiPAP) machines help regulate breathing during sleep.
Continuous positive airway pressure (CPAP) therapy may also be used in some cases.
Medications like acetazolamide or theophylline can stimulate breathing.
Lifestyle changes such as weight management and improving sleep hygiene may help alleviate symptoms.
If you or someone you know is experiencing symptoms of central sleep apnea, consulting a healthcare provider for proper diagnosis and treatment is important.
Cardiac workers lung desease
Cardiac pulmonary edema (often referred to as “cardiac worker’s lung disease”) is a condition that can occur due to heart failure, where the heart’s inability to pump blood effectively causes fluid to accumulate in the lungs, leading to breathing difficulties.
However, cardiac worker’s lung disease isn’t a widely recognized specific term in medical literature. It may refer to lung issues that arise in the context of chronic heart disease, especially in conditions where the heart’s inability to pump blood leads to secondary lung issues like pulmonary edema.
Causes of Cardiac Pulmonary Edema:
- Congestive heart failure (CHF): The most common cause, where the heart’s pumping efficiency is reduced, leading to fluid back-up in the lungs.
- Acute myocardial infarction (heart attack): Can lead to left-sided heart failure and pulmonary edema.
- Valvular heart disease: Such as mitral valve disease, which may lead to fluid retention in the lungs.
Symptoms:
Shortness of breath (especially when lying down).
Rapid breathing and a feeling of suffocation.
Coughing up frothy sputum, sometimes tinged with blood.
Wheezing and difficulty breathing.
Cyanosis (bluish color of the lips and face).
Diagnosis:
Chest X-ray: May show fluid in the lungs or other signs of pulmonary edema.
Echocardiogram: Used to assess heart function and identify any underlying heart conditions.
Electrocardiogram (ECG): To detect any arrhythmias or heart problems.
Blood tests: For BNP (brain natriuretic peptide) levels, which can be elevated in heart failure.
Treatment:
- Oxygen therapy: To help increase oxygen levels in the blood.
- Diuretics: To remove excess fluid from the body.
- ACE inhibitors or ARBs: To reduce the heart’s workload and improve pumping efficiency.
- Beta-blockers: To reduce heart rate and blood pressure, helping the heart function better.
- Vasodilators: To help relax blood vessels and reduce the heart’s workload.
- Mechanical ventilation: In severe cases, to assist with breathing.
Effective management of the underlying heart condition is crucial to preventing further episodes of pulmonary edema. Regular monitoring and appropriate treatment by healthcare professionals are essential.
Pathophysiology of left ventricular failure
Left ventricular failure (LVF), also known as left-sided heart failure, occurs when the left ventricle of the heart is unable to pump blood effectively to the rest of the body. This results in a decreased cardiac output and an inability to maintain adequate perfusion of tissues and organs.
Pathophysiology of Left Ventricular Failure:
- Impaired Contractility or Systolic Dysfunction:
Reduced Ejection Fraction (EF): The left ventricle’s ability to contract and pump blood is diminished, leading to a decrease in the ejection fraction (EF), which is the percentage of blood ejected from the ventricle with each heartbeat.
Causes: This can be caused by conditions such as myocardial infarction (heart attack), chronic hypertension, cardiomyopathy, or valvular heart diseases (e.g., aortic stenosis, mitral regurgitation).
- Increased Preload:
The reduced pumping efficiency leads to blood backing up into the left atrium and eventually into the lungs (pulmonary circulation).
Pulmonary Congestion: As blood volume accumulates in the left atrium, pressure increases, leading to fluid leakage from the capillaries into the alveoli (lung tissue). This results in pulmonary edema, causing symptoms like shortness of breath, orthopnea (difficulty breathing when lying flat), and paroxysmal nocturnal dyspnea (waking up from sleep due to difficulty breathing).
- Increased Afterload:
Systemic Vasoconstriction: The body compensates for reduced cardiac output by stimulating the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS). This causes vasoconstriction and sodium retention, which increases blood volume (fluid retention) and systemic vascular resistance (afterload).
Further Strain on the Left Ventricle: The increase in afterload makes it even harder for the left ventricle to pump blood effectively, worsening heart failure.
- Neurohormonal Activation:
The decreased cardiac output triggers the release of renin from the kidneys, which activates the RAAS. This leads to increased aldosterone and angiotensin II levels, causing:
Fluid retention (by promoting sodium reabsorption in the kidneys).
Vasoconstriction (increased peripheral resistance).
Cardiac remodeling (long-term structural changes in the heart muscle).
Sympathetic Nervous System Activation: Increased levels of norepinephrine are released, leading to vasoconstriction, tachycardia, and further myocardial workload.
- Pulmonary Symptoms:
Pulmonary Edema: Fluid accumulation in the lungs due to the elevated left atrial pressure can lead to impaired gas exchange, hypoxemia, and dyspnea.
Coughing with Frothy Sputum: A hallmark symptom of pulmonary congestion.
- Decreased Renal Perfusion:
The kidneys receive reduced blood flow due to low cardiac output, triggering renal retention of sodium and water, which increases blood volume and worsens fluid overload.
Decreased Glomerular Filtration Rate (GFR) may also occur, contributing to renal dysfunction.
- Left Ventricular Remodeling:
Chronic LVF leads to structural changes in the heart, including ventricular dilation, hypertrophy (thickening of the ventricular walls), and fibrosis. This further diminishes the heart’s ability to pump efficiently and increases the risk of arrhythmias.
- Systemic Effects:
Fatigue: Due to poor tissue perfusion and oxygen delivery.
Exercise Intolerance: Reduced ability of the heart to meet increased oxygen demands during physical activity.
Compensatory Mechanisms:
The body attempts to compensate for LVF through:
- Frank-Starling Mechanism: Initially, the heart stretches (increased preload) to pump more blood, but this can only work for a short time.
- Neurohormonal Activation: As discussed, mechanisms like RAAS and sympathetic activation aim to improve perfusion, but they can be harmful long-term if the underlying cause is not treated.
Key Features of LVF:
Backward Failure: Blood backs up into the pulmonary circulation, causing pulmonary congestion and edema.
Forward Failure: Decreased cardiac output results in poor perfusion of tissues and organs, leading to fatigue, weakness, and organ dysfunction.
Left ventricular failure can lead to both acute and chronic symptoms, and its management typically involves medications to reduce preload and afterload, improve contractility, and relieve symptoms of pulmonary congestion.
Role of respiratory therapist in pulmonary vascular desease
A respiratory therapist (RT) plays a crucial role in the management and treatment of pulmonary vascular disease (PVD), which includes conditions like pulmonary hypertension (PH), pulmonary embolism (PE), and other disorders affecting the pulmonary vasculature. Respiratory therapists work closely with physicians and other healthcare providers to optimize respiratory function, alleviate symptoms, and improve patient outcomes. Here’s how RTs contribute:
- Assessment and Monitoring:
Oxygenation and Ventilation: RTs assess the patient’s oxygenation status through pulse oximetry and arterial blood gas (ABG) analysis. In pulmonary vascular diseases, oxygen levels may fluctuate due to poor blood flow to the lungs.
Respiratory Rate and Pattern: Monitoring for signs of dyspnea, tachypnea, or labored breathing, which are common in PVD due to increased right heart strain and low oxygen levels.
Pulmonary Function Tests (PFTs): While the diagnosis of PVD is often based on imaging and clinical findings, PFTs help evaluate lung capacity and efficiency, which may be affected by vascular problems.
- Oxygen Therapy:
Administering Oxygen: Many patients with pulmonary vascular diseases (especially pulmonary hypertension) suffer from low oxygen levels. RTs administer supplemental oxygen to improve oxygenation and reduce strain on the heart and lungs.
Monitoring Oxygen Levels: Continuous monitoring ensures that patients maintain adequate oxygen saturation (SpO2), reducing the risk of hypoxemia, which can exacerbate symptoms of PVD.
- Ventilatory Support:
Mechanical Ventilation: In severe cases (such as acute pulmonary embolism or acute exacerbations of pulmonary hypertension), mechanical ventilation or non-invasive positive pressure ventilation (BiPAP or CPAP) may be required. RTs are skilled in setting up and managing these devices to help maintain optimal airway pressure and improve ventilation.
Invasive Ventilation: In cases requiring intubation, RTs are responsible for managing the ventilator settings and ensuring that ventilation is properly adjusted to the patient’s needs.
- Pulmonary Rehabilitation:
Patient Education: RTs educate patients about breathing exercises, energy conservation techniques, and proper use of inhalers or other medications, which can help manage symptoms.
Exercise and Breathing Techniques: In the case of chronic pulmonary vascular diseases (like pulmonary hypertension), RTs guide patients in controlled exercises that can help improve lung function and reduce breathlessness. These exercises are typically part of a broader pulmonary rehabilitation program.
- Medications and Treatments:
Nebulized Medications: RTs administer nebulized bronchodilators or corticosteroids to help manage symptoms like shortness of breath and wheezing, especially in cases where pulmonary vascular disease leads to bronchoconstriction.
Management of Diuretics: In pulmonary vascular diseases with fluid retention, RTs help monitor for fluid overload signs (like edema or crackles in the lungs) and collaborate with the medical team in fluid management strategies.
- Acute Care Management:
Acute Pulmonary Embolism (PE): In the case of PE, RTs play a key role in managing respiratory distress and administering therapies such as oxygen, anticoagulants, and in some cases, thrombolytic therapy.
Handling Acute Exacerbations of Pulmonary Hypertension: In acute exacerbations, where there is an increase in pulmonary pressures leading to respiratory failure, RTs assist in managing ventilation and oxygenation to improve the patient’s clinical status.
- Collaboration and Communication:
Interdisciplinary Approach: RTs work alongside cardiologists, pulmonologists, and critical care teams to provide comprehensive care for patients with pulmonary vascular disease.
Patient Monitoring and Reporting: RTs keep the medical team informed about changes in the patient’s respiratory status and assist with the interpretation of lab results, like ABGs or chest X-rays, helping in the early identification of issues such as right-sided heart failure or fluid buildup.
- Palliative and End-of-Life Care:
For patients with end-stage pulmonary vascular disease, such as severe pulmonary hypertension, RTs provide comfort measures like oxygen therapy and non-invasive ventilation, along with education on managing symptoms and improving quality of life.
Summary of Key Roles:
Assess respiratory function and provide ongoing monitoring.
Administer oxygen therapy and ventilatory support as needed.
Assist in managing medications like nebulized therapies or diuretics.
Educate patients on breathing exercises and techniques.
Collaborate with the healthcare team to optimize care for patients with pulmonary vascular disease.
Respiratory therapists are integral to improving the quality of life for patients with pulmonary vascular disease by helping manage respiratory symptoms, optimizing lung function, and preventing complications.