Pathophysiology Flashcards
What is the Patho of ACS
Acute Coronary syndrome is a spectrum of illnessess.
1) Unstable Angina
- results when the blood flow is impeded to the myocardium. Most commonly, this block can be from plaque formation, thrombosis, vasospasm, and elevated blood pressure. Often, a combination of these is the provoking factor.
Non-ST elevation MI
- Non-ST-elevation myocardial infarction (NSTEMI) is a type of involving partial blockage of one of the coronary arteries, causing reduced flow of oxygen-rich blood to the heart muscle.
STEMI
-The pathogenic mechanism typically involves plaque rupture and thrombus formation within the coronary artery, though other processes may also lead to STEMI. This is when an artery is fully occluded starving a certain part of the heart of oxygen.
What is the Patho of Pulmonary Oedema
What is the shock state of PO and why?
Cardiac Pulmonary Oedema
1. Increase in Left ventricular end diastolic pressure causing left atrium to pump harder
2. Atrium become overwhelmed leading in increase in hydrostatic pressure.
3. Pulmonary veins (at heart) begin to widen, this causes a back flow of blood into pulmonary circulation.
4. Fluid shifts into interstitial spaces (Outside of cells and compartments considered extracellular space)
5. Increase in pressure in these spaces causes fluid to shift into Alveoli.
6. This will cause fluid in the lungs, wash surfactant out.
Signs and symptoms
1. Dyspnoea (Short of breathe)
2. Orthopnoea (SOB laying down)
3. Hypertension
4. Crackles in lungs (both) Coarse indicates more fluid in the lungs.
Patients most at risk are patients with LVF. The left ventricle no longer functions as well due to a change in physiology like e.g. hypertrophy.
Shock state
Cardiogenic shock
- Cardiogenic shock occurs when the heart is unable to pump blood effectively, due to back flow of oxygenated blood in the heart, this can lead to shock. further to this the heart increase its force (BP) and thus patients are very Hypertensive causing further damage to an already damaged heart.
What is the Patho of asthma? Early phase/ Late phase and partial reversibility?
What are some signs and symptoms
What is the Shock state of asthma and why?
Reversible
Early phase
1. Inhaled exposure to trigger (Allergen/ irritant)
2. T- Helper cells release cytokins
3. This causes activation of IGE which cause mast cell degranulation
4. Degranulation causes release of Inflammatory mediators (Leukotrienes, histamine and prostaglandins).
5. Inflammatory mediators cause contraction of bronchial smooth muscle in airways (Bronchospasm)
6. Also causes fluid shift (Oedema) + Mucus production (goblet cells) which leads do further airway obstruction.
Late phase
1. Further Inflammatory cells and mediators are released leading to worsening symptoms.
2. Goblets cells become hyperreactive leading to further mucus production.
Partial Reversible
- Patients who have long term reoccurring presentation will generally only have partial reversibility due to lung remodelling
- Fibrosis (Scarring)
- Membrane thickening
- Increase volume of mucus
Signs and symptoms
1. Dyspnoea (Short of breath)
2. Coughing
3. Wheezing
4. Chest tightness
5. Increase respiratory rate (Tachypnoea)
6. Cyanosis + Fatiuge
Shock state (Asthma generally doesn’t fit into a shock state) however
- Distributive shock could occur with widespread vasodilation due to Fluid shift from inflammatory mediators
- Obstructive shock could technically occur if patients have gas trapping and hyperinflation of chest (increase in Intrathoracic pressure), this could cause a physical pressure on Vena cava reducing blood flow to heart. This would reduce preload. Thus, causing a physical obstruction/
What is the Patho of Emphysema.
What type of shock state is Emphysema
(Referring to generally COPD presentations).
Emphysema
Definition
- Abnormal and permanent enlargement of air spaces and destruction of Alveolar walls. Tis leads to reduced gas exchange, gas trapping and impaired expiratory airflow.
Pathophysiology of Emphysema:
1. Patients have generally been exposed to chemicals, smoke or other irritants that lead to alveolar wall destruction.
2. Further leading to decrease in good gas exchange due to reduced surface area of Alveolar wall.
3. This leads to decrease oxygenation of blood and gas trapping,
4. Secondary to Alveoli wall destruction is reduction/ loss of elastic recoil, which is important for expelling air during exhalation.
4. Gas trapping leads to increase in Co2 retention and hyperinflation of chest (Pink Puffer)
Signs and symptoms
1. Dyspnoea (Shortness of breathe)
2. Chronic Cough, dry or wet
3. Wheezing
4. Chest tightness
5. Barrel Chest
6. Increase respiratory rate (Tachypnoea)
7. Cyanosis + Fatigue
Shock State
Patients with COPD exacerbation can met Hypoxic shock states. Hypoxic shock state is when oxygen level become critically low and are unable to meet the demand of tissue and organ perfusion. This will lead to Cellular dysfunction (cell death) and then organ dysfunction and death.
What is the Patho of Chronic bronchitis.
Definition
- Chronic inflammation of the airways (bronchi), which leads to increased mucus production, airflow limitation, and difficulty with breathing.
- It is defined clinically as a productive cough (mucus production) for at least 3 months per year for two consecutive years or more.
Patho
1. Patients are exposure to Irritants (Smoking, chemicals, air pollutants etc) leading to persistent re-occurring infections in the lower respiratory tract.
2. Inflammation mediators released (Prostaglandins and Leukotrienes).
inflammatory mediators are released contributing to airway injury and remodeling. The inflammation leads to increase in mucus and increase in hypertrophy. This will lead to further obstruction of airways.
Mucus Hypersecretion:
The thick mucus leads to chronic productive cough, a key feature of chronic bronchitis. The cough is worse in the mornings and is often associated with sputum (mucus) production.
Due to damaged Cilia, patient often have issues clearing mucus. This means a build up of mucus and a build up of Bacteria are breeding grounds for further infections.
Inflammation and mucus buildup lead to narrowing of the bronchi, making it difficult for air to flow in and out of the lungs.
Chronic inflammation also causes remodeling of the airway wall, with fibrosis (scarring) and thickening of the airway walls, further contributing to airflow obstruction.
Bronchial Smooth Muscle Constriction:
Chronic bronchitis is often associated with bronchospasm (constriction of the bronchial smooth muscle), which further narrows the airways and increases resistance to airflow.
Decreased Gas Exchange:
The chronic narrowing and inflammation of the airways result in ventilation-perfusion mismatch. While air may enter the lungs, it cannot reach all areas of the alveoli effectively due to blocked or narrowed airways, reducing oxygen uptake and carbon dioxide clearance.
Over time, this leads to hypoxemia (low oxygen levels in the blood) and hypercapnia (increased carbon dioxide levels), especially in advanced disease.
Air Trapping and Hyperinflation:
In patients with chronic bronchitis, the collapse of small airways during exhalation leads to air trapping—the retention of air in the lungs after expiration. This causes lung hyperinflation,
What is the definitions of COPD (Emphysema and chronic bronchitis)
COPD is a term that includes 2 or more of the following 3 conditions
1. Asthma
2. Emphysema
3. Chronic Bronchitis
These 3 conditions all impact the airways and lungs, generally speaking cause widespread inflammation.
These conditions lead to long term structural changes in the airway.
What is the Patho of COPD
COPD is a combined illness of Asthma, Chronic bronchitis and Chronic Emphysema.
All 3 of this conditions are similar and all cause airway remolding.
- Inflammation (inflammatory mediators including prostaglandins, cytokines, histamines via mast cell degranulation : Prolonged exposure to irritants, This inflammation leads to damage and remodeling of the airways.
- Loss of elastic recoil: causes a reduction in assistance of expiration leading to gas trapping and increase effort on expiration. It also reduces surface area for gas exchange.
- Hypersection of mucus: From Goblet cells leads to mucus plugging and airway restriction.
Airway remodeling: The airways become inflamed and produce excess mucus, leading to mucus plugging and narrowing of the airways. Additionally, there is thickening of the airway walls, which further obstructs airflow.
What is the Patho of croup?
Croup, also known as laryngotracheobronchitis, is a common respiratory illness in children characterized by inflammation and narrowing of the upper airway, particularly the larynx, trachea, and bronchi. This condition typically results in a distinctive barking cough, stridor, and hoarseness.
Most commonly effecting ages 6 months to 6 years old.
Inflammation:
- The infection triggers inflammation of the respiratory epithelium, leading to:
Oedema and swelling of the subglottic region (below the vocal cords).
Increased mucus production.
Airway Obstruction:
-The subglottic space is naturally narrow, especially in young children.
Inflammation and swelling in this region cause significant airway narrowing, leading to increased airway resistance.
Severity:
Mild: Barking cough without stridor at rest.
Moderate: Stridor at rest with mild to moderate respiratory distress.
Severe: Significant stridor, severe respiratory distress, lethargy, or hypoxia.
What is the Patho of Hyperglycemia
Hyperglycemia occurs when blood glucose levels are too high, typically above 7.0 mmol/L (fasting) or 11.1 mmol/L (post-meal).
What Happens in Hyperglycemia:
Insufficient Insulin or Insulin Resistance:
- Type 1 Diabetes: The body doesn’t produce enough (or any) insulin, which is needed to help glucose enter cells.
-Type 2 Diabetes: The body becomes resistant to insulin, so glucose cannot enter cells effectively, even if insulin is present.
Glucose Accumulates in the Blood:
Insulin is a gate keeper for cells and allows cells to uptake glucose to use as energy. Since glucose can’t enter cells properly, it builds up in the bloodstream.
Cells are starved of energy, so the liver produces even more glucose, worsening the problem.
Osmotic Effects:
-High glucose levels pull water out of cells into the bloodstream, leading to dehydration and excessive urination (polyuria).
This can cause increased thirst (polydipsia).
Metabolic Imbalance:
In the absence of insulin, fat breakdown increases, leading to ketone production. This can result in diabetic ketoacidosis (DKA) in Type 1 diabetes.
In severe Type 2 diabetes, hyperosmolar hyperglycemic state (HHS) can develop, with very high blood sugar and severe dehydration.
What is the Patho Hypoglycemia
Reduction in Blood glucose state <4mmol/L
Caused by
- Overuse of insulin or other hypoglycemic agents (e.g., sulfonylureas) can cause an exaggerated insulin response, leading to excess glucose uptake into cells and insufficient glucose in circulation
- Insulin excess (as in insulinoma or overdose) or impaired hormonal responses can reduce glycogen breakdown.
- Minimal or no production of glucose due to issues with liver.
- Conditions like type 1 diabetes, long-standing diabetes, or damage to the pancreas may impair the release of glucagon, the primary counterregulatory hormone for glucose homeostasis.
- Decrease in available glucose, decrease in glycogen or to much insulin can lead to this.
- Brain requires ATP to function, confusion, dizziness, irritability, difficulty concentrating, visual disturbances, seizures, and even loss of consciousness can occur.
- As a result of the sympathetic nervous system’s activation, symptoms include shaking, sweating, tachycardia, and anxiety.
To address this issue, paramedics can give, Glycogen to stimulate conversion of glycogen to glucose, they can also give glucose paste or sugar water directly.
What is Hyperosmolar Hyperglycemic State (HHS)
1) Insulin Deficiency:
2) In HHS, insulin deficiency is sufficient to prevent glucose from being taken up by cells. This leads to hyperglycemia. However, there is enough insulin to prevent significant ketone formation, unlike in DKA.
3) Osmotic Diuresis:
The high blood glucose levels cause osmotic diuresis, where glucose in the urine draws water along, leading to excessive urination (polyuria). This results in significant fluid loss and dehydration.
4) Severe Dehydration:
The fluid losses lead to dehydration. Dehydration can also impair kidney function, further exacerbating the hyperglycemia and electrolyte imbalances.
5) Electrolyte Imbalances:
Dehydration and osmotic diuresis result in significant loss of electrolytes, particularly sodium, potassium.
What is Diabetic Ketoacidosis (DKA)
1) Insulin Insufficiency
2) Glucagon, adrenaline and hormones are released.
3) These hormones promote glucose production by the liver (gluconeogenesis) and breakdown of glycogen (glycogenolysis), worsening hyperglycemia.
4) Fat break down leads to fatty acid production, these are then converted to Ketones.
Ketones are acidic, causing metabolic acidosis.
The body attempts to compensate by increasing breathing rate (Kussmaul respirations) to blow off CO₂ and reduce acidosis.
4) Electrolyte Imbalances:
Hyperglycemia causes osmotic diuresis, leading to loss of water, sodium, and potassium in the urine.
5) Dehydration and Hypovolemia:
Osmotic diuresis leads to severe dehydration and loss of circulating blood volume (hypovolemia), which can cause hypotension and reduced tissue perfusion.
What is Euglycemic Ketoacidosis and how is it relevant in Prehospital care?
Euglycemic ketoacidosis (EKA) is a rare form of diabetic ketoacidosis (DKA) where blood glucose levels remain normal or only mildly elevated (typically <11 mmol/L, but significant ketosis and metabolic acidosis still occur. This condition is most commonly associated with:
- Sodium-Glucose Co-Transporter-2 (SGLT-2) Inhibitors: ( canagliflozin, dapagliflozin, and empagliflozin)
- Alcoholics
- Prolonged fasting/ Starvation
- Acute illness or stress
- Pregnancy
What is the patho of a Seizure
Seizures occur when neurons in the brain fire excessively or synchronously.
This abnormal firing disrupts the balance between excitatory (e.g., glutamate) and inhibitory (e.g., GABA) neurotransmitters.
Hyperxcitable Neurons:
In seizure-prone areas, neurons have a lower threshold for firing due to changes in:
Ion channels (e.g., sodium, calcium, and potassium channels).
Neurotransmitter systems (reduced GABA or increased glutamate).
Seizures can be focal (originating in one area)
or
generalized (involving both hemispheres of the brain).
Causes
- Certain conditions can predispose the brain to seizures, including:
Structural damage (stroke, trauma, tumors).
- Electrolyte imbalances (e.g., low sodium or calcium).
- Infections (e.g., meningitis, encephalitis).
- Genetic mutations affecting ion channels or receptors.
- Withdrawal from alcohol or sedatives.
What is the Meningococcal Disease
Meningococcal disease is caused by the bacterium, which can lead to life-threatening infections such as meningitis (infection of the protective membranes around the brain and spinal cord) and septicemia (bloodstream infection). It progresses rapidly and requires immediate medical attention.
Signs
- Fatigue
- Cold hands and feet, or mottled skin
- Petechial rash (small, red or purple spots on the skin that do not fade under pressure)
- Fever
- Severe headache
- Stiff neck
- Nausea and vomiting
- Sensitivity to light (photophobia)
- Altered mental status (confusion, lethargy, or difficulty concentrating)
- Seizures
