PATHOPHYSIOLOGY Flashcards
(15 cards)
Myocardial Infarction: Confirmed with ECG
Sudden ischemic death of myocardial tissue, often due to thrombotic occlusion from (ATHEROSCLEROSIS) plaque rupture in a coronary vessel.
Complications:
- Heart Failure: damage to heart’s pumping ability.
- Arrhythmias: potentially life threatening.
- Cardiogenic Shock: Severe heart pump failure leading
to inadequate blood flow.
Asthma
-Chronic inflammation of respiratory lining, involving tightening of respiratory smooth muscles and episodes of airway hyperresponsiveness.
-IgE antibodies respond to certain triggers in the environment.
-This exposure to irritants causes the release of inflammatory mediators such as prostaglandin, histamine, and cytokines, which cause airway swelling.
- This swelling causes goblet cells to produce excessive mucus.
Rhabdomyalisis
Rapid dissolution of damaged skeletal muscle, causing the direct release of intracellular muscle components (myoglobin, creatine kinase, aldolase, lactate dehydrogenase, electrolytes) into the bloodstream.
Complications:
- AKI
- Disseminated Intravascular Coagulation (DIC)
- Electrolyte imbalances: hyperkalaemia,
hyperphosphatemia
COPD
COPD is a progressive and permanent damage to the lung structure.
- long-term exposure to irritants like tobacco smoke, air pollution, or occupational dust irritates the airways, causing inflammation in the lungs.
-The body’s immune system responds by releasing inflammatory cells such as neutrophils and macrophages, which release enzymes (e.g., elastase) that damage lung tissue.
-In response to inflammation, goblet cells produce excessive mucus, which obstructs the airways and causes symptoms like chronic cough and sputum production.
- Emphysema is a key component of COPD. The alveoli (tiny air sacs where gas exchange occurs) lose their structural integrity. The walls between alveoli break down, reducing the surface area for oxygen exchange.
- Brnochitis : Chronic inflammation and excessive mucus production in the bronchi lead to narrowing of the airways, making it harder for air to flow in and out of the lungs.
Normally, carbon dioxide (CO2) levels in the blood are the main stimulus for breathing. Specialized chemoreceptors in the brainstem (medulla) detect rising CO2 levels, triggering an increase in the respiratory rate and depth to expel the excess CO2. This is called the hypercapnic drive.
However, in people with COPD, the hypoxic drive takes over as the primary mechanism for controlling breathing. This happens due to chronic hypercapnia (elevated CO2 levels) and reduced oxygen levels in the blood.
Blunt trauma
May result in internal or external haemorrhage depending on location and mechanism. Body has trouble clotting due to the amount of blood.
Complications:
- Severe Hypotension
- Hypovolemic shock
- Death
Penetrating trauma
Penetration: The object pierces the body, disrupting tissues, blood vessels, and organs in its path. Cavitation: Rapid movement of the penetrating object creates a temporary cavity, causing additional tissue damage.
Complications:
- Local Tissue Damage - entry site and along trajectory
- Vascular Injury & Haemorrhage - the size and location
of the injured vessels, significant bleeding may occur,
leading to hypovolemic shock
- Infection Risk: Contamination: introduces foreign
material into the body & microbial Invasion: Bacteria
from the environment or skin can enter deeper
tissues, leading to infection.
Appendicitis
Obstruction of appendiceal orifice leads to an increase in intraluminal and intramural pressure, resulting in small vessel occlusion and lymphatic stasis
Complications:
- appendix becomes ischemic and necrotic
- Bacterial infection - peritonitis
- Acidosis
Sepsis and Septic Shock
Life-threatening organ dysfunction caused by dysregulated host response to invasion of tissue by pathogens.
Dysregulation of the inflammatory mediator cascade leads to capillary integrity loss, maldistribution of microvascular blood flow, and nitric oxide production, causing organ injury and dysfunction.
Complications:
- Decreased oxygen delivery
- Impaired CO2 removal lead to acidosis.
Addisons
Hypothalamus releases corticotropin-releasing hormone (CRH) in response to stressors. CRH stimulates anterior pituitary to release adrenocorticotropin hormone (ACTH). ACTH upregulates cortisol production in the adrenal cortex.
Complications:
- Postural hypotension, compensatory tachycardia,
and potential vascular collapse.
- Reduced renal perfusion leads to water retention,
and potassium leakage = hyperkalemia and metabolic
acidosis.
- Circulatory collapse impairs waste product excretion,
elevating blood urea nitrogen and creatinine levels.
Show Questio
Cocaine toxicity
CNS Stimulant - Binds and blocks monoamine neurotransmitters (dopamine, adrenaline, noradrenaline, and serotonin) re-uptake transporters
Cocaine leads to vasoconstriction via stimulation of the alpha-adrenergic receptor of the coronary artery’s smooth muscle cells
Significantly increases myocardial oxygen requirements, heart rate, and cardiac output.
This in turn with it’s vasoconstrictive properties can result in cocaine-induced MI, and accelerated ischaemic heart disease
Anaphylaxis
Severe, life-threatening, generalised or systemic hypersensitivity reaction. This is characterised by rapidly developing life-threatening airway and/or breathing and/or circulation problems, usually associated with skin and mucosal changes.
Heart failure
When the heart struggles to pump effectively, the body activates the renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system, causing vasoconstriction, fluid retention, and further stress on the heart.
Systolic HF - ventricles cant pump hard enough during systole
Diastolic HF - ventricles cant fill endough during diastole
Conmplications:
- Pulmonary Oedema
- Death
What are some symptoms of an AMI
Sharp crushing pain
Radiating
Nausea
Treatment and dosages for MI
Asiprin 300mg
GTN - 400mcg - 800mcg
Morphine 1mg in 1ml diluted with NaCl 0.9% to make 10ml
