first ever flashcard

A 55-year-old woman with no past medical history presented with recurrent chest pains with the latest pain onset was 6 hours prior and lasted for 30 minutes. Occasionally she felt it as burning-like sensation. Vital signs were BP 140/80 mmHg, HR 90/min, RR 16/min, and SpO2 99% on room air. 12-lead ECG demonstrates sinus rhythm, no ST elevations, and a presence of isolated ST segment depression in a high lateral lead. High sensitivity troponin result is pending.

Which statement is the most correct regarding the pathophysiology of the above patient?

A. Air enters the pleural space from the lung via mediastinal tissue planes

B.Defect in esophageal mucosal defense against the refluxate and esophageal motility

C. Lack of oxygen supply to the working myocardium by thrombus formation

D.Physiological stressful state leading to demand-supply mismatch of oxygen

E.Tear in media intima of the aorta leads to formation of new lumen

What condition is indicated by recurrent chest pains in a 55-year-old woman with ST segment depression in a high lateral lead on ECG?

Demand-supply mismatch of oxygen due to physiological stressful state.

The condition indicated is typically angina pectoris, which arises from a demand-supply mismatch of oxygen to the heart muscle. In this case, the recurrent chest pains suggest that there is an imbalance where the heart's demand for oxygen exceeds the supply, particularly during stress or exertion. ST segment depression in the ECG indicates ischemia, which suggests that the heart is not receiving adequate blood flow, likely due to coronary artery disease or other factors impacting coronary perfusion.

An 11-month-old boy presented with a 1-day history of wheezing and coughing. The parents reported that this is the third episode of the year. Previous episodes were similar and resolved within a few days especially during cold or rainy days. They denied any choking episodes.

The child's vital signs were BP 82/48 mmHg, HR 110/min, RR 30/min, SpO2 94% on room air and T 36.5 ºC. On examination, the child appeared to be in mild respiratory distress with audible expiratory wheezing. The rest of the physical examination was unremarkable.

What is the most likely cause of wheezing in this patient?

A. Infective inflammation of the lung parenchyma.

B. Inhalation of a foreign object into the airways

C. Narrowing of the airways triggered by allergens

D. Regurgitation of stomach contents into the esophagus.

E. Viral infection causing obstruction of the small airways.

What is the most likely cause of wheezing in an 11-month-old boy with recent respiratory distress?

Viral infection causing obstruction of the small airways.

Wheezing in an 11-month-old boy with recent respiratory distress is most likely caused by a viral infection, such as respiratory syncytial virus (RSV), which leads to inflammation and obstruction of the small airways (bronchioles). This obstruction results in difficulty breathing and characteristic wheezing sounds during expiration. The recurrent nature of wheezing episodes in young children, especially after exposure to cold or during viral season, supports this diagnosis.

The other options are less likely based on the provided history and examination:

• A. Infective inflammation of the lung parenchyma (pneumonia) typically presents with fever and more severe respiratory distress.

• B. Inhalation of a foreign object into the airways would likely present with a sudden onset of symptoms and a history of choking.

• C. Narrowing of the airways triggered by allergens (asthma) is possible but less likely given the age and the pattern of episodes.

• D. Regurgitation of stomach contents into the esophagus (GERD) can cause wheezing but is less likely to present with recurrent episodes specifically during cold or rainy days.

A 65-year-old woman with underlying DM, HPT and ESRF on regular hemodialysis presented with reduced conscious level for one day duration. She recently missed her last dialysis session due to being unwell for the past one week. Otherwise, there was no fever, recent trauma, or neurological deficit.

Relevant laboratory results were as follows:

FBC: Hb 9.0 g/dL / WBC 11.1 X 109/L / PLT 300 X 109/L

RP: Na 130 mmol/L / K 5.5 mmol/L / Urea 35 mmol/L / Creatinine 900 μmol/L

What is the most likely pathophysiology to explain her condition?

What explains the reduced consciousness in a 65-year-old woman on hemodialysis?

A .Accumulation of uremic neurotoxin causing cerebral dysfunction

B. Cellular energy failure leading to neuronal death

C. Cytotoxic cerebral oedema following cerebral infarction

D. Disruption of blood-brain-barrier secondary to inflammatory mediators

E. Reduction in functioning hepatocytes causing ammonia accumulation

Accumulation of uremic neurotoxin causing cerebral dysfunction.

Definition: Accumulation of uremic neurotoxin causing cerebral dysfunction. This condition arises when the kidneys are unable to adequately filter waste products from the blood due to end-stage renal failure (ESRF). As a result, toxic substances, referred to as uremic toxins, accumulate in the bloodstream, leading to a range of neurological impairments including confusion, lethargy, or reduced consciousness. In this patient, factors such as missing dialysis sessions can significantly exacerbate the buildup of these toxins, ultimately affecting brain function and leading to observable cognitive changes.

A 25-year-old woman complained of fever and epigastric pain for two days. It was associated with arthralgia, myalgia and retroorbital pain. Fever temporarily relieved by paracetamol. No recent jungle trekking or travelling history.

On examination, she was alert, pink, warm peripheries with CRT <2 seconds. Her vital signs were BP 90/60 mmHg, HR 120/min, RR 22/min, SpO2 96% on room air and T 39ºC. Per abdomen examination revealed mildly tender hepatomegaly.

Which is the best pathophysiology that explains her condition?

A. Accumulation of N-acetyl-p-benzoquinone due to glutathione depletion

B. Bacterial invasion to liver via portal vein

C. Cystic duct inflammation due to bile stasis

D. Invasion of hepatocytes and Kupffer cells by virus

E. Rupture of schizont-containing erythrocytes triggering cytokine response

What pathophysiology best describes a 25-year-old woman with fever and epigastric pain?

Invasion of hepatocytes and Kupffer cells by virus.

Invasion of hepatocytes and Kupffer cells by a virus, typically associated with viral hepatitis. This condition occurs when a hepatotropic virus, such as hepatitis A, B, or C, infects the liver tissue, leading to inflammation of the liver (hepatitis). The infection results in the direct destruction of liver cells (hepatocytes) and affects the resident immune cells (Kupffer cells) in the liver. This inflammatory response triggers symptoms such as fever, malaise, fatigue, and epigastric pain due to liver enlargement and enzymatic release into the bloodstream.

A 50-year-old chronic smoker presented with limping for 2 days. He complained of pain over his right lower limb. His vital signs were BP 120/60 mmHg, HR 115/min, RR 24/min, SpO2 96% on room air, T 37.5oC and pain score 8. His right toes appeared dusky, and his right leg was swollen.

Which of the following is the most likely pathophysiology of the above condition?

A. Autoimmune vasculitis of branches of aorta

B. Complete stasis of venous blood flow

C. Embolism from irregular cardiac contractions

D. Non atherosclerotic segmental inflammation of small vessels

E. Vasospasm of arterioles provoked by stressors

What explains the dusky appearance and swelling in the right lower limb of a 50-year-old chronic smoker?

Embolism from irregular cardiac contractions.

Embolism from irregular cardiac contractions, often referred to as cardioembolic events, occurs when a thrombus or embolus forms in the heart due to conditions such as atrial fibrillation, myocardial infarction, or heart valve disease. In chronic smokers, contributing factors may include atherosclerosis and endothelial dysfunction, which can increase the risk of thrombus formation in the heart. When these emboli travel through the circulatory system, they can occlude peripheral arteries, particularly in the limbs, leading to reduced blood flow. This ischemia results in tissue hypoxia, causing a dusky (cyanotic) appearance and swelling in the affected limb due to a combination of vascular congestion, inflammatory response, and potential venous obstruction as the body attempts to compensate for the lack of oxygenation.

or Non atherosclerotic segmental inflammation of small vessels (buerger disease)

50, smoker, dusky toe with swelling limbs

• buerger is mor of a chronic process in younger generation

A 65-year-old woman presented with severe pain of the right knee associated with productive cough for 5 days. She denied any trauma. She has diabetes mellitus and is non-compliant with her treatment. Her vital signs were BP 170/90 mmHg, HR 80/min, RR 18/min, SpO2 95% on room air, T 39.5°C, and pain score 9. Clinically, her right knee was swollen, warm and tender on palpation. She refused to move the right knee.

What pathophysiological process best explains the above condition?

A. Autoimmune cell infiltration into the joint

B. Bacterial invasion of the bursa

C. Hematogenous seeding from systemic infection

D. Neutrophils act as mediators of tissue destruction

E. Progressive degradation of joint cartilage

What pathophysiological process explains a swollen and tender knee in a diabetic woman with fever?

Given the patient's history of diabetes mellitus, non-compliance with treatment, and the presence of fever, the most likely pathophysiological process is C. Hematogenous seeding from systemic infection. This condition is consistent with septic arthritis, where bacteria from a systemic infection spread through the bloodstream and infect the joint, leading to severe pain, swelling, warmth, and tenderness.

The other options are less likely based on the provided history and examination:

• A. Autoimmune cell infiltration into the joint is characteristic of autoimmune diseases like rheumatoid arthritis, which typically presents with chronic symptoms rather than acute onset.

• B. Bacterial invasion of the bursa (septic bursitis) would present with localized swelling and tenderness over the bursa, but the systemic signs of infection make septic arthritis more likely.

• D. Neutrophils act as mediators of tissue destruction is a general mechanism seen in various inflammatory conditions but does not specifically explain the acute presentation with systemic infection.

• E. Progressive degradation of joint cartilage is characteristic of osteoarthritis, which presents with chronic pain and stiffness rather than acute severe pain and systemic signs of infection.

The combination of diabetes, non-compliance with treatment, fever, and acute knee symptoms strongly suggests septic arthritis due to hematogenous seeding from a systemic infection

A 62-year-old woman presented with sudden onset of severe right eye pain, blurred vision, and nausea. She had headache and saw halos around lights. On examination, her right eye appeared red with a hazy cornea. Intraocular pressure measurement revealed significantly elevated pressure in the affected eye.

What is the best pathophysiology for the above condition?

A. Abnormal outflow of aqueous humor

B. Accumulation of inflammatory cells in the anterior chamber of the eye

C. Obstruction of blood flow to the retina by embolus

D. Progressive damage to the optic nerve axons

E. Separation between the vitreous and the retina

What is the best explanation for sudden onset severe eye pain and hazy cornea?

Abnormal outflow of aqueous humor.

Abnormal outflow of aqueous humor leading to increased intraocular pressure. This condition, often associated with acute glaucoma, occurs when the drainage pathways for aqueous humor (the clear fluid in the front part of the eye) become blocked or compromised. As a result, fluid accumulates within the eye, increasing pressure on the optic nerve and causing severe pain. The hazy appearance of the cornea is typically due to corneal edema, which occurs when the cornea swells from the excess intraocular pressure affecting its transparency. This situation requires immediate medical attention to prevent permanent vision loss.

A 16-year-old boy presented with acute hearing loss for 2 days. He listened to loud music via headphones all the time. He denied any other history. On examination, bilateral Rinne test was positive.

What is the most likely cause for his condition?

A. Eardrum perforation

B. Hair cells damage

C. Impacted ear wax

D. Middle ear infections

E. Neural damage

What is the most likely cause of acute hearing loss in a 16-year-old boy?

Hair cells damage due to loud music.

Acute hearing loss in a 16-year-old boy is most likely caused by damage to the inner ear's hair cells due to prolonged exposure to loud music, often experienced through headphones or at concerts. This damage can lead to temporary threshold shifts in hearing or permanent sensorineural hearing loss if exposure is excessive. Acute hearing loss in adolescents is commonly due to damage to hair cells in the cochlea, often resulting from exposure to loud sounds, such as music from headphones.

30-year-old man with no past medical history came in for persistent vomiting for 3 days and generalized muscle weakness. On examination, he was alert and lethargic looking. His vital signs were normal. Physical examinations of both upper and lower limbs revealed hypotonia, power 3/5 and hyporeflexia. ECG showed U wave in precordial leads.

What is the best pathophysiology contributing to his condition?

A. Absence of dystrophin leading to excessive membrane fragility

B. Autoimmune destruction of acetylcholine receptor

C. Decreased net activity of proton pumps and HCO3- exchangers

D. Increased muscle tissue breakdown

E. Reduction in efflux of potassium during repolarization phase

What pathophysiology is contributing to generalized muscle weakness in a 30-year-old man with abnormal ECG findings?

Reduction in efflux of potassium during repolarization phase.

Reduction in efflux of potassium during repolarization phase leads to prolonged action potentials in muscle cells and myocardial cells, resulting in impaired muscle contraction and generalized muscle weakness. This can occur in conditions such as hyperkalemia, where elevated potassium levels hinder the normal outflow of potassium from cells during repolarization. As a consequence, the resting membrane potential becomes less negative, making it harder for the muscle cells to reach the threshold needed for action potentials, thus contributing to muscle weakness and possibly affecting heart rhythm.

A 20-year-old man, a drug abuser without any previous medical illnesses was brought by police officer with acute agitation. His vital signs were BP 190/100 mmHg, HR 135/min, RR 25/min, SpO2 100% on room air and T 37.9oC. He was sweating. His ECG showed sinus tachycardia with broad QRS complexes.

Which of the following is the most likely pathophysiology of the above condition?

A. Coronary vasospasms

B. Excitatory effect via alpha- and beta-adrenergic stimulation

C. Increased dopamine release

D. Inhibition of serotonin reuptake

E. Sodium channel blockade

What mechanism underpins agitation in a 20-year-old man involving broad QRS complexes?

Excitatory effect via alpha- and beta-adrenergic stimulation.

The mechanism underlying agitation in a 20-year-old man with broad QRS complexes is primarily due to the excitatory effects of alpha- and beta-adrenergic stimulation, which can lead to increased sympathetic activity. This overstimulation may result in cardiac conduction abnormalities, manifesting as broad QRS complexes on an ECG.

A 52-year-old man with underlying ischemic heart disease and bronchial asthma presented with a sudden onset of shortness of breath associated with flu-like symptoms for 3 days. His vital signs were BP 120/70 mmHg, HR 120/min, RR 32/min, SpO2 91% on room air, and T 37.5oC. Lung auscultation revealed bilateral generalized rhonchi.

His ABG on arrival showed: pH 7.32, PaO2 60 mmHg, PCO2 38 mmHg, and HCO3 24 mmol/L.

Which underlying pathophysiological best explains the above condition?

A. Alveolar hypoxia leading to pulmonary vasoconstriction

B. Histamine release from mast cells leading to hyperresponsive airway

C. Hypersecretion leading to obstruction of small airway

D. Pulmonary blood flow shunting causing low ventilation to perfusion ratio

E. Reduced cardiac perfusion causing activation of the sympathetic nervous system

What is the physiological cause behind shortness of breath in a 52-year-old man with underlying health issues?

Alveolar hypoxia leading to pulmonary vasoconstriction.

Alveolar hypoxia leading to pulmonary vasoconstriction. In individuals with underlying health issues such as chronic obstructive pulmonary disease (COPD) or heart disease, the alveoli may not adequately exchange oxygen due to damage or inflammation. This results in hypoxia (low oxygen levels) in the alveoli, which in turn causes vasoconstriction of the pulmonary blood vessels as a compensatory mechanism to redirect blood flow to better ventilated areas of the lung. However, this vasoconstriction can increase pulmonary artery pressure and worsen the overall oxygenation of the blood, exacerbating feelings of shortness of breath. Furthermore, other factors such as fluid accumulation in the lungs or heart failure complicate the picture, making it crucial to address the underlying conditions affecting both the lungs and heart.

A 50-year-old woman presented with fever and productive cough for 2 days. On examination, she appeared lethargic and in respiratory distress. Her vital signs were BP 130/85 mmHg, HR 102/min, RR 28/min, SpO2 88% on room air and T 38.5°C. Lung auscultation revealed crepitations in the right lower lobe. Chest X-ray showed infiltration in the right lower zone. Her WBC was 28 x 109/L.

What is the pathophysiology that best describes the above condition?

A. Diffuse alveolar damage from destruction of pneumocytes

B. Destruction of alveolar epithelium by reactive oxygen species

C. Infection of ciliated cells in conducting airways

D. Invasion of alveolar epithelial cells via ACE-2 receptors

E. Unopposed activity of neutrophil elastase in the airways

What pathophysiology describes the lung condition in a 50-year-old woman with productive cough and lethargy?

Diffuse alveolar damage from destruction of pneumocytes.

Diffuse alveolar damage from destruction of pneumocytes resulting in alveolar collapse and impaired gas exchange. This condition typically represents acute lung injury or acute respiratory distress syndrome (ARDS), characterized by injury to the alveolar-capillary membrane. The destruction of pneumocytes, which are responsible for producing surfactant, leads to decreased surfactant levels, causing alveolar instability and collapse (atelectasis). This inflammatory process is usually triggered by various factors, such as infections (like pneumonia), toxins, or systemic inflammatory responses. The disruption of the alveolar architecture not only hampers effective gas exchange but also leads to pulmonary edema, contributing to the patient's respiratory symptoms, including productive cough, increased work of breathing, and lethargy due to hypoxia.

A 67-year-old man with underlying hypertension presented with altered sensorium for one day. On examination, he was drowsy. His vital signs were BP 230/120 mmHg, HR 80 /min, RR 18 /min SpO2 97% on room air and T 37oC. CT brain showed intracerebral hemorrhage.

Which is the best pathophysiology to explain the above condition?

A. Blood brain barrier disruption

B. Hemorrhagic necrosis of brain parenchyma

C. Impaired cerebral autoregulation secondary to ruptured vessel

D. Increased capillary leakage leading to cerebral edema

E. Sympathetic activation secondary to reduced cerebral perfusion

What best explains altered sensorium in a 67-year-old man with intracerebral hemorrhage?

Increased capillary leakage leading to cerebral edema.

Increased capillary leakage leading to cerebral edema. Intracerebral hemorrhage involves bleeding within the brain tissue, which disrupts normal vascular integrity. This disruption causes an increase in capillary permeability, allowing plasma proteins and fluids to accumulate in the interstitial space. The resulting cerebral edema (swelling of the brain) increases intracranial pressure, decreases cerebral perfusion, and compresses surrounding brain structures. This combination of effects results in altered sensorium and potentially severe neurological deficits, manifested as confusion, reduced consciousness, or coma. Immediate medical intervention is often required to manage this increased pressure and prevent permanent brain injury.

55-year-old man presented with pleuritic chest pain, cough, and gradually worsening shortness of breath for 5 days. On assessment, his vital signs were BP 92/60 mmHg, HR 120/min, RR 24/min, SpO2 90% on room air and T 39oC. Chest examination revealed stony dullness and reduced breath sounds over right lower zone.

What is the underlying pathophysiological mechanism primarily responsible for the above lung condition?

A. Blockage of lymphatic flow in the pleural cavity

B. Elevated pulmonary capillary pressure

C. Increased interstitial fluid movement due to bacterial invasion

D. Movement of ascitic fluid from peritoneal cavity into pleural space

E. Reduced plasma oncotic pressure

What pathophysiology describes lung findings in a 55-year-old man with pleuritic chest pain?

Increased interstitial fluid movement due to bacterial invasion.

Increased interstitial fluid movement due to bacterial invasion, which typically occurs in conditions such as pneumonia. When bacteria infect the lung tissue, they trigger an inflammatory response that leads to increased vascular permeability. This allows fluid and immune cells to seep into the interstitial spaces of the lung, causing inflammation and edema. The pleuritic chest pain arises as a result of irritation of the pleura surrounding the lungs, which can occur when inflammatory mediators stimulate pain receptors in the pleura. Symptoms often include sharp chest pain that worsens with deep breathing or coughing, alongside respiratory symptoms like cough and shortness of breath.

A 19-year-old man was stabbed in the left side of his chest. His vital signs were BP 90/60 mmHg, HR 130/min, RR 25/min, and SpO2 95% on room air. He had muffled heart sounds and distended jugular veins. Upon inspiration, his blood pressure dropped to 75/55 mmHg. His extremities were cool and clammy. What is the best pathophysiology to describe the injury?

A. Disruption of the tracheobronchial wall resulting in escape of air into pleural cavity

B. Laceration of intercostal arteries causing blood accumulation in pleural space

C. Rapid blood accumulation within pericardial sac causing increase in intrapericardial pressure

D. Sheer-stress mechanism resulting in avulsion type injury to the heart

E. Traumatic ventricular wall aneurysm resulting in cardiac dysrhythmia

What mechanism explains the hemodynamic instability in a patient following stab wound to the chest?

Rapid blood accumulation within pericardial sac causing increase in intrapericardial pressure.

Rapid blood accumulation within the pericardial sac leading to increased intrapericardial pressure, a condition known as cardiac tamponade. This occurs when blood from a penetrating injury fills the pericardial space, which is normally only a few milliliters of fluid. As blood accumulates, the pressure surrounding the heart rises, inhibiting its ability to fill adequately during diastole. This results in compromised cardiac output and systemic blood flow, leading to hemodynamic instability characterized by hypotension, tachycardia, and potential shock. The heart is essentially squeezed by the pressure from the fluid or blood, and without immediate intervention, such as pericardiocentesis or surgery, the patient may quickly deteriorate.

3-year-old boy who was previously well presented with a two-day history of fever and progressive shortness of breath. The patient did not have suggestive event of choking.

On examination, he had drooling saliva, low-pitched inspiratory stridor with nasal flaring, suprasternal and intercostal retractions. It was also noted that the patient had slight hyperextension of the neck. His vital signs were BP 100/60 mmHg, HR 155/min, RR 48/min, SpO2 89% on room air, and T 39°C. Lungs auscultation revealed reduced breath sounds bilaterally.

Which of the following is the most likely pathophysiology of this patient’s conditions?

A. Congenital invagination of supraglottic structures during inspiration

B. Direct invasion of the epiglottic mucosal layer by microorganisms

C. Disruption of the recurrent laryngeal nerve impulses

D. Hyper functional laryngeal reflex associated with post-nasal drip

E. Increase secretion of antigen-specific immunoglobulin E molecules

What is the likely pathophysiology when a 3-year-old presents with stridor and drooling?

Direct invasion of the epiglottic mucosal layer by microorganisms.

Direct invasion of the epiglottic mucosal layer by microorganisms, commonly associated with infections such as epiglottitis. This condition is characterized by the inflammation of the epiglottis, which is located at the base of the tongue and acts as a flap to prevent food from entering the trachea during swallowing. The inflammation can be caused by various pathogens, most notably Haemophilus influenzae type b (Hib) but also by other bacteria and viruses. Inflammation and swelling of the epiglottis can lead to narrowing of the airway, resulting in stridor (a high-pitched wheezing sound during breathing) and drooling due to the child’s inability to swallow comfortably. This situation is often an emergency, as the swelling can progress rapidly, leading to respiratory distress and potential airway obstruction.

A 64-year-old man presented with multiple episodes of vomiting and watery diarrhoea for two days after consuming food from a hawker stall. He had no known medical illness. On examination, he was dehydrated and appeared lethargic. His abdomen was soft and non-tender. His vital signs were BP 80/50 mmHg, HR 130/min, RR 28/min, SpO2 98% on room air and T 37.5°C.

What is the most likely pathophysiology of the above condition?

A. Bacterial translocation

B. Disruption of intestinal mucus membrane

C. Enteric micro-perforation

D. Microvilli destruction

E. Mast cell activation causing histamine release

What accounts for vomiting and watery diarrhoea in a 64-year-old man post food consumption?

Disruption of intestinal mucus membrane.

Disruption of the intestinal mucous membrane can lead to gastrointestinal symptoms such as vomiting and watery diarrhea. This disruption can occur due to various factors including infections (viral or bacterial), inflammatory conditions (such as inflammatory bowel disease), or exposure to toxins. The intestinal mucosa plays a crucial role in digestion and nutrient absorption, as well as serving as a barrier to pathogens and harmful substances. When the mucous membrane is disrupted, it can result in increased permeability, allowing pathogens, toxins, and undigested food particles to enter the bloodstream, triggering an inflammatory response. This response can result in symptoms such as nausea, vomiting, and diarrhea as the body attempts to expel harmful substances. Additionally, disruption of the mucosal surface can hinder the absorption of fluids and electrolytes, leading to dehydration and electrolyte imbalances, which are especially concerning in older adults.

A 50-year-old chronic alcoholic presented with nausea, vomiting of blood, malaise, and right upper quadrant pain for 2 days. On examination, he was drowsy with BP 120/90 mmHg, HR 105/min, RR 24/min, T 37.8˚C and pain score 4. Abdominal examination revealed tender hepatomegaly, splenomegaly, and signs of chronic liver disease.

Which pathophysiology best described his illness?

A. Acetaldehyde causes liver injury

B. Elevated immunoglobulin M indicates acute disease

C. Immune recognition and activation of B lymphocytes

D. Low level of T lymphocytes

E. Spread by fecal contaminated water

What pathophysiological explanation applies to a 50-year-old man with chronic alcohol use presenting with abdominal pain?

Acetaldehyde causes liver injury.

Acetaldehyde causes liver injury due to its toxic effects as a byproduct of alcohol metabolism. When ethanol is consumed, it is primarily metabolized in the liver by an enzyme called alcohol dehydrogenase, which converts ethanol into acetaldehyde, a highly reactive and toxic compound. This acetaldehyde can cause direct damage to hepatocytes (liver cells) by forming adducts with proteins and lipids, disrupting cellular function and leading to oxidative stress. Prolonged exposure to acetaldehyde, alongside the contributions of other metabolic pathways and inflammatory processes, can result in liver conditions such as fatty liver (steatosis), alcoholic hepatitis, and eventually cirrhosis. Additionally, the accumulation of acetaldehyde induces an inflammatory response characterized by the activation of Kupffer cells (liver macrophages), which further exacerbates tissue injury and promotes fibrosis. Symptoms like abdominal pain may arise due to liver inflammation or distension as a result of these pathological changes.

A 35-year-old man presented with an acute onset of severe upper abdominal pain radiating to the back with bouts of vomiting after heavy alcohol consumption. On examination, he is afebrile, tachycardic, and appears dehydrated. Abdominal examination revealed epigastric tenderness. Murphy’s sign is negative. Laboratory investigation showed serum amylase of 1200 IU/L.

Which pathophysiological process best explains the above condition?

A. Abnormal lipoprotein metabolism

B. Direct toxic effect

C. Increased cholinergic stimulation

D. Increased synthesis of chymotrypsin enzymes

E. Reflux of bile into the duct

What process explains abdominal pain after heavy alcohol consumption in a 35-year-old man?

Direct toxic effect on pancreatic tissue.

The direct toxic effect on pancreatic tissue from heavy alcohol consumption can lead to a condition known as alcoholic pancreatitis. This process involves the damage of pancreatic cells by ethanol and its metabolites, which can result in inflammation and dysfunction of the pancreas. Ethanol disrupts the normal secretion and function of digestive enzymes, causing them to become activated within the pancreas rather than in the intestine, leading to pancreatic autodigestion. This activation can trigger an inflammatory response, resulting in acute abdominal pain that is often described as severe and can radiate to the back. The inflammation may cause swelling and blockage of the pancreatic ducts, which can lead to further complications such as necrosis, infection, and pseudocyst formation. Additionally, alcohol abuse can increase the permeability of pancreatic acinar cells and the release of pro-inflammatory cytokines, compounding the injury and related symptoms. Over time, repeated episodes of pancreatitis can lead to chronic pancreatitis, resulting in permanent damage and additional gastrointestinal issues

What is the likely pathophysiology for the severe abdominal pain in a 40-year-old woman?

Obstruction of appendiceal lumen.

What defines the likely pathophysiology in a case of testicular swelling and pain in a 30-year-old man?

Loss of arterial supply of the right testis.

What explains the foul-smelling vaginal discharge in a 28-year-old woman?

Ascending infection from cervix to endometrium.

What is the most likely cause of painless per rectal bleeding in a 45-year-old woman?

Engorgement of anal arteriovenous plexus.

What best describes the condition of a patient with generalized tonic-clonic seizure not resolved with medication?

Altered excitability between neuronal structures.

What is the primary pathophysiological issue that caused seizures in a 10-month-old infant with hypoglycemia?

Reduce brain substrate leading to abnormal firing of neurons.

What pathophysiological change leads to acidosis in an 8-year-old girl with severe dehydration?

Absolute insulin deficiency.

What explains lethargy and hyperpigmentation in a 45-year-old woman with diabetes?

Diminished adrenal gland function.

What causes reduced consciousness in a motor vehicle accident patient?

Increased intracranial pressure reduces cerebral perfusion.

What physiological response occurs in a pregnant woman post-trauma?

Partial or complete detachment of placenta.

What drug mechanism of action is most significant in anaphylactic shock treatment?

Increase vascular smooth muscle contraction.

What phases of pathophysiology contribute to acute cholecystitis?

I, II, III and IV.

What likely pathophysiology explains acid-base imbalances in a morbidly obese patient?

Desensitized CO2 chemoreceptors.

What is the pathophysiological basis of hypertensive urgency?

II, III and IV.

What mechanism explains muscle stiffness following antipsychotic use?

Blockade of dopamine D2 receptors at basal ganglia.

What antiarrhythmic action is important during broad complex tachycardia?

Inhibition of adenylyl cyclase activity.

What skin layers are affected in burns resulting from an explosion?

the epidermis, dermis papillary and reticular layer.

What response is triggered by cold peripheries in post-accident abdominal pain?

Prorenin conversion to renin.

In which conditions is lung compliance decreased?

II, III and IV.

What statement about medication for hypoglycemic patient is TRUE?

It stimulates insulin secretion depending on blood sugar level.

What occurs in primary blast injury leading to delayed abdominal presentations?

I, II and IV.