1. Consider the haematemesis that Maria has been experiencing.
1. Consider the haematemesis that Maria has been experiencing.
Consider Marias history and other data and then; a) Explain her presentation by describing the physiological and pathophysiological mechanisms involved. In your answer, i) identify in brackets () the data or observations from the case scenario that support your explanations. ii) identify any other data or observations that have a similar aetiology to the observation you are explaining. Word limit: 200. Referencing required - AMA(Vancouver) style.
Maria is likely experiencing ruptured oesophageal varices secondary to acute decompensated liver sclerosis due to a history of excessive drinking, exacerbated by heavy smoking.
Pancytopenia due to bone marrow dysfunction from long term alcoholism and low red cell blood count because of acute bleed.
Serum protein
Markers of cirrhosis:
Increased INR (1.8)
Prolonged activated partial thromboplastin time (aPTT)
Hypalbuminaemia 23g/L
Thrombocytopaenia low platelet count 75x109/L
AST/ALT ratio > 1
Long term alcoholism and heavy smoking liver cirrhosis (reduced synthetic function of liver i.e. albumin and INR, caput medusa, abdominal ultrasonogram findings)
Portal hypertension.
Oesophageal varices (endoscopy findings).
Ruptured oesophageal varices and hence haematemesis.
Pancytopenia due to bone marrow dysfunction from long term alcoholism.
Red blood cell low because of acute bleed.
Serum protein usually from poor diet associated with alcoholism.
Ammonia goes up due to reduced hepatic clearance.
Blood urea nitrogen (BUN) goes up in acute upper GI bleed.
Creatinine is raised likely due to acute kidney injury (AKI) secondary to acute bleed and pre-renal injury, could also be due to other comorbidities associated with alcoholism such as hypertension which is exacerbated by smoking.
Hyponatraemia: beer potomania is a syndrome used to describe patients who present with hyponatremia along with a history of excessive beer drinking these patients are at serious risk of rapid decompensation secondary to hyponatremia and its neurological sequelae.
Chronic hepatitis C positive also pre-disposes to further sequalae of alcohol and hepatocellular carcinoma.
Chronic hepatitis C likely contracted from her tattoos in home country.
Hepatocellular carcinoma is the most common type of primary liver cancer. Hepatocellular carcinoma occurs most often in people with chronic liver diseases, such as cirrhosis caused by hepatitis B or hepatitis C infection.
Signs and symptoms of oesophageal varices:
Vomiting blood (coffee ground) a slow blood leak may show up as dried, coagulated blood aka coffee ground, whereas a ruptured vein will produce fresh, red blood in the vomit.
Jaundice of the skin and eyes yellow tinge to skin and jaundice in sclera suggests liver disease/ portal hypertension.
Ascites positive fluid intake indicates ascites in the patient suggestive of portal hypertension.
Oedema in legs and feet.
Upper abdominal pain
Confusion/ disorientation hepatic encephalopathy loss of brain function when damaged liver does not remove toxins from the blood.
Signs of shock:
Low blood pressure: 100/70mmHg
Tachycardia
Tachypnoea: 24bpm
2. Peters jugular vein is distended and pulsating. Explain Peters presentation by describing the physiological and pathophysiological mechanisms involved. In your answer, i) identify in brackets () the data or observations from the case scenario that support your explanations. ii) identify any other data or observations that have a similar aetiology to the observation you are explaining.
Word limit: 200. Referencing required - AMA(Vancouver) style.
Obstruction in upper airway
Acute pulmonary oedema
Bronchospasm
Peripheral oedema
Heart failure:
Dyspnoea shortness of breath and difficulty breathing
Fatigue, tired, exhaustion
Fluid retention and oedema
Jugular veinous pressure (JVP):
Jugular vein distention
JVD occurs when there is a backup of blood in the superior vena cava or heart itself, where slowed blood flow in the heart of superior vena cava can cause blood to back up into the jugular veins, increasing jugular venous pressure and causing it to bulge outward.
