Reference no: EM133117400 , Length: word count:1500

NURS90153 Human Anatomy and Physiology - University of Melbourne

Case Study One: Monty

Monty is a 34-year-old male with a history of immune deficiency diagnosed in early childhood and on lifelong intravenous immunoglobulin (IVIg) therapy. Monty also suffers from chronic sinusitis and is treated with clarithromycin prophylactically. He lives with his partner James and their cat Theo.

Monty complained of feeling ill reporting fatigue, muscle aches and pains, headaches, and feverish. His partner was concerned so they went to their local Emergency Department.

In the Emergency Department, Monty was febrile (38.9ºC), Blood pressure was 130/ 80mmhg, Pulse post 90bpm Respiration 20 bpm. He denied having any vision changes, abdominal pain, vomiting, urinary or bowel changes. He also had swollen lymph nodes around the neck.

Monty's initial laboratory evaluation was within normal limits, with the exception of an elevated white blood cell (WBC) count of 12,800 cells/ and C-reactive protein (CRP) of 20 mg/L.

Magnetic resonance imaging (MRI) of the brain showed innumerable enhancing lesions scattered throughout the cerebral and cerebellar hemispheres, with involvement of the cortex, subcortical and periventricular white matter, bilateral basal ganglia, thalami and brainstem, with target and nodular enhancement.

Lumbar puncture and cerebrospinal fluid analysis for Toxoplasma revealed 2,600 copies/mL. Serologies were negative for HIV, Epstein-Barr virus, hepatitis B and hepatitis C. T. gondii IgG was positive (145 IU/mL: normal 0.0-7.1 IU/mL). T. gondii IgM was normal.Monty has been diagnosed with cerebral toxoplasmosis.

He was commenced on Clindamycin (an antibiotic). During his course of treatment, Monty had two episodes of tonic-clonic seizures within one hour and then became unresponsive. A head CT revealed a large, left thalamic, intraparenchymal haemorrhage with intraventricular extension causing obstructive hydrocephalus.

Question a) Describe and rationalise how and why Monty has developed cerebral toxoplasmosis
(approx. 250 words)

Question b) Explain the physiology behind why Monty has developed seizures and is now unresponsive.
(approx. 250 words)

Question c) Explain why Monty has swollen lymph nodes and what are their usual functionof the lymph nodes, rationalise why they are swollen

Case Study Two: Lynn

Mrs Lynn Murdoch is a 58-year-old admitted into hospital with cellulitis to her left lower leg. Lynn has a history of hypertension, has a BMI of 35, type 2 diabetes mellitus, a sedentary lifestyle, and a family history of cardiovascular disease (mother died young from AMI).
On day 3 of her admission, Lynn rings the call bell complaining of chest discomfortpain is radiatingbetween her scapula. On your initial assessment, Lynn looks pale and diaphoretic and does not look like her normal bright cheery self.

As her nurse, you undertake a patient assessment including vital signs:
• Heart rate 98 bpmand irregular
• BP (MAP) 145/86 mmHg (105)
• RR 26 pm
• SpO2 (%) 95% on FiO2 0.21
• Temperature 37.6 ºC
• Pain score 6/10.
Her ECG indicates ST elevation in leads II, III, aVF indicative of a right coronary artery occlusion and thus is called an inferior STEMI (ST Elevated Myocardial Ischemia).

Question a) Identify and describe the area and structures of the heart that is vascularised by the right coronary artery. Include in your answer the implications of the disruption of blood supply from the right coronary artery to this area.
(approx.250 words)

Question b) Explain and rationalise Lynn's symptoms that relate to the acute condition
(approx.250 words)

Question c) Lynn has a diagnosis of type 2 diabetes. Identify the organ that is malfunctioning and give an explanation as to why this is occurring, include in your answer a brief outline of the two other organs that are affected with type2 diabetes and why they are affected.