2808NRS : Human Pathophysiology and Pharmacology 2 A2 Written Assignment

Assessment Overview

This assessment is designed to develop your skills in critically analysing a patient case study. You will be expected to differentiate between normal and abnormal findings and identify evidence-based diagnostic investigations and treatment strategies. This assignment will help you integrate and apply your understanding of human pathophysiology and pharmacology through the creation of a single-page concept map and a 500-word written explanation.

This assessment will cover all the learning outcomes of the course.

Instructions

There are TWO parts to this task, both of which require interpretation and analysis of a case study.

Case Study

George Russell is a 72-year-old man with a history of type 2 diabetes mellitus, diagnosed 12 years ago. He was found at home in a confused and dehydrated state after not being seen for several days. Paramedics reported he was disoriented, minimally responsive, and had a dry mouth, sunken eyes, and poor skin turgor. His vital signs were: blood pressure 86/54 mmHg, heart rate 122 bpm and shallow breathing at a rate of 24/min. He had not urinated for more than 12 hours. George had no current diabetes medications in use, with his weekly medication pack untouched for two weeks. His home contained many empty sugary drink bottles and takeout containers, suggesting poor nutrition and hydration. His neighbour mentioned he became socially withdrawn after his wife died six months ago and stopped attending social activities. A finger-prick blood glucose reading was too high to register and he was diagnosed in hospital with Hyperosmolar Hyperglycaemic State (HHS), a serious complication of type 2 diabetes.

Part 1: Concept Map

• Develop a single-page, color-coded concept map (whatdoesagoodconceptmap assignmentlooklike?)

• Identify the three (3) patient risk factors (RF) from the case study and demonstrate how these link to the aetiology and/or pathophysiology of the diagnosed disease.

• Provide a step-by-step pathophysiological sequence that links the aetiology (cause) of the diagnosed disease (Hyperosmolar Hyperglycaemic State – HHS) to the five (5) clinical manifestations (CMs) described in the case study.

Group Clinical Manifestations by Body System

These CMs can be grouped by:

• Cardiovascular

• Metabolic/Endocrine

• Neurological

• Integumentary

• Renal

This will support a clear and logical flow from the underlying cause (the aetiology) to how it affects different parts of the body.

Each body system should show:

• How it is affected by the disease process

• What specific clinical sign or symptom results

Part 2: Written Explanation (500 words)

• Explain and justify two (2) evidence-based diagnostic investigations to confirm the diagnosis.

• Explain and justify (2) evidence-based approaches to treat and manage the patient's condition based on your analysis and interpretation of evidence-based research. One of these management approaches must be pharmacological.

• Use at least four scholarly references for the written explanation section.

Other Instructions

• Adhere strictly to the 500-word limit for your written explanation, including in-text citations and quotations. The reference list is not included in the word limit. The marker will stop marking once 500 words are reached.

• You do not need to include in-text references in Part 1 (concept map component).

• Submit Parts 1 and 2 as a single document – we recommend using PowerPoint to create your concept map, and for your written section (howdoIdothis?).

• We highly recommend saving and submitting your PowerPoint slides as a PDF single document to avoid unwanted reformatting when you submit your assignment via the submission portal.

• Use scholarly literature published within the last ten years (2015 - 2025 inclusive).

• Use APA7 referencing style, as per the Griffith Health Writing and Referencing Guidelines.

• You may use headings and subheadings to organise your written explanation; a formal introduction and conclusion are not required.

• Use academic language throughout; do not write in the first person.

• Refer to the marking rubric at the end of this document to understand the ‘weighting’ of each section.

What you must submit

• Two parts in one file (PDF recommended):

  • Part 1: Single-page, colour-coded concept map

    • Identify 3 patient risk factors (RFs) from the case study and link them to the aetiology/pathophysiology of Hyperosmolar Hyperglycaemic State (HHS).

    • Build a step-by-step pathophysiological chain from aetiology to 5 clinical manifestations (CMs) grouped by body systems (cardiovascular, metabolic/endocrine, neurological, integumentary, renal).

    • For each system: show how it’s affected and the specific sign/symptom.

  • Part 2: 500-word written explanation

    • Explain & justify two diagnostic investigations to confirm HHS.

    • Explain & justify two management approaches (one must be pharmacological), using evidence-based research.

    • Use ≥4 scholarly references (≤10 years).

Evidence, format, and submission

• Word limit: Strict 500 words for Part 2 (incl. in-text citations/quotes; reference list excluded). Marking stops at 500.

• Sources: Scholarly literature 2015–2025; APA 7 referencing.

• Style: Academic language; no first person; headings/subheadings allowed in Part 2; no in-text refs needed for the concept map.

• File & submission: Create in PowerPoint, export as single PDF, and submit to the A2 FINAL portal (use A2 DRAFT first to check originality).

• Learning focus: Differentiating normal vs abnormal findings, selecting diagnostics & treatments, integrating pathophysiology + pharmacology, and communicating reasoning visually and in writing.

Key Pointers to Cover

Concept Map 

• Risk factors (from the case):

  • Medication omission/poor glycaemic control: Weekly pack untouched; no diabetes meds in use.

  • Dehydration/poor intake: Dry mouth, sunken eyes, poor skin turgor; empty sugary drink bottles; no urine >12 h.

  • Psychosocial stressors/age: Bereavement, social withdrawal; older adult with T2DM (12 years).

• Pathophysiology chain (HHS):

  • Insulin deficiency + counter-regulatory hormone excess → marked hyperglycaemia → osmotic diuresis → profound free-water loss → hyperosmolality → cellular dehydration, especially CNS.

• CMs grouped by body system (link cause → effect):

  • Cardiovascular: Severe volume depletion → hypotension (BP 86/54), tachycardia (HR 122).

  • Metabolic/Endocrine: Extreme hyperglycaemia (too high to register) with minimal ketosis → hyperosmolar state.

  • Neurological: Confusion, minimal responsiveness from neuronal dehydration.

  • Integumentary: Dry mucosa, poor skin turgor from dehydration.

  • Renal: Oliguria/anuria (>12 h no urine) from prerenal azotaemia and reduced renal perfusion.

• Design tips: Use colour codes for RF → Pathway → System effects → CMs; arrows for flow; keep text concise.

Written Explanation 

• Diagnostics (choose any two, justify with evidence):

  1. Serum glucose & effective osmolality (2 × Na + glucose/18): Confirms marked hyperglycaemia and hyperosmolality (hallmarks of HHS) and correlates with mental status changes.

  2. Venous/arterial blood gas + serum/urine ketones: Differentiates HHS (minimal acidosis/ketosis) from DKA (metabolic acidosis, elevated β-hydroxybutyrate); guides insulin/fluid strategy.

  • (Supportive labs often cited: electrolytes (Na, K), urea/creatinine, serum osmolality, infection screen.)

• Management (two approaches; one pharmacologic):

  1. Aggressive IV fluid resuscitation (non-pharmacologic): Start 0.9% saline to restore intravascular volume, then adjust (e.g., 0.45% saline) based on corrected Na/osmolality; aim to gradually reduce osmolality to avoid cerebral oedema.

  2. Low-dose IV insulin infusion (pharmacologic): Initiate after initial fluids and once K⁺ ≥3.3 mmol/L; titrate to safely lower glucose while monitoring K⁺ and adding dextrose when glucose ~14 mmol/L to continue osmolality correction.

  • Integrate electrolyte replacement (esp. K⁺), frequent monitoring, and treat precipitating causes (e.g., infection, missed meds).

How the Academic Mentor Guided the Student 

Decode the brief and rubric

• Read the task line-by-line, highlighting deliverables, word limits, evidence rules, and submission format.

• Extract what each criterion assesses (conceptual accuracy, pathophysiological logic, evidence use, clarity).

Extract clinical data from the case

• Build a data table: signs, vitals, behaviours, meds, social context.

• Label RFs vs CMs and flag which body system each CM belongs to.

Map the pathophysiology

• Draft the aetiology → mechanism → system effect → sign/symptom chain for HHS.

• Validate with current guidelines/reviews and simplify to fit one page.

Design the concept map

• Choose a colour legend (RFs, pathways, systems, CMs).

• Use arrows and numbered steps to show causality; minimize text; ensure immediate readability.

Select diagnostics & treatments (evidence-based)

• Prioritise two diagnostics that confirm HHS vs DKA and guide therapy (osmolality, glucose, acid-base, ketones).

• Choose two treatments aligned with standards (fluids + insulin), with safety caveats (potassium thresholds, rate of osmolality correction).

Write the 500-word explanation

• Structure: 2–3 sentences context → Diagnostics (justification) → Management (justification) → 1 closing sentence.

• Insert ≥4 scholarly references (≤10 years), format APA 7, stay ≤500 words.

Quality checks and submission

• Cross-check against rubric; verify recency of sources; ensure no first person.

• Export PowerPoint → PDF, run draft submission for originality, then submit final to A2 FINAL.

Outcome Achieved

• Clear, visual concept map linking RFs to HHS mechanisms and to system-specific clinical signs.

• Concise, 500-word, evidence-based write-up explaining why chosen diagnostics confirm HHS and how the selected treatments mitigate pathophysiological derangements.

• File meets formatting, evidence, word limit, and submission requirements.

Learning Objectives Covered

• Clinical reasoning: Differentiated normal vs abnormal findings; mapped cause-effect pathways for HHS.

• Integration of pathophysiology & pharmacology: Explained fluid shifts, hyperosmolality, insulin action, and electrolyte management.

• Evidence-based practice: Selected and justified diagnostics and treatments using recent scholarly literature.

• Professional communication: Conveyed complex mechanisms in a one-page concept map and a precise academic paragraph with APA 7 compliance.

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