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Concept Map instructions
The purpose of this assignment is to create a graduate-level concept map of a condition you will see as an APRN in your practice. A concept map is a diagram or visual outline detailing pathophysiological concepts and the cellular-level significance of a selected disease. This allows you to explore the physiology of a condition in-depth and the resulting changes in normal pathology and physical exam findings.
Instructions
In Week 1 you selected a pathophysiologic condition and were required to obtain faculty approval. To complete this project, create a concept map (Word document or PDF) illustrating the nature of the disease. Be sure to include:
1. The etiology (risk factors) and common causes of the pathological condition.
2. The prevalence of the disease (statistics), including worldwide distribution.
3. The severity of the disease (morbidity, mortality).
4. Physical exam findings associated with the condition. Be specific on how each exam finding is created by the pathological changes by using your arrow connections.
5. Common laboratory or diagnostic abnormalities associated with the condition. Be specific and show how each laboratory abnormality is created by the pathological condition and what you would expect to see as the APRN. It is not enough to say “low hemoglobin,” for example. Start thinking like an APRN and use actual values (Hgb <8.0 mg/dl, SaO2 <90%, CXR with bilateral lower lobe infiltrates, etc.). Link these findings to your physical exam findings and the cellular changes that lead to them using your arrow connections.
6. The pathophysiology of the disease to the cellular level. This is different from etiology. Rather, this is what changes happen at the cellular level in this specific disease process. Start broad and work to the most specific as you move outward or downward. For example: Trunk of tree → branches of tree → stems on branches → leaves on stems.
7. A brief discussion of treatment and management of the chosen disease process.
8. Demonstrate (with arrows) the interconnections of all of these items. It is okay if this makes it look messy, as long as the boxes remain readable. Remember, this map should be comprehensive, as it demonstrates your critical thinking into how things are related.
9. You must cite all concepts within your map using APA 7th edition in-text citations and provide a separate reference list in a Word document that follows APA 7th edition professional format. A minimum of two scholarly references are required; there is no maximum. You may use as many scholarly resources as needed to provide a comprehensive map. Sources that are not accepted include Medscape, WebMD, Wikipedia, Healthline, and so forth. Your sources must be scholarly—think journals, textbooks, UpToDate, PubMed, NIH.gov, and so on.
In the past, students have used MindMup, Miro, and MindMeister as mapping software for this project. There is no need to pay for anything. You can work to completion on the map, then take a screenshot if the software doesn’t allow free download. You can also use Word or PowerPoint and create your own map using boxes or a template. (You can Google “free concept map template” for Word or PowerPoint and use a created template.) You can also submit a handwritten version as long as it is readable. Regardless of the format, please be sure that the faculty can easily zoom in and read the text in your boxes and that all of the map fits on your viewable page.
Please note that use of AI is prohibited on this assignment. If AI use is suspected, student will receive a zero on this assignment and be reported to the Office of Academic Integrity. Use of your or another student's previous map constitutes plagiarism/cheating and will be handled in the same manner. Concept Maps will be put through TurnItIn for faculty review.
Concept Map Student Examples
Below are examples of concept maps created by students who earned an A on this assignment. Your map does not need to look exactly like these, but they should give you an approximate idea of the level of detail and complexity your map should contain. Keep in mind that some conditions will be more detailed than others due to the nature of the pathophysiology of that disease. In some of these examples the connecting arrows may have been removed for clearer visualization of the boxes but were present when the student submitted their map along with a reference page.
Rubric is linked below
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Concept Map Rubric |
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Concept Map Rubric |
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Criteria |
Ratings |
Pts |
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Comprehensiveness and Completeness of Concept Map Concept map includes (with graduate-level detail): 1. Etiology/risk factors/causes of chosen disease, 2. Physical exam findings, 3. Laboratory and diagnostic findings with expected values/data, 4. Pathophysiologic changes to the cellular level, 5. Morbidity/mortality, 6. Prevalence (statistics), and 7. Brief discussion of treatment/management. |
70 to >65 pts Exemplary Fully answers all the focus questions presented in the assignment instructions with scholarly graduate-level rigor and comprehensiveness. 65 to >50 pts Satisfactory Adequately addresses questions presented in the assignment instructions but missing detail or comprehensiveness in some areas. 50 to >0 pts Unsatisfactory Inadequately addresses questions presented in the assignment instructions or is not comprehensive or graduate-level work. |
/ 70 pts |
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Critical Thinking Connections (arrows) are present between concepts (explaining the why). Complexity of the map should be high and at the graduate level. |
20 to >16 pts Exemplary Demonstrates logical, thorough, and accurate interconnections of disease pathology. 16 to >10 pts Satisfactory Demonstrates some logical, thorough, and accurate interconnections of disease pathology but missing connections between some concepts. 10 to >0 pts Unsatisfactory Does not demonstrate logical, thorough, and accurate interconnections of disease pathology. |
/ 20 pts |
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Professionalism/Format Format of concept map is clear/readable. In-text citations are cited correctly in map and reference page included following APA 7th edition format. Two scholarly references are provided. |
10 to >7 pts Exemplary Format is clear and readable and flows logically (can follow it easily). Fully supports conclusions using in-text APA citations. Reference page provided and follows APA 7th edition format. Two scholarly references used. 7 to >5 pts Satisfactory Provides some support for conclusions but minor issues with APA format, grammar, professional appearance, or flow. All references may not be scholarly sources. 5 to >0 pts Unsatisfactory Does not provide support for conclusions using in-text citations, or significant issues with APA format, grammar, or professionalism. Map unreadable or unable to be downloaded/viewed. References and/or reference page missing. |
/ 10 pts |
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Total Points: 0 |
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Iron Deficiency Anemia (IDA)
Etiology (Risk Factors)
Clinical Manifestations (Physical Exam
Findings)
Prevalence
Severity (Morbidity & Mortality)
Labs & Diagnostics
Pathophysiology
Treatment
Most common nutritional disorder worldwide (affects
10-20% of the population) (McCance &
Huether, 2023)
Living in poverty & developing countries (McCance & Huether,
2023)
Increased requirements during pregnancy & excessive menstrual
bleeding (McCance & Huether, 2023)
Progression causes more severe structural & functional
changes in epithelial tissue (McCance & Huether, 2023)
Early symptoms: shortness of breath, weakness, fatigue, & pallor of mucous membranes, skin, & palm
creases (pale earlobes, palms, & conjunctivae) (McCance & Huether, 2023)
Dietary deficiency (McCance & Huether, 2023)
Impaired iron absorption (McCance & Huether, 2023)
Chronic blood loss (McCance & Huether, 2023)
Increased iron requirements (McCance &
Huether, 2023)
Chronic diarrhea (McCance & Huether, 2023)
Premenopausal females; adolescents & women of
childbearing age (McCance & Huether, 2023)
Infants, children, & adolescents (McCance & Huether, 2023)
IDA secondary to bleeding from GI diseases (i.e. duodenal or gastric ulcers, hiatal hernias, esophageal
varices, hemorrhoids, cirrhosis, cancer, or IBS) (McCance &
Huether, 2023)
Surgical procedures & trauma (McCance & Huether, 2023)
Parasite infestations (McCance & Huether, 2023)
H. pylori infections impair uptake of iron (McCance & Huether, 2023)
Children exposed to unsafe toxins in resource-poor conditions (i.e. exposure to & absorption of lead
prevents addition of iron to heme molecules), contributing to IDA (McCance & Huether, 2023)
A hypochromic-microcytic (small erythrocytes & low hemoglobin
concentration) anemia caused by iron store depletion (McCance &
Huether, 2023)
Depleted iron stores do not meet hemoglobin production needs as a
result of excess blood loss & inadequate dietary
intake (McCance & Huether, 2023)
Iron deprivation for erythrocytes & other tissues (McCance & Huether, 2023)
Inadequate iron (Fe) delivery to meet body's needs in cases with sufficient iron stores (McCance &
Huether, 2023)
Inability to maintain heme synthesis produces relative or
functional iron deficiency (McCance & Huether, 2023)
Systemic iron balance regulated by hepcidin peptide. Hepcidin inhibits iron
transfer to plasma through binding with feroportin, endocytosis, & degradation
(McCance & Huether, 2023)
Iron is contained in hemoglobin & stored for
future hemoglobin synthesis (McCance & Huether, 2023)
Stage I: Decreased iron stores in bone marrow
(serum iron & hemoglobin remain normal) (McCance &
Huether, 2023)
Stage II: Iron-deficient erythropoiesis occurs,
due to diminished transportation of iron
to bone marrow (McCance & Huether,
2023)
Stage III: Hemoglobin-deficient cells enter circulation to replace normal erythrocytes that have
been removed due to aging (McCance & Huether, 2023)
A decrease in hepcidin related to the immune response to infection is possible, causing hypoferremia
(lack of iron in blood), which hinders the growth of pathogens that require iron for survival. However,
adequate iron is also required for the innate immune response to function appropriately (McCance &
Huether, 2023)
Consumption of cow's milk decreases bioavailability of iron in
infants & toddlers (McCance & Huether, 2023)
Restricted diets ingested by older adults (McCance & Huether, 2023)
Eating disorders (over- & underweight) (McCance &
Huether, 2023)
Gradual onset of symptoms (medical attention usually sought when hemoglobin
level is around 7-8g/dL) (McCance & Huether, 2023)
Koilonychia (spoon-shaped, brittle fingernails) due to impaired ciliary
circulation (McCance & Huether, 2023)
Cheilosis (fissures/scales of the mouth) (McCance & Huether, 2023)
Stomatis (inflammation of mouth) (McCance & Huether, 2023)
Glossitis (painful ulcers of buccal mucosa & burning tongue) (McCance &
Huether, 2023)
Dysphagia (difficulty swallowing) (McCance & Huether, 2023)
Worsened by hyposalivation (McCance & Huether, 2023)
Other symptoms include gastritis, headache,
neuromuscular changes, numbness, tingling, irritability,
& vasomotor disturbances (McCance & Huether, 2023)
Gait alterations are rare (McCance & Huether, 2023)
Complications
Lab tests (McCance & Huether, 2023)
Decreased hemoglobin & hematocrit (<7-8 start to see symptoms) (McCance & Huether, 2023)
Microcytic (low MCV) & hypochromic (low MCHC) erythrocytes found in blood (McCance & Huether, 2023)
Symptom evaluation (McCance & Huether, 2023)
Decreased serum iron, ferritin, & transferritin saturation levels
(McCance & Huether, 2023)
Sensitive indicator of heme synthesis: Amount of free erythrocyte
protoporphyrin (FEP) in erythrocytes (McCance & Huether, 2023)
Identify & eliminate source(s) of blood loss
(McCance & Huether, 2023)
Oral iron replacement therapy (McCance &
Huether, 2023)
Parenteral (IV) iron replacement therapy
(McCance & Huether, 2023)
Hematocrit levels should improve within 1-2 months with oral iron replacement therapy
(McCance & Huether, 2023)
More precise measurement of improvement: Serum ferritin (SF) levels
(McCance & Huether, 2023) A rapid decline in symptoms
(fatigue, weakness, etc) usually seen within first month of therapy
(McCance & Huether, 2023)
Menstruating women may need daily oral iron until menopause
(McCance & Huether, 2023)
Fat absorption disorders (McCance & Huether, 2023)
Celiac disease (McCance & Huether, 2023)
Bariatric surgery & surgeries that decrease stomach acidity (McCance & Huether, 2023)
Menstruation, especially in adolescent girls (Lee, 2020)
Estimated 30-50% of global population has
IDA (Lee, 2020)
IDA prevalence was 0.7% for men & 8.0% for women in a
2014 Korean domestic report survey (Lee, 2020)
Poor diets in teenagers (i.e. junk foods) (McCance & Huether, 2023)
Period of rapid growth – nutrition/adequate intake of iron is crucial (Lee, 2020)
Period of active growth – increased need for quality
nutrition (Lee, 2020)
Weight loss is influenced by social/peer pressures,
especially in adolescent girls who already have
increased iron loss from menstruation (Lee, 2020)
Low birth weight & prematurity (Lee, 2020)
Strict vegan & vegetarian diets (iron not absorbed as well as it is from meat, fish, & poultry) (Lee,
2020)
Regular blood donation (Lee, 2020)
Certain medications (Lee, 2020)
Genetics (Kumar et al., 2022)
Blood loss should be evaluated for an occult source if IDA is
otherwise unexplained (McCance & Huether, 2023)
Occult blood test (McCance & Huether, 2023)
PPIs interfere with absorption of iron & NSAIDs increase risk of blood loss
(Lee, 2020)
Replenish iron deficiency & iron stores (Lee, 2020)
Higher cost for IV iron than oral iron therapy, but decreased number of
hospital/outpatient visits (Lee, 2020)
Hepcidin is affected by inflammation &
iron metabolism (Lee, 2020)
Chronic inflammatory conditions (Lee, 2020)
Normal hemoglobin (Hb) concentrations
(Bathla & Arora, 2021)
Adult males: Hb > 13g/dL; Adult females: Hb > 12 g/dL (Bathla &
Arora, 2021)
Children 9-24 months: Hb 105-135g/ L; Children 2-16 years: Hb 115-150 g/
L (Mattiello et al., 2020)
More adolescents in India (10-20%) diagnosed with
IDA than in other countries as a result of insuffiecent
dietary intake of iron (Kumar et al., 2022)
Inherited hemoglobinopathies (Kumar et al., 2022); Family history of
iron-refractory IDA (Lee, 2020)
Maternal deaths are 3x higher in women with
IDA (Kumar et al., 2022)
Vegetarians have a greater lack of bioavailable heme iron
in their diets (Kumar et al., 2022)
33% of adults in South Asia compared to 2.4%
in the US population (Kumar et al., 2022)
The Centers for Disease Control & Prevention (CDC) recommends
screening nonpregnant females for anemia every 5-10 years by
measurement of hemoglobin level (Weyand et al., 2023)
Low iron is associated with an increased all-
cause rate of mortality (Weyand et al., 2023)
Screenings & iron supplements improve
risk of developing anemia (Weyand et al.,
2023)
Food insecurity (Weyand et al., 2023)
More non-white race & hispanic ethnicity affected (Weyand et al.,
2023)
In developing & developed countries, IDA is more prevalent in women &
children, but men are also susceptible (Bathla & Arora, 2021)
IDA affects 20-25% of pre-school aged
children (< 5 years) worldwide, with the
highest prevelance in Africa & South Asia (Gedfie et al., 2022)
6,021 deaths in the United States (1.8
deaths per 100,000 population) (CDC, 2024)
With low iron stores, iron is used for hemoglobin synthesis, leaving the brain & other organs/tissues
at risk for adverse effects (i.e. decreased perfusion/oxygenation)
(Jefferds et al., 2022)
Minority groups with low incomes/SES (Jefferds et al., 2022)
i.e. Obesity, CHF, CKD, & IBS (Kumar et al., 2022)
IDA is common & a "major cause of
morbidity worldwide" (Snook et
al., 2021)
Treatment goals: Restore hemoglobin level/iron stores,
improve functioning & quality of life (Snook et al., 2021)
Consider blood transfusion (Snook et al., 2021)
Treatment not effective? Investigate
further; change regimen for persistent or recurrent IDA with
unknown or irreversible cause (Snook et al.,
2021)
Take doses on an empty stomach to help absorption (Snook et al., 2021)
Additional testing may be warranted to identify
cause of IDA (ASH, n.d.)
Look for GI tract abnormalities (i.e. endoscopy, capsule enteroscopy,
etc) (ASH, n.d.)
Test urine for blood/hemoglobin (ASH, n.d.)
Gynecologic evaluation (i.e. pelvic ultrasound, uterine biopsy) (ASH,
n.d.)
Dietary counseling/Increase dietary intake of iron (ASH,
n.d.)
Iron-rich foods (i.e. meat, poultry, fish, leafy greens, legumes,& iron- enriched grains/pastas) (ASH, n.d.)
Help diagnose IDA severity & determine treatment plan (McCance & Huether, 2023)
Choice for poor adherence/ intolerance of oral iron
replacement, uncontrolled chronic blood loss, or intestinal
malabsorption (McCance & Huether, 2023)
Most asymptomatic (Lee, 2020)
Iron supplements (McCance & Huether, 2023)
See irregularly shaped erythrocytes (McCance & Huether, 2023)
IDA symptoms occur at stage III as a result of iron store depletion, reduced hemoglobin
production, & reduced oxygen carrying capacity to body tissues (McCance &
Huether, 2023)
Results in reduced hemoglobin synthesis (McCance & Huether,
2023)
Poor exercise tolerance & increased heart rate
(Warner & Kamran, 2023)
Overall US prevalence among females aged 12-21 years old: 6.3% (Weyand et al., 2023)
Due to blood loss with menstruation, the rate of IDA in
women of childbearing age is 10% in the US (Warner & Kamran,
2023)
IDA in children: cognitive impairments (might be long-lasting & irreversible)
(McCance & Huether, 2023)
Increased risk of infection (Warner & Kamran, 2023)
Pregnancy complications (Warner & Kamran, 2023)
Heart conditions (Warner & Kamran, 2023)
Depression (Warner & Kamran, 2023)
Low birth weight, premature delivery, &
maternal mortality (Warner & Kamran, 2023)
Can lead to death from underlying heart or
lunch disorders (Warner & Kamran, 2023)
US mortality rates with IDA as the cause of
death grew from ~0.04 in 1999 to ~0.08 in 2018 per 100,000 people (Sun
& Weaver, 2021)
Higher bioavilability fron breast milk than cow's milk (McCance & Huether, 2023)
SF levels < 12 mcg/L in children under 5 years old, & <15 mcg/L in individuals over 5 (Mattiello
et al., 2020)
,
Addison's Disease
Pathophysiology
Adrenal cortex is under the control of two
different regulatory circuits: HPA axis and
the renin-angiotensin- aldosterone system
(RAAS) (Hahner et al., 2021).
Circadian and stress inputs converge on the
hypothalamus's paraventricular nucleus
(PVN), inducing the release of corticotropin-
releasing hormone (CRH) and arginine
vasopressin (Hahner et al., 2021).
CRH stimulates adrenocorticotropic
hormone ACTH release, inducing secretion of
corticosteroids, mainly cortisol, but also
dehydroepiandrosterone (DHEA) and aldosterone
(Hahner et al., 2021). The HPA axis is
regulated by cortisol via feedback regulation in the hypothalamus and pituitary (Hahner et al.,
2021). Glucocorticoid
deficiency leads to a loss of the negative
feedback of cortisol on the hypothalamus and pituitary, resulting in
increased CRH and ACTH levels (Hahner et
al., 2021). Decreased aldosterone
secretion results in increased renin (>4.1ng/ mL/hr) release from the kidney (Gomella, 2022;
Hahner et al, 2021).
Autoimmune destruction of
adrenocortical tissue is caused by
autoantibodies, most frequently autoantigen, 21-hydroxylase (Hahner
et al., 2021).
Circulating CD4+ and CD8+ T cells with
autoreactivity against 21-hydroxylase, and
with contributions from dendritic cells and
macrophages, mediates destruction of the
adrenal cortex (Hahner et al., 2021).
Activation of B cells in local draining lymph
nodes leads to the production of
autoantibodies against the enzyme 21
hydroxylase (Hahner et al., 2021).
Circulating CD4+ and CD8+ T cells targeting
21-hydroxylase- expressing
corticotrophs mediate the destruction of the
adrenal cortex (Hahner et al., 2021).
Environmental factors not known, but viruses
might be involved (Hahner et al., 2021).
Addison's disease is associated with major
histocompatibility complex (MCH)
genotypes such as DR3- DQ2 and DrR4-DQ8. Variants in CTLA4, PTPN22, CIITA, and
CLEC16A (Hahner et al., 2021).
The heritability of Addison disease is high
(Hahner et al., 2021).
Lack of aldosterone leads to loss of sodium
in the body, with decreased intravascular
fluid volume and hypotension (Hahner et
al., 2021).
Loss of negative feedback by cortisol results in increased