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1. Choose a disease + 6 terms Disease: Hypertension 1. Etiology The cause of hypertension is often unknown (primary), but can be related to genetics, diet (high sodium), and lifestyle. 2. Pathogenesis Hypertension develops due to increased peripheral resistance and/or increased cardiac output, leading to sustained high blood pressure. 3. Risk factors Factors such as obesity, smoking, stress, and family history increase the likelihood of developing hypertension. 4. Signs Objective findings include elevated blood pressure readings (e.g., >130/80 mmHg). 5. Symptoms Often none, but may include headaches, dizziness, or vision changes. 6. Complications Long-term hypertension can lead to stroke, heart failure, and kidney damage. 2. Definitions + Examples a. Etiology Cause of a disease Example: Smoking is the etiology of many lung diseases. b. Incidence Number of new cases in a population over a specific time Example: The incidence of influenza increases during winter months. c. Precipitating factor
A condition that triggers the onset of a disease Example: Stress can be a precipitating factor for a heart attack. d. Complication A secondary problem that develops due to a disease Example: Diabetes can lead to neuropathy as a complication. e. Prognosis Expected outcome of a disease Example: Early-stage cancer has a better prognosis than late-stage cancer. f. Iatrogenic A condition caused by medical treatment Example: Infection after surgery is an iatrogenic complication. g. Sequelae Long-term effects after a disease or injury Example: Paralysis after a stroke is a sequela.
3. Metaplasia vs Malignant Neoplasm Metaplasia Reversible change where one cell type is replaced by another Usually due to chronic irritation Not cancer Example: Smoking causing respiratory cells to change type Malignant Neoplasm Cancerous growth
6. Preventive Practices Hand hygiene Vaccination Healthy diet Regular exercise Avoid smoking and alcohol Routine health screenings Stress management 7. Case Study (CJ) Match each term: Diagnosis: malignant breast tumor Medical history: high blood pressure, family history of breast cancer Etiology: genetic predisposition (mother and aunt had breast cancer) Prognosis: depends on stage and response to treatment
Benign neoplasm: not present in this case
Iatrogenic: possible complications from surgery or medications Signs: breast lump Complication: possible spread of cancer or surgical complications Treatment: surgery to remove tumor Cancer: malignant breast tumor Examination of living tissue: biopsy
1. Locations of fluids Intracellular fluid (ICF): inside cells Extracellular fluid (ECF): outside cells o Interstitial fluid (between cells)
o Intravascular fluid (blood plasma)
2. Which is higher? 👉 Intracellular fluid (ICF) Makes up about **2/3 of body fluid
- Fluid changes with age** Infants → more body water Elderly → less body water 👉 Older adults → higher risk for dehydration 4. Why dehydration affects cells Less fluid = poor nutrient and oxygen delivery Waste removal decreases Cells shrink → impaired function 5. Function of sodium (Na ⁺ ) Controls water balance Maintains ECF volume Important for nerve impulses and muscle function 👉 Sodium = “water follows sodium” 6. Hypernatremia effects ↑ sodium in ECF → pulls water out of cells 👉 Results: ECF volume increases ICF volume decreases (cells shrink)
↓ chloride → ↑ bicarbonate 👉 Leads to metabolic alkalosis
12. Normal pH ranges Blood: 7.35 – 7. Urine: 4.5 – 8. 13. Slow, shallow respirations a. PCO₂ Increases (CO₂ retained) b. Serum pH Decreases → respiratory acidosis 14. Causes of metabolic acidosis Diarrhea Diabetic ketoacidosis (DKA) Renal failure 15. Ketoacidosis (DKA) a. Effect on bicarbonate & pH ↓ bicarbonate (buffer used up) ↓ pH → acidosis b. Compensation Lungs try to remove CO₂ Kidneys excrete acid (if able)
c. Signs of compensation Rapid, deep breathing ( Kussmaul respirations )
16. Purpose of Kussmaul respirations Blow off CO₂ Help raise pH (reduce acidosis) 17. Unconscious diabetic (DKA) a. Serum pH 👉 Low (acidic) Reason: buildup of ketoacids b. Serum potassium 👉 High (hyperkalemia) Potassium shifts out of cells during acidosis 18. Effect of insulin on potassium 👉 Lowers potassium levels Moves potassium **into cells
- Dehydration effects (DKA)** Tachycardia (fast heart rate) **Weak, thready pulse
- Cool-down after exercise** Helps maintain circulation Removes lactic acid gradually
Brings WBCs to infection site Destroys pathogens Removes damaged tissue Begins healing process
3. Warmth & fever a. Warmth Caused by vasodilation Increased blood flow brings immune cells a. Fever Caused by pyrogens Helps: o Kill bacteria o Increase immune response b. Systemic signs Fever Fatigue ↑ WBC (leukocytosis) 4. Why lab values are limited Show inflammation is present BUT do NOT identify: o Exact cause o Location o Specific organism
5. Inflammation vs infection a. Why inflammation → infection risk Tissue damage = easier for microbes to enter Fluid buildup = poor circulation b. Classify: Sunburn → inflammation Rash under tape → inflammation Common cold → infection (viral) Red eye + pus → **infection
- Peritoneal fluid** Normal: clear, minimal fluid Abnormal: thick, yellow fluid = **pus (infection)
- Fluid shift effects** Blood volume ↓ Hematocrit ↑ (more concentrated blood) 8. Joint movement impaired Swelling + pain Pressure in joint 👉 Limits movement 9. Fever mechanisms Vasoconstriction (retain heat)
14. Effects of scar tissue a. Small intestine ↓ absorption Possible obstruction b. Brain Loss of function Permanent damage c. Cornea Vision impairment (opacity) d. Mouth Reduced flexibility Difficulty speaking/eating e. Lungs ↓ gas exchange ↓ elasticity Reduced oxygenation **🚨 BURNS
- Pain & redness a.** Nerve endings stimulated → pain Vasodilation → redness
b. Low protein after burn Protein loss through damaged skin Increased metabolism Poor nutrition intake
16. Chemical burn a. Immediate removal stops chemical damage 👉 prevents deeper tissue injury b. Healing factors Good blood supply Proper wound care Adequate nutrition No infection 17. Complications of major burn Infection (loss of skin barrier) Fluid loss → shock Electrolyte imbalance 18. Facial burn complications Difficulty breathing (airway damage) Vision problems Speech/eating difficulties
a. Bone marrow damage ↓ WBC production 👉 Less ability to fight infection b. Circulatory impairment ↓ blood flow 👉 ↓ oxygen, nutrients, immune cells c. Puncture wound Breaks skin barrier 👉 Direct entry for microorganisms
3. Benefits of resident flora Prevent growth of harmful bacteria (competition) Help maintain normal body function (ex: vitamin production in gut) 4. Infection vs inflammation Infection = invasion by microorganisms Inflammation = body’s response to injury or infection 👉 You can have inflammation WITHOUT infection 5. Reduce respiratory infection transmission Hand hygiene Wearing masks Covering cough/sneezing Avoid close contact 6. Explanations
a. Why no immediate symptoms? Incubation period Microorganisms need time to multiply b. Why infections can resolve without drugs? Immune system can destroy pathogens c. Why antibiotics are prescribed? Kill or inhibit bacterial growth 👉 Prevent complications
7. Why finish antibiotics Ensures ALL bacteria are killed Prevents resistance Prevents recurrence 8. Why viral infections are hard to treat Viruses live inside host cells Hard to target without damaging cells Fewer antiviral drugs available 9. Influenza signs Local: Sore throat Nasal congestion Systemic:
Types & purpose: B cells → produce antibodies T cells → destroy infected cells & regulate immune response
3. Active natural vs passive artificial immunity Active natural immunity Body produces its own antibodies after infection Example: recovering from chickenpox Passive artificial immunity Antibodies are given to the person Example: immune globulin injection Key difference: Active = body makes antibodies Passive = antibodies are given 4. Purpose of booster vaccine Stimulates memory cells Increases antibody levels Provides longer-lasting immunity 5. Purpose of gamma globulins Provide immediate protection Contain antibodies 👉 Used when rapid immunity is needed
6. Location of IgA Found in body secretions : o saliva o tears o breast milk o mucus 👉 Protects mucosal surfaces 7. Type III hypersensitivity (how it develops) Antigen + antibody form complexes Complexes circulate in blood Deposit in tissues Trigger inflammation 8. Hay fever (allergic reaction) 1. First exposure → IgE antibodies formed 2. IgE attaches to mast cells 3. Re-exposure → pollen binds IgE 4. Mast cells release histamine 👉 Results: Sneezing Runny nose Itching 9. Why anaphylaxis is life-threatening Massive histamine release Causes:
