Final Exam Pathophysiology 2200 - Curry College 2025

Curry College 2025 BSN

☆☆Compare and contrast morbidity and mortality

1. Morbidity = effects of illness on life (impact)

2. Mortality = causes of death in a population

☆ List the levels of disease prevention and provide an example

• Primary – prevent disease (immunizations, remove risk factors)

• Secondary – early detection (Pap smear, screening tests)

• Tertiary – reduce complications (antibiotics, radiation, rehab)

☆☆Clinical Manifestations: signs and symptoms

1. Signs (Objective) – seen/measured (fever, swelling, pupil change)

2. Symptoms (Subjective) – patient reports (pain, dyspnea, dizziness)

☆☆What is Etiology?

1. Cause of disease (genetic, environmental, biological, etc.)

☆☆What is incidence and Prevalence?

• Incidence = NEW cases

• Prevalence = EXISTING cases

☆☆What are the 3 types of cell surface Receptors?

• G-protein linked – On/off switch

• Enzyme-linked – Hormone receptors

• Ion-channel linked – Neurotransmitter signaling (nerve/muscle)

☆☆What are the 2 types of Cell metabolism?

1. Glycolysis (cytoplasm) – Anaerobic → 2 ATP → lactic acid

2. Citric Acid Cycle (mitochondria) – Aerobic → 34–36 ATP → CO₂ + H₂O + ATP

☆☆What are the 2 types of cell membrane movement?

Passive (No energy)

• Diffusion (O₂/CO₂)

• Facilitated diffusion (glucose, ions)

• Osmosis (water)

Active (Requires energy)

• Na⁺/K⁺ pump

☆What are the 3 Ion channels?

• Autocrine – cell affects itself

• Paracrine – nearby cells

• Endocrine – hormones via bloodstream

☆☆What are the 4 types of skins?

• Epithelial – protect, absorb, secrete

• Connective – most abundant; supports/binds

• Muscle – movement; actin/myosin

• Nervous – communication (neurons + neuroglia)

☆☆Describe cell changes to injury and aging

1. Injury

   • Atrophy – ↓ cell size

   • Hypertrophy – ↑ cell size

   • Hyperplasia – ↑ number of cells (e.g., BPH)

   • Metaplasia – replacement of adult cells (Chronic diseases)

   • Dysplasia – disordered growth (pre-cancerous)

2. Aging

   1. *Apoptosis (fallen apart): cell-suicide

☆☆What are the three mechanisms of cell dying?

1. Free radicals – DNA + membrane damage

2. Hypoxia – most common, ↓ ATP

3. Calcium imbalance – enzyme activation → cell damage imbalance (enzyme)

☆What is Reversible Cell Injury?

1. Function impaired but cell can recover

   1. Cellular swelling

   2. Fatty change (esp. liver)

☆☆What are the 2 Programmed Cell Death

1. Apoptosis (fallen apart): cell-suicide

2. Necrosis: cell death of an organ or tissue that is still part of a living person.

   1. Gangrene

☆What are the cardinal signs of Inflammation? (Local 5 vs 3 Sysemic)

Local (vasodilation = earliest sign)

• Rubor – redness

• Tumor – swelling

• Calor – heat

• Dolar – pain

• Loss of function

Systemic (acute-phase response)

• Fever

• Fatigue

• Sepsis (severe bacterial infection)

☆**What is Acute vs Chronic inflammation?

Acute

• Short, self-limiting

• Exudation (pus), plasma proteins

• Neutrophils = first responders

Chronic

• Long duration

• Lymphocytes + macrophages (main workers)

• Angiogenesis, tissue necrosis, fibrosis (scarring)

☆What are the cells of inflammation?

Endothelial cells

• Prevent sticking (antiplatelet/antithrombotic)

• Control vasodilation/constriction

Platelets (Thrombocytes)

• Release inflammatory mediators:

  • Histamine

  • Cytokines

  • Prostaglandins (pain)

☆What are the types of Leukocytes (WBC)?

Granulocytes

• Neutrophils – first responders; most abundant (60–70%)

• Eosinophils – parasites & allergic reactions (arrive after neutrophils)

• Basophils – precursors to mast cells

• Mast cells – abundant in lungs, GI, skin (major inflammatory role)

Agranulocytes

• Monocytes → Macrophages

  • First phagocyte

  • Release vasoactive mediators: leukotrienes, prostaglandins

• Lymphocytes – adaptive immunity

• Natural killer cells – target cancer cells

☆What are the 3 cellular mediators? What is the process causing the reactions called?

Released during degranulation

• Histamine – vasodilation/constriction

• Prostaglandins – pain

• Cytokines – communication

☆What is the 4 Cellular Response of Leukocytes?

• Margination/Adhesion – WBCs line vessel wall

• Transmigration – move through vessel

• Chemotaxis – move toward injury

• Activation/Phagocytosis – engulf & destroy debris

☆**What is the Complement system?

1. Brings Innate and Adaptive / local and systemic systems together

2. Causes vasodilation

☆What are the 4 types of Exudate?

• Serous – watery, low protein

• Serosanguinous – blood → pink → clear

• Hemorrhagic – RBC leakage

• Purulent – pus (WBCs, proteins, debris)

☆What is Granulation tissue?

• Red, moist connective tissue

• Contains: new capillaries, fibroblasts, residual inflammatory cells

• Indicates healing

☆What are the 3 stages of Wound Healing?

• Inflammatory phase – clot forms; WBCs migrate

• Proliferative phase (Granulation) – fibroblasts build collagen & ECM

• Wound contraction & remodeling – scar formation

☆What are the Agents of Infectious Disease?

Viruses

• Smallest pathogens

• Hardest to cure

• Protein coat; require host to replicate

Eukaryotes (Fungi)

• Yeasts + molds

• Have true nucleus

Prokaryotes (Bacteria)

• No true nucleus

• Contain DNA & RNA

☆What are the 4 portals of entry?

1. Penetration – break in skin/mucosa

   • Burns, wounds, surgery, bites

2. Direct Contact – infected tissue → intact mucosa

   • STIs, mother-to-child (vertical/congenital)

3. Ingestion – oral/GI route

   • Contaminated food/water

4. Inhalation – bypass respiratory defenses

   • Pneumonia, meningitis, TB

☆What is the 5 Disease Course in Infection?

• Incubation – pathogen replicates

• Prodromal – vague, early symptoms

• Acute – rapid pathogen growth; max symptoms

• Convalescent – containment & healing

• Resolution – pathogen eliminated

☆What are the different types of locations of receiving Infectious disease?

1. Nosocomial: develop in hospitalized patients (Inside of hospital) 

2. Community acquired: acquired outside of healthcare facilities

☆What are the types of Immunity?

1. Innate (Born with)

   1. Local Inflammation / Vascular (Redness, Swelling, Heat, Pain, Loss of function)

1. Systemic Responses

   • Fever

   • Fatigue

   • Lethargy

   • Anorexia

4. Adaptive (Antibodies/Pathogens)

   1. Develop over the course of time

      1. Cell-Mediated Immunity – T Lymphocytes

         • Develop in: Thymus

         • Cytotoxic T cells – kill infected cells

         • Helper T cells – activate B cells & immune response

         • Regulatory T cells – suppress/regulate immune activity

         Humoral Immunity – B Lymphocytes

         • Develop in: Bone marrow

         • Produce:

           • Antibodies (Immunoglobulins)

           • Memory B cells (rapid response on re-exposure)

☆What is the difference between active and passive immunity?

Active Immunity (Acquired)

• Produced by your own body

• Long-lasting

• Example:

  • Infection

  • Vaccination

Passive Immunity (Transferred)

• Given from another source

• Immediate but short-lived

• Examples:

  • Maternal antibodies (placenta, breast milk)

  • Immunoglobulin injections

☆☆What is the travel of blood through the SVC and IVC?

1. Right Side (SVC/IVC → Lungs: Pulmonary circulation, low pressure)

   SVC/IVC → RA → Tricuspid valve → RV → Pulmonary valve → Pulmonary artery → Lungs

   2. Left Side (Lungs → Body: Systemic circulation, high pressure)

   Pulmonary veins → LA → Mitral valve (prevents the backflow during systole) LV → Aortic valve → Aorta → Body

☆What are the symptoms of left and right sided heart failure?

Right-Sided HF

• Edema

• Weight gain

• ↑ Peripheral venous pressure

Left-Sided HF

• Tachycardia

• Crackles

• Cough

• Shortness of breath (dyspnea)

☆☆What is Cardiac output?

1. The quantity of blood pumped by the heart in a given period of time

2. CO = SV × HR

3. BP = CO × PR

4. ↑ PR = most common cause of ↑ BP (Atherosclerosis)

5. ↓ SV → ↓ BP → ↑ HR (compensation)

☆☆What is Preload, Afterload, Contractility?

• Preload:
  End-diastolic volume (stretch before contraction)

• Afterload:
  Pressure the heart must pump against

• Contractility:
  Heart’s ability to eject stroke volume

☆☆What controls blood flow?

1. Autoregulation (Short-term)
   Humoral mechanisms
   Endothelial control
   Collateral circulation

Key Mediators

• Histamine – vasodilation

• Norepinephrine – vasoconstriction

• Epinephrine – vasodilation

• Angiotensin II – strongest vasoconstrictor

☆☆Know the 5 Cardiac Conduction pathway through the heart?

1. SA Node (Pacemaker)  heart rate 60-100 bpm*

2. AV Node

3. AV Bundles

4. R & L Bundle Branch 

5. Purkinje Fibers

☆Dyslipidemia causes an imbalance of what lipid components?

1. Triglyceride 

2. Phospholipids

3. Cholesterol

☆What is Dyslipidemia and what can it cause?

Imbalance of lipids →

Causes:

• Atherosclerosis

• Stroke

• PVD

• Ischemic heart disease

  • HDL high = good

  • LDL high = bad

☆What is the greatest risk factor for the development of atherosclerosis?

High cholesterol

☆What are the Nonmodifiable and Modifiable risk factors for Atherosclerosis?

1. Nonmodifiable 

   1. Age

   2. Male gender

   3. Genetic disorder

   4. Family hx of premature CAD

2. Modifiable 

   1. Smoking

   2. Obesity

   3. Hypertension

   4. Hyperlipidemia

   5. Diabetes mellitus

☆☆Distinguish between 3 Systemic Arterial and 3 Systemic Venous disorders.

1. Arterial (Lower)

   • Atherosclerotic occlusive disease (PAD)

   • Raynaud disease/phenomenon

   • Acute arterial occlusion (Sudden blockage)

   Venous

   • Varicose veins (Dilated veins)

   • Chronic venous insufficiency (CVI)

   • Venous thrombophlebitis → pulmonary embolism (Dead-Air space)

☆What causes an aneurysm?

• Weak arterial wall → dilation (outpouching)

• Most common cause: Atherosclerosis (HTN)

• Dissecting aneurysm: sudden tearing pain, internal bleeding

☆☆Know the definitions of systole, diastole.

• Systole: Contraction (blood out)

• Diastole: Relaxation (heart fills)

☆Define Chronic Venous Insufficiency vs peripheral artery disease(Symptoms)

1. Chronic Venous Insufficiency (Constriction and elevation)

   • Congestion

   • Edema

   • Pooling

   • Varicose veins

   • Skin changes

   2. Peripheral Artery Disease

   • Intermittent claudication

   • Pallor on elevation

   • Intermittent claudication (Pain when walking)

   • Rubor on dependency

   • ↓ pulses

   • Pain

☆☆What is Virchow’s Triad?

1. Increases the risk of a DVT

   1. Stasis of blood (Immobility) -> Ambulate 

   2. Increased blood coagulability -> Anticoagulante 

   3. Vessel wall injury

☆☆Name the short term and long term BP

1. Short Term

   1. Autoregulation (ANS)

2. Long Term

   1. Kidneys

☆☆What are the risk factors for Coronary Artery Disease (CAD)?***

smoking, HTN, high LDL, low HDL, diabetes, age, obesity, physical inactivity, Dyslipidemia

☆☆What are the 2 types of Coronary Heart Disease?

1. Chronic Ischemic Heart Disease

   1. Chronic stable angina

   2. Silent myocardial ischemia, and variant or vasospastic angina

      1. Angina is chest pain

2. Acute Coronary Syndromes (ACS)

   1. Unstable angina (UA) 

   2. Myocardial infarction (Heart attack)

☆What are the 5 Sympathetic nervous system responses to a heart attack?

1. GI distress

2. Tachycardia (vasoconstriction)

3. Anxiety

4. Hypotension and shock

5. Weakness in limbs

☆☆Be able to describe / identify the 3 layers of the heart wall.

1. Epicardium

   1.  visceral layer of serous pericardium

2. Myocardium

   1. bundles of contractile cardiac muscle cells

3. Endocardium

   1. innermost layer; Lines heart chambers

☆What are the primary and secondary Cardiomyopathies (CM)?

1. Primary: Heart muscle diseases of unknown origin (genetic or acquired)

   1. Types: HCM, AVRD, Dilated, Restrictive 

   2. Secondary: Conditions in which the cardiac abnormality results from another cardiovascular disease

☆☆What are the 2 Valve Defects?

Stenosis

1. Narrowing of the valve opening, so it does not open properly valve

   1. Blood goes back down

1. Regurgitation

   1. valve will not close all the way; it leaks when it should be closed

☆☆What are the functions of the lungs/Respiratory system?

1. Gas exchange -> Alveoli 

   1. **Peripheral Chemoreceptors- Oxygen moves from alveolar air into blood

   2. Central Chemoreceptors- Carbon dioxide moves from blood into alveolar air

☆What is the difference between Alveolar 1 and 2?

1. Type I Alveolar Cells

   1. Cell surface

2. Type II Alveolar Cells

   1. Produce surfactant

☆What are the types of ventilation-perfusion mismatching?

• Dead space → ventilated, NOT perfused

• Shuntting → perfused, NOT ventilated → hypoxia

☆Define ventilation, perfusion, and respiration.

1. Ventilation → movement of air in/out

2. Perfusion → blood flow through lungs

3. Respiration → gas exchange

☆☆What are the Cough reflexes and Cheyne-stoke?

1.  Cough reflexes 

   1. Protection 

2. Cheyne-stoke

   1. Abnormal pattern of breathing

☆☆What are the types of pleural disorders?

1. Pleuritis- Inflammation of the pleura (pain) 

2. Pleural Effusion- Fluid

   1. Chyle- Lymph Fluid 

3. Hemothorax- Blood

4. Pneumothorax- Air

☆☆What are Spontaneous and Traumatic Pneumothorax?

1. Spontaneous: an air-filled blister on the lung ruptures

2. Traumatic: air enters through chest injuries

   1. Tension: cannot leave on exhalation (tracheal deviation)

   2. Open:  leaves on exhalation

☆☆What are the 2 Chronic Obstructive Pulmonary Disorders?

1. Emphysema (“Pink puffer”) → dead space

   • Alveolar wall destruction

   • Loss of elasticity

   • Enlarged air spaces

   Symptoms

   • Decreased breath sounds

   • Barrel chest

   • Cor pulmonale

   • Cough

2. Chronic Bronchitis (“Blue bloater”) → shuntting

   • Inflammation of bronchioles

   Symptoms

   • ↑ mucus

   • Cough

   • Dyspnea

   • Narrow airways

   • Rhonchi

☆☆What is Acute Respiratory distress syndrome (ARDS)?

1. Fluid-filled alveoli → severe gas exchange failure

2. Caused by sepsis, trauma

3. Refractory hypoxemia

☆☆What are the ways to prevent and recognize a Pulmonary Embolism?

1. Prevent

   1. Ambulate 

   2. Anticoagulante 

   3. Prevent DVT (Most common reason) 

   4. Compression 

2. Recognize 

   1. Sudden shortness of breath

   2. Chest pain

   3. Increase RR

   4. Increased heart rate

☆☆What is Atelectasis? (Name the 5 symptoms)

1. Incomplete expansion

   1. Atelectasis leads to Obstruction Compression 

2. Symptoms

   1. Tachypnea

   2. Tachycardia

   3. Dyspnea

   4. Cyanosis (Late sign)

   5. Absence of breath sounds

☆☆What are the 4 types of treatment for Atelectasis?

1. Deep breathing

2. Coughing

3. IS

4. Ambulate

☆☆What is Asthma? And the two types?

• Chronic airway inflammation

• #1 cause: Allergens

  • Causes shunting

Type 1 – Extrinsic

• Allergens

• Antigens

Type 2 – Intrinsic

• Infection

• Exercise

• Cold air

1. ☆☆What is the function of the kidney? 

1. Urine formation

2. Excreting waste 

3. Production in red blood cell (erythropoiesis)

4. Synthesis of Vitamin D

☆Why is Renin produced?

• Released due to hypotension / low perfusion

• Holds onto Na+ → ↑ BP

☆What is the functional unit of the kidneys?

Nephron (High pressure)

☆What is the Vascular and Tubular component?

Vascular

• Glomerulus = filtration

• Bowman’s capsule → filtrate is protein & RBC-free

Tubular

• Reabsorption & secretion

• Eliminates K+

☆What are the 4 Tubular components consist of? **

Proximal – majority of reabsorption
Loop of Henle – concentration

• Normal SG: 1.010–1.025

• Low = dilute

• High = concentrated

Distal – site of Renin release (JG cells)
Collecting duct – final urine concentration

☆What is secreted in our urine?

Potassium (K+)

☆Which diagnostic tests are used to assess kidney function (list and describe)

BUN

• High BUN = poor kidney function

Specific Gravity

• Measures urine concentration

• Normal: 1.005–1.025

Serum Creatinine

• Best indicator of kidney function

• From muscle metabolism

GFR

• Normal ~ 125 mL/min

• Daily urine output ~ 1.5 L

☆What is Antidiuretic Hormone (ADH)? ** (Urine Production)

Responds to ↑ blood osmolality

• Low water intake → ↑ ADH → ↑ water reabsorption

• High water intake → ↓ ADH → diuresis

☆What do the Juxtaglomerular cells release?

Renin

☆☆What is Cystic disease?

• Fluid-filled sacs in nephron

• Causes obstruction → stasis → pain (abd/back)

☆☆What are some of the types of obstructions of the urinary tract?

1. Calculi (stones)

2. Pregnancy

3. Scar tissue

4. Tumors

5. Benign prostatic hyperplasia (BPH)

6. Neurologic disorders

☆What are the manifestations of a urinary obstruction? **

1. Pain

2. Signs and symptoms of UTI (Burning)

3. Renal dysfunction (Increased BUN, Increase Creatine, Decrease GFR)

   1. Causes = Hypertension and infection

☆☆What is Hydronephrosis?

Urine filled dilation of the renal pelvis

1. ☆**Symptoms:

   1. Anuria = no urination

   2. Oliguria= Decrease in urination (<50 mL/day)

   3. Polyuria = excess urination

   4. Nocturia = waking at night to urinate 

   5. Diuresis = excessive production of urine

☆What are the clinical manifestations of Renal Calculi (Kidney Stones)?

• Renal colic (severe pain)

• Cool/clammy skin

• Nausea/vomiting

• Stones 1–5 mm

• Non-colicky pain

• dull flank ache, worse with fluid intake

☆☆What are the treatments for kidney stones?

1. Hydration 

2. Diet change

☆☆What is Cystitis and Pyelonephritis?

1. Cystitis=Lower UTIs

2. Pyelonephritis=Upper UTIs

☆Define dysuria, pyuria, hematuria, Proteinuria, Anuric, Uremia.

1. Dysuria: Burning and pain on urination

2. Pyuria: Pus in urine

3. Hematuria: Blood in urine 

4. Proteinuria: Protein in urine

5. Anuric: making no urine

6. Uremia: Urea in urine

What is Azotemia?

Build up of nitrogenous wastes in the blood

☆☆What is the cause of Nephrotic Syndrome? What’s the result? **

1. Damage to the glomeruli (Cause- Generalized edema)

   1. Result: High Protein 

☆What is the difference between Acute pyelonephritis and Chronic pyelonephritis?

Acute: sudden kidney infection, casts present
Chronic: recurrent/persistent infection → scarring

☆☆What is Hyperkalemia? **

1.  Increase in potassium  (Caused by decreased function of kidney; acute renal failure) 

Cause; Arrhythmias

☆☆What happens when the kidneys fail? **

• ↓ Waste removal

• Cannot regulate fluid, electrolytes, pH

• Nitrogenous wastes ↑ → ↑ BUN & ↑ Creatinine

☆What is acute renal failure and chronic renal failure?

Acute Kidney Injury (AKI)

• Sudden onset

• Key sign: Azotemia (↑ nitrogenous wastes in blood)

Chronic Kidney Disease (CKD)

• Permanent nephron loss

• Progressive, irreversible

☆☆Define prerenal, intrinsic, and postrenal. (Acute)

Prerenal = Problem BEFORE kidney

• ↓ Blood flow

• Causes: dehydration, blood loss, hypovolemia, heart failure

Intrinsic = Problem INSIDE kidney

• Direct damage

• Causes: glomerulonephritis, acute tubular necrosis, nephrotoxic drugs

Postrenal = Problem AFTER kidney

• Obstruction

• Causes: stones, BPH, pregnancy

☆☆What are the 4 phases of the AKI? (Acute)

1. Onset: precipitating

2. Oliguric: decreased urine output 

3. Diuretic: kidneys try to heal and urine output increases

4. Recovery:  tubular edema resolves

What is Chronic kidney Disease?

1. Causes a permanent loss of nephrons

2. ☆☆Causes: decrease in erythropoietin = fatigue, pallor, low hemoglobin.

☆☆What are the causes of Chronic kidney Disease? Treatment? **

1. Hypertension

2. Diabetes mellitus

3. Polycystic kidney disease

4. Obstructions of the urinary tract

5. Glomerulonephritis

6. Chronic use of pain medication

   1. Dialysis

      1. Hemodialysis

      2. Peritoneal dialysis

☆What is the function of the parasympathetic and sympathetic?

• Parasympathetic: promotes bladder emptying

• Sympathetic: promotes bladder filling

☆What are the involuntary and voluntary controls?

• Involuntary: Autonomic nervous system

• Voluntary: Somatic nervous system

☆What are Neurogenic Bladder Disorders?

1. Spastic Bladder Dysfunction

   1. Unable to Store urine in the bladder

      1. Neurologic lesions above level of the sacral cord 

2. Flaccid Bladder Dysfunction

   1. Unable to empty the bladder

      1. affect motor neurons in the sacral cord

Where is each enzyme found and what is it responsible for digesting? <3

1. Amylase

   1. Mouth (Breakdown of carbohydrates)

2. Lipase

   1. Pancreas (Break down fats)

3. Pepsin

   1. Stomach (Breaking down proteins)

4. Lysozyme

   1. Salivary (Defend against bacteria)

5. Trypsin

   1. Duodenum (Breakdown of proteins)

☆What are the 5 types of GI secretions?

• Salivary – lubrication; amylase/ptyalin

• Gastric – gastrin → HCl

• Pancreatic – enzymes (trypsin, lipase, amylase)

• Biliary – bile

• Intestinal – neutralizes acid, protects duodenum

What are the 2 types of GI hormones? <3

1. Gastrin

   1. Produced by G cells in stomach 

      1. Stimulates secretion of gastric acid by secreting parietal cells

         1. Disorder of gastric acid- excess gastric acid secretion leads to ulcers and diarrhea.

2. Ghrelin

   1. Peptide hormone produced in fundus of stomach

☆What are the 3 cells in the stomach mucosal layer and what do they secrete?

1. Parietal cells

   1. Gastric acid (result of gastrin production) 

2. Chief cells

   1. Pepsin

   2. Lipases

3. G-Cells 

   1. Gastrin (Hormone) 

☆What is the difference between Dysphagia, Achalasia, Esophageal Lacerations, and Esophageal Diverticula?

• Dysphagia – difficulty swallowing; choking/coughing; food sticks

• Achalasia – LES fails to relax; food stuck

• Esophageal diverticula – outpouching; gurgling, halitosis, food stops early

Esophageal Lacerations

• Boerhaave syndrome – non-penetrating mucosal tears after forceful vomiting (alcoholics)