2025 Pathophysiology Pathcards to keep for
easy studying at any time.
, lOMoARcPSD|40025598
Condition: Atherosclerosis
Pathophysiology cards Condition: Dyslipidemia (Hyperlipidemia)
Pathophysiology: Formation of fatty streaks (accumulation of Pathophysiology: Elevation of plasma cholesterol, triglycerides (TG), or
lipid-lade foam cells in intimal layer) of the artery. This progresses both, OR a low HDL cholesterol, contributing to the development of
into an atherosclerotic plaque (3 components). atherosclerosis,
Layman’s explanation: Layman’s explanation:
High level of fat in your blood.
Build-up of fat, cholesterol, and other substances in and on your
Risk Factors:
artery walls, which can restrict blood flow. Primary: Genetic—single or multiple gene mutations that result in either
Risk Factors: overproduction or defective clearance of TG & LDL, or underproduction or
Non-modifiable: Age. Family history. Male gender. excessive clearance of HDL.
Modifiable: Certain dyslipidemias. DM. HTN. Smoking. Excessive Secondary: Sedentary lifestyle w/excessive intake of saturated fat,
alcohol consumption. Heart transplant. ↓ intake of fruits & veggies. cholesterol, and trans-fat. DM. Excessive alcohol use. CKD. Hypothyroidism.
Obesity. Psychosocial factors (Type A personality, depression, Primary biliary cirrhosis and other cholestatic liver diseases. Drugs
anxiety, work, socioeconomic factors). Renal insufficiency. (thiazides, beta blockers, retinoids, highly active antiretrovirals,
Sedentary lifestyle. cyclosporine, tacrolimus, estrogen, progestin, & glucocorticoids).
Diagnostic Tests:
Diagnostic Tests: Serum lipid profile (total cholesterol, TG, HDL, LDL, VLDL). For primary,
Symptomatic: History & physical exam. Fasting lipid profile. Plasma physical exam, hx, and serum cholesterol.
glucose & HgbA1C. Clinical Manifestations:
Asymptomatic: Screening. CT scan. Corneal arcus (grayish white opacification at periphery of cornea). Milky
Clinical Manifestations: white appearance of retina. Tendinous xanthomas. Tuberous &
S/S develops when lesions impede blood flow. Transient ischemic tuberoeruptive xanthomas (firm, non-tender [sub]cutaneous nodules that
symptoms (stable exertional angina, TIA, intermittent claudication) are yellowish-orange hue). Planar xanthomas (elevated cutaneous
may develop when stable plaques grow and reduce lumen to less yellowish-orange deposits, often on eyelids). Eruptive xanthomas (painless
yellowish papules on an erythematous base on torso, esp. elbows, chest,
than 70%. Symptoms of unstable angina, MI, ischemic stroke, or rest
and buttocks).
pain in limbs may develop when unstable plaques rupture and Complications:
occlude a major artery. CAD. CVA. PAD. Acute pancreatitis.
Complications: Treatment:
Death. Aneurysms. Arterial dissection. MI. CVA. TIA. Risk assessment criteria. Lifestyle changes (exercises & diet). For ↑ LDL, use
Treatment: statins, sometimes bile acid sequestrants, niacin, and others. For ↑ TG,
Lifestyle changes (diet, smoking, physical activity). Drug treatment niacin, fibrates, omega-3 fatty acids, and others.
of diagnosed RFs. Antiplatelet drugs. Statins. Possibly ACEI or beta Nursing Interventions:
blockers. Monitor lab values. Monitor VS (esp. BP). Encourage a ↓ cholesterol & ↑
Nursing Interventions: fiber diet. Encourage exercise.
References:
Assess chest pain (if present). Monitor LOC. Encourage patient to ↓ https://www.merckmanuals.com/en-ca/professional/endocrine-and-
RF. Monitor S/S based on parts of body affected (coronary— metabolic-disorders/lipid-disorders/dyslipidemia#v990122
angina or acute MI; brain—CVA).
References:
https://www.merckmanuals.com/en-
ca/professional/cardiovascular-
disorders/arteriosclerosis/atherosclerosis#v933891
, lOMoARcPSD|40025598
Pathophysiology cards
Condition: Pernicious anemia/Vitamin B12 deficiency Condition: Gastroesophageal reflux disorder (GERD)
Pathophysiology: Pathophysiology:
↓ in RBCs that occurs when intestines cannot absorb vitamin B12 Incompetence of lower esophageal sphincter (LES) allows reflux
properly, because parietal cells located in gastric mucosa are of gastric contents into esophagus, casing burning pain.
destroyed. This leads to intrinsic factor (IF) not being produced (1) Increased pressure: obesity. Pregnancy. Delayed gastric
and vitamin B12 cannot be absorbed without IF production. emptying.
Layman’s’ explanation: (2) Defective barrier: hypotensive LES. Hiatal hernia.
Causes a person to have too few RBCs (anemia) because their (3) Decreased pressure: chronic pulmonary disorders. Chronic
intestines cannot absorb vitamin B12 properly. cough. Professional signs.
Risk Factors: Layman’s’ explanation:
Addison’s. Graves’. Hypoparathyroidism. Hypothyroidism. Long-term condition where acid from stomach comes up into
Myasthenia gravis. Post gastric bypass. Atrophic gastritis. esophagus.
Autoimmune disorders. Primary ovarian failure (before 40). T1DM. Risk Factors:
Testicular dysfunction. Vitiligo. Sjogren syndrome. Hashimoto’s. Gravity (sit upright= better). Weight gain. Fatty foods. Caffeinated
Celiac disease. or carbonated beverages. Alcohol use. Smoking. Drugs
Diagnostic Tests: (anticholinergic, antihistamines, TCAs, CCBs, progesterone, &
CBC. Reticulocyte count. LDH level. Bilirubin. MMA level. nitrates).
Homocysteine level. Vitamin B12 level. Level of antibodies against Diagnostic Tests:
IF. History. Endoscopy (not responding to treatment). 24-hr pH testing.
Clinical Manifestations: Esophageal manometry.
Mild: diarrhea. Constipation. N&V. Fatigue. Lack of energy. Clinical Manifestations:
Lightheadedness when standing up or on exertion. Anorexia. Heartburn with or without regurgitation of gastric contents into
Pallor/mild jaundice. SOB (mostly OE). Heartburn. Swollen red mouth. Cough. Voice hoarseness. Wheezing. Esophagitis.
tongue and bleeding gums. Esophageal hemorrhage.
Complications: Complications:
Gastric cancer. Nerve damage. GI tract problems. Memory Esophagitis. Peptic-esophageal ulcer. Esophageal stricture. Barrett
problems, confusion, or other neuro symptoms. Heart damage. esophagus. Esophageal adenocarcinoma. Aspiration.
Treatment: Treatment:
Shot of B12 once a month. Oral B12 supplements. Nasal spray B12. Elevate HOB. Avoid coffee, alcohol, and fats. Avoid smoking.
Nursing Interventions: Medications—PPI, H2 blockers. Anti-reflux surgery.
Maintain/encourage good oral hygiene. Monitor VS (esp. SpO2). Nursing Interventions:
Fall risks precautions. Monitor lab values. Pain assessment. 12-lead EKG (to rule out chest pain causes).
References: Good oral hygiene. Nutritional history. Elevate HOB (30-degrees).
https://medlineplus.gov/ency/article/000569.htm Respiratory assessment (SOB, cough, voice hoarseness).
https://www.registerednursern.com/pernicious-anemia-nclex- References:
review-notes/ https://www.merckmanuals.com/en-
ca/professional/gastrointestinal-disorders/esophageal-and-
swallowing-disorders/gastroesophageal-reflux-disease-gerd
https://emedicine.medscape.com/article/176595-overview#a4
, lOMoARcPSD|40025598
Condition: Osteoporosis
Pathophysiology cards Condition: Hearing loss
Pathophysiology: Pathophysiology: 4 types
↓ in total bone mass. Porous, brittle, fragile bones develop (1) Conductive: Secondary to lesions in external auditory canal, TM, or
progressively. Calcitonin and estrogen ↓. PTH ↑, increasing bone middle ear. Lesions prevent sound from being effectively into inner
ear.
turnover and resorption.
(2) Sensorineural: Caused by lesions of either A) inner ear [sensory] or B)
Layman’s’ explanation:
auditory/8th cranial nerve. Sensory: sometimes reversible. Seldom
Reduction in skeletal mass caused by an imbalance between life threatening. Neural: rarely recoverable. May be d/t a
bone resorption and formation. potentially life-threatening brain tumor. Auditory neuropathy
Risk Factors: spectrum disorder.
Genetics: small framed, non-obese Caucasian women. Asian (3) Mixed: Caused by severe head injury with or without fracture of
women of slight build. African American women are less skull or temporal bone, chronic infection, or by one of many
susceptible. Age: Men are a ↓ incidence. Older age & ↓ genetic disorders.
testosterone/estrogen. Nutrition: ↓ calcium & vitamin D intake. ↑ (4) Age-related/Presbycusis: (A) noise induced (B) HTN or DM (C)
Ototoxic medications (D) Structural abnormalities (E) Changes in
phosphorus intake. Inadequate calories. Physical exercise:
inner ear as we age or along nerve pathways.
sedentary lifestyle. Lack of weight-bearing. Low weight & BMI. Layman’s’ explanation:
Lifestyle: ↑ consumption of caffeine & alcohol. Smoking. Lack of Damage to ear or conditions causing a loss of hearing in one or both ears.
exposure to sunlight. Meds: corticosteroids. Antiseizure. Heparin. Risk Factors:
Thyroid hormone (all of the meds affect calcium absorption & Long-term exposure to loud noise without proper protection. Older age.
metabolism). Infection. Autoimmune disorders. Ototoxic drugs.
Diagnostic Tests: Diagnostic Tests:
Dual-energy x-ray absorptiometry (DXA)—bone mineral density. Hearing Handicap Inventory for Elderly-Screening Version. Physical exam.
BMD testing—response to therapy and progression. Labs— Whisper test (CN8). Tuning forks test. Audiometer test.
Clinical Manifestations:
calcium, phosphate, ALP, urine calcium excretion, hematocrit, ESR,
Inability to hear high-pitched sounds. Difficulty hearing women,
& x-ray.
background noises, others speak clearly, in loud areas, & the difference
Clinical Manifestations: between “s” and “th” sounds. Increased sensitivity to certain sounds
Compression fractures. Kyphosis (progressive)/Dowager’s hump. ↓ (seeming overly loud). Tinnitus. Asking people to repeat themselves.
calcitonin & estrogen. ↑ PTH. Complications:
Complications: Depression/isolation. Full deafness.
Fractures. Deformities. Osteoarthritis. Heart failure. Bone cancer. Treatment:
Treatment: Hearing aids. Cochlear implants. Assistive learning devices. Brain stem
Diet (↑ calcium and vit D). Weight-bearing exercises. Biphosphates. implants.
Nursing Interventions:
Calcitonin (nasal, subQ, IM). Raloxifene (SERMs). Teriparatide.
Patient history. Subjective questions/chief complaint. Observation/signs &
Nursing Interventions:
cues. Whisper test (CN8). Environmental modifications (minimize
Supine/side-lying bed rest. Firm, non-sagging mattress. Knee flexion background noise & echoes). Adaptive techniques (face them directly,
(↑ comfort). Intermittent local heat & back rubs (promote muscle ensure you have their attention, enunciate, rephase instead of repeat).
relaxation). Posture. Improving BM (↑ fiber/fluids, stool softeners). References:
References: https://www.nidcd.nih.gov/health/age-related-hearing-loss
https://nurseslabs.com/osteoporosis/
easy studying at any time.
, lOMoARcPSD|40025598
Condition: Atherosclerosis
Pathophysiology cards Condition: Dyslipidemia (Hyperlipidemia)
Pathophysiology: Formation of fatty streaks (accumulation of Pathophysiology: Elevation of plasma cholesterol, triglycerides (TG), or
lipid-lade foam cells in intimal layer) of the artery. This progresses both, OR a low HDL cholesterol, contributing to the development of
into an atherosclerotic plaque (3 components). atherosclerosis,
Layman’s explanation: Layman’s explanation:
High level of fat in your blood.
Build-up of fat, cholesterol, and other substances in and on your
Risk Factors:
artery walls, which can restrict blood flow. Primary: Genetic—single or multiple gene mutations that result in either
Risk Factors: overproduction or defective clearance of TG & LDL, or underproduction or
Non-modifiable: Age. Family history. Male gender. excessive clearance of HDL.
Modifiable: Certain dyslipidemias. DM. HTN. Smoking. Excessive Secondary: Sedentary lifestyle w/excessive intake of saturated fat,
alcohol consumption. Heart transplant. ↓ intake of fruits & veggies. cholesterol, and trans-fat. DM. Excessive alcohol use. CKD. Hypothyroidism.
Obesity. Psychosocial factors (Type A personality, depression, Primary biliary cirrhosis and other cholestatic liver diseases. Drugs
anxiety, work, socioeconomic factors). Renal insufficiency. (thiazides, beta blockers, retinoids, highly active antiretrovirals,
Sedentary lifestyle. cyclosporine, tacrolimus, estrogen, progestin, & glucocorticoids).
Diagnostic Tests:
Diagnostic Tests: Serum lipid profile (total cholesterol, TG, HDL, LDL, VLDL). For primary,
Symptomatic: History & physical exam. Fasting lipid profile. Plasma physical exam, hx, and serum cholesterol.
glucose & HgbA1C. Clinical Manifestations:
Asymptomatic: Screening. CT scan. Corneal arcus (grayish white opacification at periphery of cornea). Milky
Clinical Manifestations: white appearance of retina. Tendinous xanthomas. Tuberous &
S/S develops when lesions impede blood flow. Transient ischemic tuberoeruptive xanthomas (firm, non-tender [sub]cutaneous nodules that
symptoms (stable exertional angina, TIA, intermittent claudication) are yellowish-orange hue). Planar xanthomas (elevated cutaneous
may develop when stable plaques grow and reduce lumen to less yellowish-orange deposits, often on eyelids). Eruptive xanthomas (painless
yellowish papules on an erythematous base on torso, esp. elbows, chest,
than 70%. Symptoms of unstable angina, MI, ischemic stroke, or rest
and buttocks).
pain in limbs may develop when unstable plaques rupture and Complications:
occlude a major artery. CAD. CVA. PAD. Acute pancreatitis.
Complications: Treatment:
Death. Aneurysms. Arterial dissection. MI. CVA. TIA. Risk assessment criteria. Lifestyle changes (exercises & diet). For ↑ LDL, use
Treatment: statins, sometimes bile acid sequestrants, niacin, and others. For ↑ TG,
Lifestyle changes (diet, smoking, physical activity). Drug treatment niacin, fibrates, omega-3 fatty acids, and others.
of diagnosed RFs. Antiplatelet drugs. Statins. Possibly ACEI or beta Nursing Interventions:
blockers. Monitor lab values. Monitor VS (esp. BP). Encourage a ↓ cholesterol & ↑
Nursing Interventions: fiber diet. Encourage exercise.
References:
Assess chest pain (if present). Monitor LOC. Encourage patient to ↓ https://www.merckmanuals.com/en-ca/professional/endocrine-and-
RF. Monitor S/S based on parts of body affected (coronary— metabolic-disorders/lipid-disorders/dyslipidemia#v990122
angina or acute MI; brain—CVA).
References:
https://www.merckmanuals.com/en-
ca/professional/cardiovascular-
disorders/arteriosclerosis/atherosclerosis#v933891
, lOMoARcPSD|40025598
Pathophysiology cards
Condition: Pernicious anemia/Vitamin B12 deficiency Condition: Gastroesophageal reflux disorder (GERD)
Pathophysiology: Pathophysiology:
↓ in RBCs that occurs when intestines cannot absorb vitamin B12 Incompetence of lower esophageal sphincter (LES) allows reflux
properly, because parietal cells located in gastric mucosa are of gastric contents into esophagus, casing burning pain.
destroyed. This leads to intrinsic factor (IF) not being produced (1) Increased pressure: obesity. Pregnancy. Delayed gastric
and vitamin B12 cannot be absorbed without IF production. emptying.
Layman’s’ explanation: (2) Defective barrier: hypotensive LES. Hiatal hernia.
Causes a person to have too few RBCs (anemia) because their (3) Decreased pressure: chronic pulmonary disorders. Chronic
intestines cannot absorb vitamin B12 properly. cough. Professional signs.
Risk Factors: Layman’s’ explanation:
Addison’s. Graves’. Hypoparathyroidism. Hypothyroidism. Long-term condition where acid from stomach comes up into
Myasthenia gravis. Post gastric bypass. Atrophic gastritis. esophagus.
Autoimmune disorders. Primary ovarian failure (before 40). T1DM. Risk Factors:
Testicular dysfunction. Vitiligo. Sjogren syndrome. Hashimoto’s. Gravity (sit upright= better). Weight gain. Fatty foods. Caffeinated
Celiac disease. or carbonated beverages. Alcohol use. Smoking. Drugs
Diagnostic Tests: (anticholinergic, antihistamines, TCAs, CCBs, progesterone, &
CBC. Reticulocyte count. LDH level. Bilirubin. MMA level. nitrates).
Homocysteine level. Vitamin B12 level. Level of antibodies against Diagnostic Tests:
IF. History. Endoscopy (not responding to treatment). 24-hr pH testing.
Clinical Manifestations: Esophageal manometry.
Mild: diarrhea. Constipation. N&V. Fatigue. Lack of energy. Clinical Manifestations:
Lightheadedness when standing up or on exertion. Anorexia. Heartburn with or without regurgitation of gastric contents into
Pallor/mild jaundice. SOB (mostly OE). Heartburn. Swollen red mouth. Cough. Voice hoarseness. Wheezing. Esophagitis.
tongue and bleeding gums. Esophageal hemorrhage.
Complications: Complications:
Gastric cancer. Nerve damage. GI tract problems. Memory Esophagitis. Peptic-esophageal ulcer. Esophageal stricture. Barrett
problems, confusion, or other neuro symptoms. Heart damage. esophagus. Esophageal adenocarcinoma. Aspiration.
Treatment: Treatment:
Shot of B12 once a month. Oral B12 supplements. Nasal spray B12. Elevate HOB. Avoid coffee, alcohol, and fats. Avoid smoking.
Nursing Interventions: Medications—PPI, H2 blockers. Anti-reflux surgery.
Maintain/encourage good oral hygiene. Monitor VS (esp. SpO2). Nursing Interventions:
Fall risks precautions. Monitor lab values. Pain assessment. 12-lead EKG (to rule out chest pain causes).
References: Good oral hygiene. Nutritional history. Elevate HOB (30-degrees).
https://medlineplus.gov/ency/article/000569.htm Respiratory assessment (SOB, cough, voice hoarseness).
https://www.registerednursern.com/pernicious-anemia-nclex- References:
review-notes/ https://www.merckmanuals.com/en-
ca/professional/gastrointestinal-disorders/esophageal-and-
swallowing-disorders/gastroesophageal-reflux-disease-gerd
https://emedicine.medscape.com/article/176595-overview#a4
, lOMoARcPSD|40025598
Condition: Osteoporosis
Pathophysiology cards Condition: Hearing loss
Pathophysiology: Pathophysiology: 4 types
↓ in total bone mass. Porous, brittle, fragile bones develop (1) Conductive: Secondary to lesions in external auditory canal, TM, or
progressively. Calcitonin and estrogen ↓. PTH ↑, increasing bone middle ear. Lesions prevent sound from being effectively into inner
ear.
turnover and resorption.
(2) Sensorineural: Caused by lesions of either A) inner ear [sensory] or B)
Layman’s’ explanation:
auditory/8th cranial nerve. Sensory: sometimes reversible. Seldom
Reduction in skeletal mass caused by an imbalance between life threatening. Neural: rarely recoverable. May be d/t a
bone resorption and formation. potentially life-threatening brain tumor. Auditory neuropathy
Risk Factors: spectrum disorder.
Genetics: small framed, non-obese Caucasian women. Asian (3) Mixed: Caused by severe head injury with or without fracture of
women of slight build. African American women are less skull or temporal bone, chronic infection, or by one of many
susceptible. Age: Men are a ↓ incidence. Older age & ↓ genetic disorders.
testosterone/estrogen. Nutrition: ↓ calcium & vitamin D intake. ↑ (4) Age-related/Presbycusis: (A) noise induced (B) HTN or DM (C)
Ototoxic medications (D) Structural abnormalities (E) Changes in
phosphorus intake. Inadequate calories. Physical exercise:
inner ear as we age or along nerve pathways.
sedentary lifestyle. Lack of weight-bearing. Low weight & BMI. Layman’s’ explanation:
Lifestyle: ↑ consumption of caffeine & alcohol. Smoking. Lack of Damage to ear or conditions causing a loss of hearing in one or both ears.
exposure to sunlight. Meds: corticosteroids. Antiseizure. Heparin. Risk Factors:
Thyroid hormone (all of the meds affect calcium absorption & Long-term exposure to loud noise without proper protection. Older age.
metabolism). Infection. Autoimmune disorders. Ototoxic drugs.
Diagnostic Tests: Diagnostic Tests:
Dual-energy x-ray absorptiometry (DXA)—bone mineral density. Hearing Handicap Inventory for Elderly-Screening Version. Physical exam.
BMD testing—response to therapy and progression. Labs— Whisper test (CN8). Tuning forks test. Audiometer test.
Clinical Manifestations:
calcium, phosphate, ALP, urine calcium excretion, hematocrit, ESR,
Inability to hear high-pitched sounds. Difficulty hearing women,
& x-ray.
background noises, others speak clearly, in loud areas, & the difference
Clinical Manifestations: between “s” and “th” sounds. Increased sensitivity to certain sounds
Compression fractures. Kyphosis (progressive)/Dowager’s hump. ↓ (seeming overly loud). Tinnitus. Asking people to repeat themselves.
calcitonin & estrogen. ↑ PTH. Complications:
Complications: Depression/isolation. Full deafness.
Fractures. Deformities. Osteoarthritis. Heart failure. Bone cancer. Treatment:
Treatment: Hearing aids. Cochlear implants. Assistive learning devices. Brain stem
Diet (↑ calcium and vit D). Weight-bearing exercises. Biphosphates. implants.
Nursing Interventions:
Calcitonin (nasal, subQ, IM). Raloxifene (SERMs). Teriparatide.
Patient history. Subjective questions/chief complaint. Observation/signs &
Nursing Interventions:
cues. Whisper test (CN8). Environmental modifications (minimize
Supine/side-lying bed rest. Firm, non-sagging mattress. Knee flexion background noise & echoes). Adaptive techniques (face them directly,
(↑ comfort). Intermittent local heat & back rubs (promote muscle ensure you have their attention, enunciate, rephase instead of repeat).
relaxation). Posture. Improving BM (↑ fiber/fluids, stool softeners). References:
References: https://www.nidcd.nih.gov/health/age-related-hearing-loss
https://nurseslabs.com/osteoporosis/
