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Final Path
Final Pathophysiology
| Question | Answer |
|---|---|
| Leukemia is a cancer of the blood cells that starts where? | BOne marrow |
| Acute Leukemia Onset | Progresses quickly and aggressively; requires immediate treatment. |
| Acute Leukemia's cell maturity | involves immature blood cells (blasts) that cannot mature and function properly. |
| Acute Leukemia's cell type | Can be further classified as Lymphocytic or Myelogenous based on the cell origin |
| Chronic Leukemia onset/progression | Progresses slowly; may not require immediate treatment. |
| Chronic leukemia cell maturity | Involves mature or partially mature cells that multiply more slowly. |
| Chronic leukemia cell type | Can be further classified as Lymphocytic or Myelogenous based on the cell origin |
| What are the 4 main leukemia | Acute Lymphocytic Leukemia (ALL), Acute Myeloid Leukemia (AML), Chronic Lymphocytic Leukemia (CLL), and Chronic Myeloid Leukemia (CML |
| The Virchow triad describes the three broad categories of factors that contribute to the formation of? | a thrombus (blood clot) within a blood vessel: 1.Endothelial Injury/Vessel Wall Damage 2. Alterations in Blood Flow (Stasis/Turbulence) 3. Hypercoagulability (Increased Tendency to Clot) |
| Endothelial Injury/Vessel Wall Damage: | Damage to the inner lining of the blood vessel (endothelium) exposes underlying collagen, triggering the clotting cascade. |
| Alterations in Blood Flow (Stasis/Turbulence) | Slowing or stopping of blood flow (stasis), or turbulent flow (e.g., around irregular plaques or in areas of bifurcation), allows clotting factors to accumulate and promotes platelet contact with the vessel wall. |
| Hypercoagulability (Increased Tendency to Clot): | An imbalance between pro-coagulant and anti-coagulant factors, which can be inherited or acquired (e.g., cancer, pregnancy, certain medications, immobility). |
| Atherosclerosis | Atherosclerosis is the thickening or hardening of the arteries caused by a buildup of plaque in the inner lining (intima). |
| Thrombus | A blood clot that forms and remains attached to the wall of a blood vessel or the heart. |
| Location of thrombus | Forms in situ (in its original place). |
| Embolus | An unattached mass (often a piece of a thrombus, but also fat, air, or other foreign material) that travels through the bloodstream |
| Location of embolus | Originates elsewhere and travels to a different site. |
| Thrombus consequence | Causes localized obstruction of blood flow at the site of formation |
| Embolus consequences | Lodges in a distant, narrower vessel, causing sudden, complete obstruction (embolism) and distal ischemia/infarction. |
| disseminated intravascular coagulation (DIC) | DIC is a condition where tiny blood clots form throughout the bloodstream, blocking small vessels and using up clotting factors and platelets, leading to excessive bleeding |
| Laboratory tests for DIC would show: D-dimer | Elevated D-dimer: A fibrin degradation product, highly sensitive for the presence of clots. |
| Laboratory tests for DIC would show: platelet count | Decreased Platelet Count (Thrombocytopenia): Platelets are consumed in the clotting process. |
| Laboratory tests for DIC would show: PT | Prolonged Prothrombin Time (PT) / International Normalized Ratio (INR) |
| Laboratory tests for DIC would show: aPTT | Activated Partial Thromboplastin Time (aPTT): Clotting factors are used up faster than they can be produced. Reduced Fibrinogen Levels: Fibrinogen (a key clotting protein) is depleted. |
| Laboratory tests for DIC would show: fibrinogen levels | Reduced Fibrinogen Levels: Fibrinogen (a key clotting protein) is depleted. |
| Shift-to-the-left phenomena | Shift-to-the-left" (or "left shift") refers to a laboratory finding in a complete blood count (CBC) with differential, specifically in the white blood cell (WBC) count. |
| Shift-to-the-left phenomena explanation | It indicates a higher-than-normal number of immature neutrophils (specifically band neutrophils or stabs) present in the blood. |
| Shift-to-the-left phenomena cause | This typically happens when the bone marrow is releasing neutrophils into the bloodstream too quickly to keep up with a severe infection or inflammatory process, forcing the release of young, less mature cells into circulation. |
| Pathophysiology of polycythemia | Polycythemia is a condition resulting in an increased number of red blood cells (RBCs) in the blood. |
| Primary Polycythemia (Polycythemia Vera) | A chronic, progressive bone marrow malignancy where a mutation (commonly the JAK2 gene) causes hematopoietic stem cells to overproduce RBCs, and often WBCs and platelets, independent of normal regulatory mechanisms (like erythropoietin levels). |
| Secondary Polycythemia | lead to increased production of (EPO), which stimulates RBC production. often a normal physiological response to chronic hypoxia (low oxygen levels), such as living at high altitudes, chronic lung disease (e.g., severe chronic bronchitis), or smoking |
| Leukemias clinic manifestation | Fatigue, pallor, frequent infections (due to non-functional WBCs), easy bruising/bleeding, swollen lymph nodes, fever, weight loss, bone pain. |
| Leukemia eval/dx | Complete Blood Count (CBC) with differential, bone marrow biopsy (confirms diagnosis and type), flow cytometry, cytogenetic analysis |
| Multiple Myeloma clinic manifestation | CRAB" criteria: Calcium elevation, Renal failure, ****A**nemia, Bone lesions (pain, fractures). Also fatigue, recurrent infections |
| Multiple myeloma eval/dx | Serum/Urine protein electrophoresis (M-protein spike), bone marrow biopsy (>10% plasma cells), Bence Jones protein in urine, imaging studies (X-ray, MRI) for bone lesions |
| Burkitt Lymphoma clinic manifestation | Very fast-growing tumor, often presenting as a large mass in the jaw/facial bones (endemic form), or abdomen (sporadic form), leading to bowel obstruction/pain |
| Burkitt lymphoma eval dx | Biopsy of tumor mass, morphology review (starry sky appearance), immunophenotyping, detection of C-MYC gene translocation (confirmatory) |
| Leukemia patho | Uncontrolled proliferation of malignant white blood cells originating in the bone marrow, crowding out normal hematopoietic cells and impairing normal immune function |
| Disseminated Intravascular Coagulation (DIC) patho | Widespread activation of the coagulation cascade by a primary disease (e.g., sepsis, trauma, cancer), leading to systemic microthrombi formation. Clotting factors and platelets are rapidly consumed, causing severe bleeding elsewhere in the body |
| Essential Thrombocythemia | A chronic myeloproliferative neoplasm characterized by the overproduction of platelets by megakaryocytes in the bone marrow, often due to a JAK2 gene mutation, leading to risk of both thrombosis and hemorrhage |
| Hemochromatosis | A disorder of iron metabolism resulting in excessive iron absorption from the diet. The iron accumulates in parenchymal cells of organs (liver, heart, pancreas), causing tissue damage, fibrosis, and organ failure |
| Clinical presentation of lymphoma Lymphomas generally present with: (lymph) | Painless swelling of lymph nodes (lymphadenopathy), commonly in the neck, armpit, or groin. |
| Clinical presentation of lymphoma Lymphomas generally present with: Bsymptoms | B Symptoms": Systemic symptoms that indicate more advanced disease, including unexplained fever, drenching night sweats, and unexplained weight loss |
| Clinical presentation of lymphoma Lymphomas generally present with: (percent) | ≥10%is greater than or equal to 10 % ≥10% in 6 months). Fatigue, pruritus (itching). Symptoms related to the site of involvement (e.g., shortness of breath if chest nodes involved |
| Risk factors associated with non-Hodgkins lymphoma | Immunosuppression: HIV/AIDS, organ transplant recipients on immunosuppressive drugs. |
| Risk factors associated with non-Hodgkins lymphoma | Autoimmune diseases: Sjogren syndrome, Rheumatoid arthritis, Systemic lupus erythematosus. |
| Risk factors associated with non-Hodgkins lymphoma | Infections: Certain viral infections like Epstein-Barr virus (EBV), Human T-cell leukemia virus type 1 (HTLV-1), and Helicobacter pylori (linked to gastric lymphoma). |
| Risk factors associated with non-Hodgkins lymphoma | Chemical exposures: Exposure to pesticides, herbicides, and certain chemotherapy agents. Age (risk increases with age). |
| thrombotic thrombocytopenic purpura (TTP)-Pathophysiology: | a deficiency in the ADAMTS13 enzyme, which normally breaks down large von Willebrand factor (vWF) multimers. |
| thrombotic thrombocytopenic purpura (TTP)-Pathophysiology: | Without this enzyme, these large multimers accumulate, causing platelets to excessively aggregate and form microthrombi in small blood vessels throughout the body. |
| TTP Lab Findings (The Pentad): | Thrombocytopenia (low platelet count). Microangiopathic Hemolytic Anemia (MAHA - damaged RBC fragments seen on blood smear). Neurological symptoms. Renal abnormalities. Fever (rare |
| acquired immunodeficiency syndrome (AIDS) patho | final stage of HIV infection. The (HIV) primarily infects &destroys CD4+ T-lymphocytes, which are crucial for the immune system's function. The progressive loss of these cells leads to profound immunosuppression, making the individual susceptible to oppo |
| How is AIDS Dx? | AIDS is diagnosed when the CD4 count drops below 200 cells/mm |
| How to monitor AIDS? | CD4+ T-cell count: Measures the extent of immune system damage. Viral Load (HIV RNA assay): Measures the amount of active virus in the blood, used to monitor disease progression and effectiveness of antiretroviral therapy (ART |
| Anemia | deficiency in the number of red blood cells or the amount of hemoglobin |
| Pernicious Anemia (PA): cause | An autoimmune disorder where the body produces antibodies against parietal cells in the stomach lining or against intrinsic factor (IF), a protein necessary for Vitamin B12 absorption in the small intestine. |
| Pernicious Anemia (PA): Patho | Lack of IF leads to a critical deficiency in Vitamin B12 (cobalamin). B12 is essential for DNA synthesis in RBC production. |
| Pernicious Anemia (PA): Patho | This deficiency causes impaired RBC maturation, resulting in large, immature RBCs (megaloblastic or macrocytic anemia) and neurological damage |
| Anemia is broadly classified using three main approaches | morphological (cell size), kinetic (production vs. destruction), and by severity. |
| Anemia: Morphological Classification (Cell Size) | most common clinical approach, based on the Mean Corpuscular Volume (MCV), which measures the average size of red blood cells (RBCs) |
| Microcytic Anemia | MCV < 80 fL): Cells are smaller than normal. |
| Microcytic Anemia : Cause | Common Causes: Iron deficiency anemia (most common), Thalassemia, Anemia of chronic disease (late stage), and Sideroblastic anemia. |
| Normocytic Anemia | (MCV 80–100 fL): Cells are of normal size, but the count is low. |
| Normocytic Anemia : Cause | Acute blood loss, Anemia of chronic disease (early stage), Aplastic anemia, and Chronic kidney disease. |
| Macrocytic Anemia | (MCV > 100 fL): Cells are larger than normal. |
| Anemia: Megaloblastic: | Often due to Vitamin B12 or Folate deficiency. |
| Anemia Non-megaloblastic: Causes | Causes include alcohol use, liver disease, and hypothyroidism. |
| valvular stenosis | Valvular stenosis is the narrowing, stiffening, or obstruction of a heart valve opening. |
| valvular stenosis: what happens when failure of valve to open? | This failure of the valve to open fully forces the heart chamber behind the valve to work harder to push blood through the narrowed opening, leading to increased pressure, hypertrophy of the heart muscle, and potentially heart failure. |
| what is the most common form of valvular heart disease? | Aortic stenosis |
| Aortic stenosis: description | Narrowing of the aortic valve opening, which obstructs blood flow from the left ventricle into the aorta during systole (heart contraction). |
| Aortic stenosis: Cause | Calcification of the valve leaflets (age-related degeneration) or congenital bicuspid valve. |
| Aortic stenosis:Classic Symptoms | The Triad of Syncope (fainting), Angina (chest pain), and Dyspnea (shortness of breath) on exertion |
| Primary Hypertension (Essential): Cause | No identifiable single cause; multifaceted interaction of genetics, environment, diet (high salt), obesity, stress, and lifestyle factors. |
| Secondary Hypertension Cause | Caused by an underlying identifiable medical condition or medication |
| Secondary Hypertension: examples of cause | Kidney disease (renal artery stenosis, chronic kidney disease), endocrine disorders (Cushing's syndrome, hyperthyroidism), sleep apnea, certain drugs. |
| Coronary artery disease risk | atherosclerosis of the heart arteries—are categorized as modifiable and non-modifiable: |
| Coronary artery disease:Modifiable: | Major/Controllable: Hyperlipidemia (high cholesterol, especially LDL), cigarette smoking, hypertension (high blood pressure), diabetes mellitus. Contributing: Obesity, physical inactivity, unhealthy diet, excessive alcohol consumption |
| Coronary artery disease:Non-Modifiable/Uncontrollable: | Age (risk increases with age). Sex (men typically at higher risk earlier in life). Family history/Genetics. |
| orthostatic hypotension | (or postural hypotension) is a sudden drop in blood pressure that occurs when a person quickly changes position, usually moving from lying down or sitting to standing up. |
| orthostatic hypotension:Mechanism: | Gravity causes blood to pool in the lower extremities. |
| orthostatic hypotension:Mechanism: | The normal body response is rapid vasoconstriction and increased heart rate to maintain cerebral perfusion. In orthostatic hypotension, this compensatory response is slow or inadequate, leading to lightheadedness, dizziness, or syncope (fainting). |
| orthostatic hypotension: Definition (clinical) | A drop in SBP of at least 20 mmHg or DBP of at least 10 mmHg within 3 minutes of standing. |
| Complicated hypertension involves sustained high blood pressure that results in target | Cardiovascular:Left ventricular hypertrophy (LVH), Angina pectoris, Myocardial infarction, Heart failure, Aneurysms (aortic dissection) |
| Complicated hypertension involves | Cerebrovascular:Stroke (ischemic or hemorrhagic), Transient ischemic attack (TIA), Hypertensive encephalopathy. |
| Complicated hypertension involve | Renal Nephrosclerosis, Chronic kidney disease, Renal failure. |
| Myocardial ischemia | occurs when the supply of oxygen and nutrients to the heart muscle (myocardium) is insufficient to meet its demands. |
| Myocardial ischemia : cause | Most often caused by atherosclerosis of the coronary arteries (CAD). |
| Myocardial ischemia Effect: | The heart muscle becomes hypoxic (oxygen-deprived), leading to reversible cell injury, accumulation of lactic acid, and clinical symptoms like angina pectoris (chest pain). |
| Myocardial ischemia Effect: | If blood flow is not restored, the ischemia progresses to irreversible cell death (myocardial infarction, or heart attack) |
| Hypoxemia | s low levels of oxygen in the arterial blood. The relationship between air getting into the lungs (ventilation, and blood flowing around the alveoli (perfusion is crucial |
| Hypoxemia | s a condition characterized by low levels of oxygen in the arterial blood (typically \(PaO_{2}<80\text{\ mmHg}\)). |
| Hypoxemia: common physiological | The most common physiological cause is ventilation-perfusion (\(V/Q\)) mismatch, where the balance between air reaching the alveoli (\(V\)) and blood reaching the capillaries (\(Q\)) is disrupted. |
| A low \(V/Q\) ratio occurs when | ventilation is decreased relative to blood flow. This is the primary driver of hypoxemia in many common lung diseases. |
| Low Ventilation-Perfusion Ratio (\(V/Q<0.8\)) : mechanism | Blood passes through areas of the lung that are not adequately refreshed with oxygen, resulting in poorly oxygenated blood returning to the heart. |
| Low Ventilation-Perfusion Ratio (\(V/Q<0.8\)): Common Causes: | Asthma, chronic bronchitis, and COPD, where narrowed airways limit airflowwhere blood bypasses ventilation entirely and does not respond well to supplemental oxygen. |
| Low Ventilation-Perfusion Ratio (\(V/Q<0.8\)): Common Causes: | Alveolar Filling: Pneumonia (pus/fluid), pulmonary edema (fluid from heart failure) |
| Low Ventilation-Perfusion Ratio (\(V/Q<0.8\)): Common Causes: | aspiration foreign objects.Extreme Case (Shunt): A \(V/Q\) of zero is called a shunt (e.g., complete alveolar collapse or ARDS), |
| High Ventilation-Perfusion Ratio (\(V/Q>0.8\)) | A high \(V/Q\) ratio occurs when perfusion is decreased relative to air intake. While these areas are well-ventilated, the lack of blood flow means oxygen cannot be picked up |
| High Ventilation-Perfusion Ratio (\(V/Q>0.8\)): Mechanism | this creates "dead space"—ventilation that is "wasted" because it doesn't participate in gas exchange |
| High Ventilation-Perfusion Ratio (\(V/Q>0.8\) : Common causes | Vascular Obstruction: Pulmonary embolism (blood clot) is the most common cause of a sudden increase in \(V/Q\), as it physically blocks blood flow to a section of the lung. |
| High Ventilation-Perfusion Ratio (\(V/Q>0.8\) : Common causes | Destruction of Capillaries: Emphysema, which destroys the alveolar walls and the capillaries within them. li and compress surrounding capillaries. |
| High Ventilation-Perfusion Ratio (\(V/Q>0.8\) : Common causes | Hemodynamic Factors: Low cardiac output, severe hypotension, or hypovolemia (low blood volume). |
| High Ventilation-Perfusion Ratio (\(V/Q>0.8\) | Mechanical Factors: Excessive Positive End-Expiratory Pressure (PEEP) during mechanical ventilation can over-distend alveoli |
| clubbing | is the painless, uniform, bulbous enlargement of the distal (far ends) segments of a digit (fingers or toes). The nail plate angle increases, and the nail bed becomes spongy. |
| Clubbing-is associated with chronic conditions causing hypoxemia, | Lung cancer Chronic obstructive pulmonary disease (COPD) - but not typically emphysema Cystic fibrosis Congenital heart disease (cyanotic types) Inflammatory bowel disease |
| Dyspnea | A subjective sensation of uncomfortable breathing or "shortness of breath." It is a common symptom of respiratory and heart disease. |
| Orthopnea: | Occurs when lying flat (supine position). The individual usually needs to sit up or use multiple pillows to breathe comfortably. It is a classic sign of left-sided heart failure (fluid shifting into the lungs when recumbent) or severe lung disease |
| Pathophysiology of cor pulmonale | Cor pulmonale is right-sided heart failure caused by pulmonary hypertension, which is in turn caused by diseases of the lung or pulmonary vasculature. |
| cor pulmonale: underlying lung disease | (e.g., severe COPD, cystic fibrosis) causes chronic hypoxia. This hypoxia leads to generalized pulmonary vasoconstriction (narrowing of blood vessels in the lungs), increasing resistance to blood flow. |
| what happens to the right ventricle with cor pulmonale? | The right ventricle of the heart must pump harder against this increased pressure, eventually hypertrophying |
| Lung cancer risk factors | Cigarette smoking (active and secondhand). Occupational exposures (asbestos, radon, arsenic). Genetics, older age, preexisting lung disease. |
| Lung cancer: Clinical Manifestations: | Symptoms often appear late in the disease: Persistent cough (most frequent symptom). Hemoptysis (coughing up blood). Chest pain, shortness of breath. Weight loss, fatigue, recurrent respiratory infections. Hoarseness (due to nerve involvement). |
| Pathophysiology of ARDS | Acute Respiratory Distress Syndrome (ARDS) is a severe, life-threatening inflammatory injury to the lungs, often following a primary insult like sepsis, pneumonia, or trauma. |
| Acute Respiratory Distress Syndrome Pathophysiology: | Widespread inflammation causes severe damage to the alveolar-capillary membrane. This increases permeability, allowing fluid, proteins, and inflammatory cells to leak into the alveoli (pulmonary edema that is non-cardiogenic). |
| Acute Respiratory Distress Syndrome Pathophysiology: | This influx inactivates surfactant, causing alveolar collapse (atelectasis), impaired gas exchange, and severe hypoxemia that is resistant to oxygen therapy |
| Chronic bronchitis | A type of COPD defined clinically as a productive cough that lasts for at least 3 months of the year for two consecutive years. |
| Chronic bronchitis Pathophysiology: | Chronic irritation (usually tobacco smoke) causes hypertrophy of mucus-producing glands in the bronchi, leading to excessive mucus production. |
| Chronic bronchitis Pathophysiology: What happens to bronchial walls? | The bronchial walls thicken, and cilia function is impaired. This leads to chronic airway obstruction, increased susceptibility to infection, and V/Q mismatching. Patients are |
| Deep vein thrombosis | Deep vein thrombosis (DVT) is the formation of a blood clot (thrombus) in a deep vein, most commonly in the legs or pelvis. The pathophysiology involves the factors of the Virchow triad |
| Deep vein thrombosis risk factors | Immobility (long flights, bed rest), surgery, trauma, cancer, pregnancy, hormonal therapy. |
| Deep vein thrombosis : major concerns | The thrombus can break loose and travel to the lungs, causing a pulmonary embolism (PE). |
| Pulmonary embolism | A pulmonary embolism (PE) is the blockage of a main artery in the lung or one of its branches by a substance that has traveled from elsewhere in the body (usually a DVT from the leg). |
| Pulmonary embolism Pathophysiology: | The blockage causes a high V/Q mismatch (dead space—see topic 25) because air can enter the affected lung segment, but blood cannot flow past the clot for gas exchange. This causes hypoxemia and can lead to pulmonary hypertension and right heart failure. |
| Hemoptysis | coughing up of blood or blood-tinged mucus from the respiratory tract (larynx, trachea, bronchi, or lungs). |
| Hemoptysis mucous ranges from? | It ranges from streaky sputum to massive hemorrhage. Causes include infections (bronchitis, tuberculosis, pneumonia), lung cancer, and pulmonary embolism. |
| Hemoptysis : Cause | infection with the bacterium Mycobacterium tuberculosis, an airborne pathogen. |
| Hemoptysis : Pathophysiology: | The bacteria multiply in the alveoli. The body's immune system usually walls off the infection, forming a granuloma (a Ghon focus) in the lung, leading to latent TB (asymptomatic, not contagious). |
| Hemoptysis : Pathophysiology: What happens when immune is compromised? | If the immune system is compromised, the bacteria can reactivate, destroying lung tissue, leading to active TB disease with symptoms like chronic cough, night sweats, fever, and weight loss. |
| Hypocapnia | there are abnormally low levels of carbon dioxide (CO |
| Hypocapnia : Cause | Cause: It is typically caused by hyperventilation (breathing too fast or too deep), which blows off excessive CO |
| Hyperventilation can be triggered by ? | anxiety, pain, hypoxemia, or a metabolic acidosis (e.g., diabetic ketoacidosis) where the body tries to compensate by increasing respiration. |
| Pneumothorax | presence of air or gas in the pleural space (the area between the lungs and the chest wall), which causes the lung to collapse, partially or fully. |
| Pneumothorax : Types-Spontaneous: | Occurs suddenly without injury, often due to rupture of small air sacs (blebs) on the lung surface. |
| Pneumothorax : Traumatic: | Caused by blunt or penetrating chest injury. |
| Pneumothorax : Tension: | A life-threatening emergency where air enters the pleural space but cannot escape, building up pressure that collapses the lung and pushes the heart and major blood vessels to the opposite side of the chest (mediastinal shift). |
| Flail chest | life-threatening injury that occurs when a segment of the chest wall is unstable and moves separately from the rest of the rib cage. |
| Flail Chest: Mechanism: | This results from multiple consecutive ribs being fractured in two or more places, or a fracture of the sternum combined with fractures of the adjacent ribs. |
| Flail Chest: Effect | During breathing, the flail segment moves paradoxically (sucks in during inhalation, pushes out during exhalation), which severely impairs ventilation and causes pain. |
| Empyema | accumulation of pus in the pleural cavity (the space surrounding the lungs). It is a type of complicated pleural effusion caused by an infection (usually bacterial pneumonia that spreads into the pleural space) |
| Empyema Treatment | Treatment requires antibiotics and drainage of the pus. |
| Adenocarcinoma | of malignant tumor originating in the glandular tissue or mucus-producing cells of an organ. |
| Adenocarcinoma : In the Lungs: | most common type of lung cancer, especially in non-smokers and women, typically found in the outer edges of the lungs. |
| Small cell lung carcinoma | Small cell lung carcinoma (SCLC) is a highly malignant type of lung cancer. |
| Small cell lung carcinoma Characteristics: I | It grows very rapidly, metastasizes early, and is strongly associated with cigarette smoking. It often arises near the center of the chest. |
| Small cell lung carcinoma : frequently cause: | It frequently causes paraneoplastic syndromes (e.g., SIADH, Cushing's syndrome) due to hormone secretion by the tumor cells. |
| Alveolar dead space | Alveolar dead space is the volume of air in alveoli that are ventilated but not perfused with blood. |
| Pulsus paradoxus | abnormally large decrease in systolic blood pressure (more than 10 mmHg) during inspiration (inhaling). |
| Pulsus paradoxus -Significance: | It is a key clinical sign of conditions that restrict the filling of the heart chambers, most notably cardiac tamponade (fluid accumulation around the heart), but also severe asthma or tension pneumothorax. |
| Restrictive versus obstructive lung disease -Obstructive | Obstructive Lung Disease Airflow out of the lungs is obstructed/slowed. |
| Restrictive versus obstructive lung disease -Restrictive | Restrictive Lung Disease Lung expansion is restricted; volume in the lungs is reduced. |
| Obstructive Lung Disease Mechanism | Narrowed airways, mucus, loss of elastic recoil. |
| Restrictive Lung Disease Mechanism | Stiff lungs, stiff chest wall, weak breathing muscles |
| Obstructive Lung Disease- examples | COPD (Emphysema, Chronic Bronchitis), Asthma, Cystic Fibrosis. |
| Restrictive Lung Disease-examples | Interstitial Lung Disease (Fibrosis), Sarcoidosis, Scoliosis, Neuromuscular diseases. |
| Define hydronephrosis: | swelling due to urine backup caused by an obstruction in the urinary tract: Dilation (swelling) of the ureter (the tube connecting the kidney to the bladder) due to blocked urine flow. |
| hydroureter | Hydronephrosis: Dilation&expansion of the renal pelvis &calyces (the central collecting structures) of the kidney, with accompanying parenchymal atrophy (tissue wasting) due to urine backup. |
| Ureterohydronephrosis: | swelling due to urine backup caused by an obstruction in the urinary tract: Dilation of both the ureter and the renal pelvis/calyces. |
| Postobstructive diuresis | A rapid and excessive production of urine (diuresis) that occurs after a long-standing urinary tract obstruction has been relieved (e.g., after removing a kidney stone or catheterizing a blocked bladder). |
| Postobstructive diuresis: concern | If not monitored closely, this massive fluid and electrolyte loss can cause dehydration, electrolyte imbalances, and potentially shock |
| Overactive bladder syndrome | urinary urgency usually accompanied by frequency (urinating often) and nocturia (waking up to urinate at night), with or without urgency urinary incontinence (leaking urine with urgency), in the absence of infection or other obvious pathology. |
| Neurogenic bladder | dysfunction (either failure to store urine or empty urine) caused by neurological damage/disease (spinal cord injury, multiple sclerosis, stroke, Parkinson's disease, diabetes neuropathy). proper signaling between the bladder and the brain. |
| Neurogenic bladder: What happens if the nerves that control the bladder are impaired? | The nerves that control bladder function are impaired, preventing proper signaling between the bladder and the brain. |
| Cystitis | inflammation of the bladder, most commonly caused by a bacterial urinary tract infection (UTI). Symptoms typically include urinary frequency, urgency, dysuria (painful urination), and possibly suprapubic pain. |
| Urinary Tract Infection (UTI) | Bacteria entering the urinary tract via the urethra. The primary pathogen is Escherichia coli (E. coli), accounting for 75-90% of UTIs. Other causes include Klebsiella, Proteus, and Staphylococcus |
| UTI Diagnosis | Urinalysis (checks for leukocytes, nitrites, blood), urine culture (identifies specific bacteria and antibiotic sensitivity). |
| UTI Treatment | Antibiotics (e.g., Trimethoprim-sulfamethoxazole, Nitrofurantoin, Ciprofloxacin) |
| Pyelonephritis | bacterial infection of the kidney (renal pelvis, calyces, and medulla). |
| Acute Pyelonephritis | Sudden, active infection, often ascending from lower UTI. Fever, chills, flank pain (CVA tenderness), UTI symptoms (dysuria, urgency). |
| Chronic Pyelonephritis | Persistent/recurrent infections leading to progressive renal scarring/fibrosis. May be asymptomatic or have vague symptoms, often leads to kidney failure over time. |
| Glomerulonephritis | inflammation of the glomeruli (the kidney's filtering units). This damage causes the filters to become leaky, allowing protein and blood to pass into the urine. |
| Glomerulonephritis cause: | Often an autoimmune reaction or post-infectious response (e.g., post-streptococcal glomerulonephritis) |
| Glomerulonephritis Manifestations | Hematuria (blood in urine), proteinuria (protein in urine), hypertension, edema (swelling), and potentially kidney failure. |
| Kidney stones | nephrolithiasis, renal calculi) are masses of crystals, protein, or other substances that form in the kidney and may obstruct the urinary tract |
| Types of kidney stones: | Calcium oxalate (most common), magnesium ammonium phosphate (struvite, associated with UTIs), uric acid, and cystine |
| Kidney stone :Symptoms | Classic symptom is excruciating flank pain (renal colic) that radiates to the groin, nausea, vomiting, hematuria |
| Primary Amenorrhea | Failure to begin menstruation by age 15 (with normal growth) or by age 13 (with absence of secondary sexual characteristics) |
| Secondary Amenorrhea | The cessation of menstruation for 3 months or more in a woman who has previously menstruate |
| Primary Amenorrhea: causes | Chromosomal abnormalities (Turner syndrome), congenital structural defects, endocrine disorders |
| Secondary Amenorrhea: causes | Pregnancy (most common cause), hormonal imbalances (PCOS), stress, excessive exercise, significant weight loss, menopause |
| Risk factors for endometrial cancer | Obesity (adipose tissue converts hormones into estrogen). Early menarche &late menopause.;Nulliparity (never having given birth).;Use of unopposed estrogen therapy (w/o progesterone).Fam hx: DM, Lynch syndrome (hereditary cancer syndrome) |
| Prostate cancer - major risk factors | Risk increases sharply after age 50. Race: Higher incidence & mortality in Blk men. Fam Hx: Having a first-degree relative w/prostate CA doubles the risk. Genetics: Presence of BRCA1/BRCA2 mutations. Diet/Lifestyle (possibly high red meat/fat diet). |
| Polycystic Ovarian Syndrome | complex endocrine disorder characterized by three key features (requires at least two for diagnosis) |
| Polycystic Ovarian Syndrome -key features | Oligo- or Anovulation: Infrequent or absent ovulation/periods. |
| Polycystic Ovarian Syndrome (PCOS) | Hyperandrogenism: High levels of male hormones (androgens), leading to hirsutism (excess hair growth), acne, and male-pattern baldness. |
| Polycystic Ovarian Syndrome | Polycystic Ovaries: Ovaries containing many small follicles/cysts seen on ultrasound. |
| Polycystic Ovarian Syndrome Pathophysiology | COS is strongly associated with insulin resistance and obesity. |
| Precocious Puberty | Onset of puberty earlier than normal (before age 8 in girls; before age 9 in boys). |
| Precocious Puberty: Cause | Central (hypothalamic/pituitary activation is early), or Peripheral (hormone production outside normal pathway, e.g., tumor) |
| Delayed Puberty | Absence of puberty signs by age 13 in girls (no breast buds) or age 14 in boys (no testicular enlargement) |
| Delayed Puberty cause | Often functional delay (genetics), chronic illness, malnutrition, or endocrine disorders (hypogonadism) |
| Hydrocele | A collection of serous fluid in the tunica vaginalis (the sac surrounding the testes), causing painless swelling of the scrotum. Common in newborns, often goes away on its own |
| Spermatocele | A benign, painless cyst or mass that forms in the epididymis (the coiled tube on top of the testicle) and contains a milky fluid and sperm |
| Varicocele | An enlargement of the veins within the loose bag of skin (pampiniform plexus) that holds the testicles (looks like a "bag of worms"). Often on the left side and a common cause of male infertility |
| Galactorrhea | inappropriate production & spontaneous flow of breast milk (milk discharge) in individuals who are not preg/breastfeeding. Caused by excessive prolactin levels (hyperprolactinemia), often d/t pituitary tumors, meds, or endo disorders like hypothyroidism. |
| Adenomyosis | where the endometrial tissue (lining of the uterus) grows into the myometrium (muscular wall of the uterus). causes the uterus to become enlarged, tender, and boggy. It results in painful periods (dysmenorrhea) and heavy menstrual bleeding (menorrhagia |
| Leiomyoma | benign tumors of the smooth muscle of the myometrium (uterine wall). They are extremely common. Symptoms vary depending on size and location and can include heavy bleeding, pelvic pain, pressure on the bladder/bowel, and infertility issues. |
| Endometrial polyps | benign, hyperplastic growths of the endometrial lining that project into the uterine cavity. They are often associated with abnormal uterine bleeding or intermenstrual spotting. |
| Endometriosis | where endometrial tissue (glandular and stromal tissue similar to the uterine lining) is found outside of the uterus, most commonly on the ovaries, fallopian tubes, and pelvic ligaments |
| Endometriosis : Pathophysiology | ectopic tissue responds to hormonal cycles by growing and bleeding each month, causing inflammation, pain, scarring, adhesion formation, and potentially infertility. |
| Gynecomastia | enlargement of breast tissue in males d/t an imbalance of hormones (more estrogen relative to androgen activity). It can be physiological (newborns, puberty, older age) pathological (meds, liver disease, kidney disease, endo disorders, testicular cancer |
| Balanitis | inflammation of the glans penis (the head of the penis). It is typically caused by poor hygiene in uncircumcised men, leading to bacterial or fungal (e.g., Candida albicans) infections, often associated with diabetes |
| Cryptorchidism | condition of having one/both testicles undescended (remaining in the abd or inguinal canal instead of descending into the scrotum) at birth. |
| Cryptorchidism -if untreated | If untreated, it increases the risk of testicular cancer and infertility d/t the higher temperature outside the scrotum |
| Phimosis | uncircumcised males where the foreskin (prepuce) is too tight and cannot be retracted back over the glans penis. It can be congenital (normal in infancy) or pathological (due to scarring from infection or poor hygiene). |
| Pancreatitis | inflammation of the pancreas. |
| Pancreatitis Acute Pathophysiology | gallstones or alcohol abuse. The obstruction or injury leads to the premature activation of digestive enzymes within the pancreas itself. These activated enzymes begin to autodigest the pancreatic tissue, causing severe inflammation, necrosis, and pain. |
| Chronic pancreatitis | progressive and permanent destruction of the pancreas by fibrotic tissue, resulting in irreversible impairment of both endocrine function (diabetes) and exocrine function (malabsorption). It is most commonly caused by chronic alcohol abuse. |
| Small bowel obstruction | partial or complete blockage of the small intestine. |
| Small bowel obstruction Common Causes: | Adhesions (scar tissue from previous surgery), hernias, tumors, or inflammation |
| Small bowel obstruction :Effect | Prevents the normal flow of digested contents, fluids, and gas, leading to distension, pain, vomiting, and dehydration |
| Paralytic ileus | (or adynamic ileus) is the functional obstruction of the intestine caused by the failure of intestinal motility (peristalsis) rather than a physical blockage |
| Paralytic ileus :Causes: | Common after abdominal surgery, electrolyte imbalances (especially low potassium), peritonitis, or certain medications (opioids). The bowel simply stops moving temporarily. |
| Peptic ulcer disease | involves breaks or ulcerations in the protective mucosal lining of the lower esophagus, stomach, or duodenum (first part of the small intestine) |
| Peptic ulcer disease :Cause: | An imbalance between factors that damage the mucosa and factors that protect it. Major causes are infection by Helicobacter pylori (H. pylori) bacteria and use of Nonsteroidal Anti-inflammatory Drugs (NSAIDs). Acid and pepsin contribute to the damage. |
| Constipation | having infrequent or difficult bowel movements, characterized by small, hard stools, straining, or a sensation of incomplete evacuation. It is often caused by low fiber diet, inadequate fluid intake, immobility, medications, or underlying diseases. |
| Crohn Disease-Location | Any part of GI tract (mouth to anus); most often small intestine/colon. |
| Crohn Disease-Pattern | "Skip lesions" (healthy tissue interspersed with diseased areas) |
| Crohn Disease-depth- | Transmural (affects all layers of bowel wall). |
| Crohn Disease- Key Feature | "Cobblestone" appearance, strictures, fistulas, anal lesions common. |
| Ulcerative Colitis (UC) | Location: Only in the Colon/Large Intestine (starts rectum, moves upward) |
| Ulcerative Colitis (UC)-pattern | Continuous inflammation |
| Ulcerative Colitis (UC)-depth | Mucosal and submucosal only (superficial) |
| Ulcerative Colitis (UC) key feature | Pseudopolyps, bloody diarrhea common |
| Portal hypertension | abnormally high blood pressure in the portal venous system (the network of veins that carry blood from the digestive organs to the liver). |
| Portal hypertension Cause | Most commonly caused by liver cirrhosis (scarring). The scarred liver obstructs blood flow, increasing pressure in the portal system. |
| Portal hypertension effect | Leads to complications like esophageal varices (enlarged veins in the esophagus that can bleed dangerously), ascites (fluid in the abdomen), and hepatic encephalopathy (brain dysfunction due to toxin buildup) |
| Types of abdominal pain | parietal, visceral, and referred |
| Visceral | vague, dull, or aching pain; poorly localized. Stems from stretching or distending internal organs |
| Visceral location | Midline (epigastric, periumbilical, suprapubic), corresponds to embryonic origin of organ |
| Parietal | Sharp, intense, localized pain. Stems from inflammation of the parietal peritoneum (lining of the abdominal cavity) |
| Parietal Location | Directly over the inflamed organ/area; sharp and worsens with movement/coughing |
| Referred pain | Pain felt in an area distant from the origin of the stimulus but supplied by the same spinal segment |
| Referred pain location | Gallbladder pain felt in right shoulder; Pancreatitis pain radiating to the back |
| Liver cirrhosis | rreversible end stage of chronic liver disease (e.g., chronic hepatitis C, alcohol abuse, non-alcoholic fatty liver disease). |
| Liver cirrhosis | Healthy liver tissue gradually replaced by diffuse fibrosis tiss& regenerative nodules. mpairs bld flow (causing portal hypertension) & prevents the liver frm performing its vital metabolic, detoxification, & synthetic fx, leading to liver failure. |
| Colorectal cancer | arises in the colon or rectum |
| Colorectal cancer Risk Factors | Age (>50), fam hx, genetics (Lynch syndrome, FAP), inflammatory bowel disease (UC/Crohn's), diet (high red/processed meat, low fiber), obesity, smoking, alcohol. Most often starts as benign polyps (adenomatous polyps) that become malignant over time. |
| Colorectal cancer risk factors | starts as benign polyps (adenomatous polyps) that become malignant over time. |
| GERD | stomach acid and contents frequently flow back up into the esophagus (acid reflux). |
| GERD cause: | Incompetence or weakening of the lower esophageal sphincter (LES), the valve between the esophagus and stomach. |
| GERD Symptoms | Heartburn, regurgitation of sour fluid, chest pain, difficulty swallowing. Chronic GERD can lead to esophagitis, strictures, or Barrett's esophagus (a precancerous condition) |
| Fracture-Open (Compound) | The bone breaks through the skin. |
| Closed fracture (Simple): | The bone breaks, but the skin remains intact. |
| Complete fracture | Bone fragments separate completely |
| Incomplete fracture("Greenstick") | Bone is bent but only partially broken (common in children). |
| Displaced fracture: | Bone fragments are misaligned |
| Non-displaced fracture | Bone fragments remain in alignment. |
| Specific Patterns fractures | Transverse (straight across), Oblique (angled), Spiral (twisting), Comminuted (multiple fragments/shattered), Compression (crushed, e.g., in vertebrae). |
| Osteoporosis | a skeletal disease characterized by decreased bone mineral density (BMD) and deterioration of bone microstructure, making the bones weak and fragile, leading to an increased risk of fractures (especially hip, spine, wrist). |
| Osteoporosis pathophysiology | Bone resorption (breakdown by osteoclasts) exceeds bone formation (building by osteoblasts), resulting in porous bone. |
| Osteomyelitis | infection of the bone |
| Osteomyelitis Cause: | ften caused by bacteria (most commonly Staphylococcus aureus), which reaches the bone via the bloodstream (hematogenous) or direct contamination (trauma, surgery, adjacent soft tissue infection). |
| Osteomyelitis Effect: | the infection causes inflammation, bone destruction, and the formation of sequestra (dead bone fragments) |
| Duchenne (DMD) | Early childhood (3-5 years), X-linked recessive Rapid progression, muscle weakness, inability to walk by age 12, heart/respiratory muscle failure (fatal). |
| Myotonic | Adolescence/adulthood Autosomal dominant "Myotonia" (difficulty relaxing muscles), weakness in face/limbs, cataracts, cardiac issues, endocrine problems. |
| Facioscapulohumeral (FSHD) | Childhood/early adulthood Autosomal dominant Progressive weakness in face (cannot whistle/close eyes tightly), shoulders (scapular winging), and upper arms. |
| Gout | painful type of inflammatory arthritis caused by hyperuricemia (elevated levels of uric acid in the blood). |
| Gout Pathophysiology | Uric acid crystallizes and deposits as monosodium urate crystals in joints (most commonly the big toe), causing acute, severe inflammatory attacks (gout flares) |
| Rhabdomyolysis | rapid breakdown of damaged skeletal muscle tissue, releasing large amounts of intracellular contents into the bloodstream |
| Rhabdomyolysis Released substances | Myoglobin (a muscle protein), potassium, and creatinine kinase (CK). |
| Rhabdomyolysis Danger: | Myoglobin is toxic to the kidneys and can cause acute kidney injury (AKI) or failure. Causes include severe trauma, extreme exertion, certain medications (statins), or prolonged immobility |
| Compartment syndrome | Compartment syndrome is a painful and dangerous condition caused by increased pressure within a confined muscle compartment (usually in the lower leg or forearm). |
| Compartment syndrome Pathophysiology | The fascia (tough connective tissue) surrounding the muscles doesnt stretch. Injury/inflammation causes swelling&edema w/in the compartment. The pressure becomes high enough to impede blood flow (ischemia) &nerve fx, leading to tissue necrosis if not trea |
| Osteomalacia | softening of the bones in adults due to inadequate mineralization of the bone matrix. |
| Osteomalacia Cause: | Usually a deficiency of Vitamin D (which is needed for calcium absorption) or resistance to Vitamin D action. The equivalent condition in children is called rickets |
| Rheumatoid arthritis | chronic, systemic autoimmune disease that primarily causes inflammation and damage to the joints. |
| Rheumatoid arthritis Pathophysiology | The immune system mistakenly attacks the synovium (the lining of the joints), causing persistent inflammation, swelling, &eventual erosion of cartilage &bone, leading to joint deformity & functional impairment. It is often symmetrical |
| Osteoarthritis | most common form of arthritis, characterized by the breakdown and eventual loss of cartilage in one or more joints. |
| Osteoarthritis Pathophysiology | degenerative "wear-and-tear" disease, often related to age, obesity&joint injury. , pain, stiffness&reduced ROM.Unlike RA, typically asymmetrical ¬ systemic (no "B" sxs. |
| Osteoarthritis Pathophysiology-what happens to the cartilage surface? | The cartilage surface becomes rough &wears away, leading to bone rubbing on bone, inflammation |
| A nurse is reviewing a new dx of Acute Myeloid Leukemia. Which characteristic best describes this type of cancer?A. involves mature bld cells&progresses slowly over years.B. It involves immature bld cells &req immediate, aggressive tx.C. primarily affects | B. It involves immature blood cells and requires immediate, aggressive treatment. |
| Leukemia is classified as | acute or chronic |
| A patient has a thrombosis. While reviewing the history, the nurse found the patient has atherosclerosis. To which component of the Virchow triad does the atherosclerosis correlate? | Endothelial injury. Endothelial injury to blood vessels can result from atherosclerosis (plaque deposits on arterial walls). |
| Hypersplenism occurs when: | the spleen is overactive |
| The best treatment for multiple myeloma | chemotherapy |
| What type of cell is most affected by acute leukemia? | blast cell |
| You observe a platelet count of 9,000/mm3, which condition must you monitor for in this patient? | spontaneous bleeding |
| Which symptoms should you assess for in a patient with Hodgkin's lymphoma? | Night sweats, low-grade fevers, and weight loss |
| A patient has lymphoblastic lymphoma. Which organ is most affected? | Thymus-The disease arises from a clone of relatively immature T cells that becomes malignant in the thymus. |
| A patient has multiple myeloma. Which area in the body does the nurse closely monitor for the tumor masses? | bones |
| A patient has acquired immunodeficiency syndrome (AIDS). Which laboratory report should the nurse monitor closely in this patient? | Lymphocyte counts-Lymphocytopenia is a major problem in acquired immunodeficiency syndrome (AIDS). |
| Aortic stenosis results in the incomplete emptying of the: | Left ventricle Blood from the left ventricle is pumped through the aortic valve into the aorta. Aortic stenosis results in the incomplete emptying of the left ventricle |
| One complication of sustained hypertension is | heart attack or stroke. |
| A middle-aged patient has a tumor that infiltrates trabeculae in spongy bone. Which diagnosis will the nurse observe documented on the chart?a. Chondrosarcoma b. Leukemia c. Lymphoma d. Osteosarcoma | a. Chondrosarcoma |
| If a patient with diabetes has advanced glycosylation end products (AGEs), what does the nurse suspect is happening in the patient's body? a. Increased ketone formation b. Tissue/cellular injury c. Dawn phenomenon d. Reduction of chronic complications | b. Tissue/cellular injury |
| A patient has a cystocele. What other condition should the nurse assess for in this patient? a. Stress incontinence b. Significant problems defecating c. The descent of the rectum into the vaginal canal d. Infertility | a. Stress incontinence |
| A patient has a fracture that broke into several fragments. Which type of fracture did the patient sustain? a. Comminuted b. Open c. Greenstick d. Occult | a. Comminuted |
| A patient has atherosclerosis. Which factor associated with endothelial injury will the nurse observe written in the history? a. Anemia b. Autoimmunity c. BP 110/70 d. Nonsmoker | b. Autoimmunity |
| A patient has heparin-induced thrombocytopenia (HIT). Which condition is a priority to assess? a. Pulmonary infarction b. Pulmonary hypertension c. Pulmonary edema d. Pulmonary embolism | d. Pulmonary embolism |
| A patient has a recent spinal cord injury. Which term should the nurse use to describe the loss of reflex function below the level of injury/lesion? a. Autonomic hyperreflexia b. Spinal shock c. Degenerative disk disease d. Low back pain | b. Spinal shock |
| The most important risk factor in the development of prostate cancer is: a. older age. b. smoking. c. low-fat diet. d. urethral stricture. | a. older age. |
| A patient with HIV has painful burning dysesthesias and paresthesias,in the extremities. What condition will the nurse see documented in the chart? a. CNS neoplasms b. HIV neuropathy c. HIV-associated dementia/cognitive disorders d. Opportunistic in | b. HIV neuropathy |
| A patient has pleuritic chest pain, shortness of breath, and hemoptysis. The pcp suspects a pulmonary embolus. Which laboratory test should the nurse check to help confirm this diagnosis?a. D-dimer levels b. RBC c. Potassium levels d. IgE count | a. D-dimer levels |
| A patient has acute leukemia. A nurse recalls the cell most affected by this disease is a: a. mature cell. b. blast cell. c. differentiated cell. d. hypochromic cell. | b. blast cell. |
| A nurse is describing the pathophysiology of duodenal ulcers. Which information shouldthe nurse include? a. Chronic inflammation inhibits the proton pumps in the gastric lining to decreased acid levels. b. The presence of bacteria in the stomach causes th | c. H. pylori |
Created by:
Charm Trinidad