• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/210

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

210 Cards in this Set

  • Front
  • Back
Acute Pericarditis
Inflammation of the pericardium lasting around 2 weeks
Chronic Pericarditis
Long term inflammation of the pericardium
Effusion
Increase in fluid in the pericardial space
Coronary Artery Disease
Impairment of coronary blood flow
Myocardial Infarction
Interruption of cardiac flow
Chronic Ischemic Heart Disease
Reduced blood supply to the heart muscle
Cardiomyopathy
A mechanical or electrical dysfunction of the heart
Hypertrophic Cardiomyopathy
Enlargement in muscle mass of the left ventricle
Arrhythmogenic Right Ventricular Cardiomyopathy
Replacement of myocytes with fatty tissue in the right ventricle
Left Ventricular Noncompaction
Enlargement due to problems with embryonic development
Ion Channelopathy
Dysfunction caused by an ion channel mutation
Dilated Cardiomyopathy
Enlargement and stretching of the heart
Restricted Cardiomyopathy
Decreased ventricular filling due to rigidity or noncompliance
Myocarditis
Acquired inflammation of the heart
Infective Endocarditis
Inflammation of the inner heart lining or valves caused by microbial colonization
Rheumatic Heart Disease
Damage caused by antigenic mimicry
Mitral Valve Stenosis
Failure of mitral valve leaflets to open properly
Mitral Valve Regurgitation
Incomplete closure of the mitral valve
Mitral Valve Prolapse
Displacement of thickened mitral leaflet into left atrium during systole
Aortic Valve Stenosis
Incomplete opening of the aortic valve
Aortic Valve Regurgitation
Incomplete closing of the aortic valve
Stable Angina
Fixed obstruction that causes deficits to metabolic demands
Variant Angina
Ischemic damage occurs during rest
Silent Ischemia
Ischemia in the absense of angina
Dysphagia
Difficulty or pain during swallowing
Hernia
Protrusion of tissue through a muscular wall
Gastroesophageal Reflux Disease
Backward movement of gastric contents into esophagus
Esophageal Cancer
Carcinoma of the esophagus
Acute Gastritis
Inflammation of the gastric mucosa
Peptic Ulcer
Ulcer affecting one or all layers of the stomach or duodenum
Gastric Carcinoma
Stomach cancer
Irritable Bowel Syndrome
Chronic and recurrent intestinal symptoms unexplained by structural or biochemical properties
Ulcerative Colitis
Nonspecific inflammatory condition of the colon
Chron's Disease
Recurrent granulomatous inflammation affecting the GI tract
Infectious Enterocolitis
Inflammation of the small intestine and colon caused by a microbial agent
Diverticulitis
Mucosal layer of colon herniates through muscularis layer
Appendicitis
Appendix becomes inflammed, swollen and gangrenous
Acute Diarrhea
Excessively frequent passage of stools for less than 2 weeks
Chronic Diarrhea
Excessvely frequent passage of stools for 3 to 4 weeks
Constipation
Infrequent or difficult passage of stools
Fecal Impaction
Retention of hardened stools in the colon and rectum
Peritonitis
Inflammation of the membrane lining the abdominal cavity
Steatorrhea
Inability to absorb fats
Celiac Disease
Immune disorder triggered by the ingestion of gluten
Adenomatous Polyps
Benign neoplasms of the intestinal epithelium
Colorectal Cancer
Cancer of the colon and rectum
Cholestasis
A decrease in bile flow
Jaundice
High levels of bilirubin in blood
Drug Induced Hepatic Disease
Liver damage caused by drugs and environmental chemicals
Acute Hepatitis
Short term inflammation of the liver
Chronic Hepatitis
Long term inflammation of the liver (more than 3 months)
Biliary Cirrhosis
Replacement of bile ducts with fibrous scar tissue
Ethanol Hepatic Disease
Liver damage caused by excessive alcohol consumption
Cirrhosis
Replacement of functioning liver with fibrous scar tissue
Portal Hypertension
Sustained portal vein pressure above 12 mm Hg
Hepatocellular Carcinoma
Cancer of liver cells
Cholangiocarcinoma
Cancer of the epithelial cells that line the bile ducts
Metastatic Tumors
Spreading of tumors to the liver
Cholelithiasis
Precipitation of substances found in the bile (gall stones)
Cholecystitis
Inflammation of the gall bladder
Choledocholithiasis
Stones in the common bile duct
Cholangitis
Inflammation of the common bile duct
Acute Pancreatitis
Reversible autodigestion of pancreatic tissue by activated enzymes
Chronic Pancreatitis
Progressive destruction of the exocrine and endocrine pancreas
Pancreatic Cancer
Cancer of the acinar cells in the exocrine pancreas
Neutropenia
Abnormally low number of neutrophils
Infectious Mononucleosis
Self limiting viral infection that causes an increase in leukocytes
Non-Hodgkin Lymphomas
Group of cancers that arise in multiple nodes and spread to various tissues
Hodgkin Lymphomas
Group of cancers that arise in a single node and then spread to neighboring nodes
Acute Leukemias
Cancers of hematopoietic progenitor cells
Chronic Leukemias
Cancers of more fully differentiated myeloid and lymphoid cells
Leukostasis
White blood cell counts increase to where blood flow is affected
Multiple Myeloma
Proliferation of malignant plasma cells in bone marrow
Transient Hypoglobulinemia
Immune cells cannot undergo class switching
X-Linked Hypogammaglobulinemia
Pre B cells cannot differentiate into mature B cells
Common Variable Immunodeficiency
Plasma cells cannot be generated
IgG Subclass Deficiency
Cannot differentiate into IgG subclasses
DiGeorge Syndrome
Failure of the thymus to develop
X-Linked Immunodeficiency with Hyper IgM
Low IgG & IgA
High IgM
Combined Immunodeficiency Disorder
Low T cell function
Severe Combined Immunodeficiency Disorder (SCIDs)
Absent T cell function
Complement Dysfunction
Absence or alterations in complement proteins
Chronic Granulomatous Disease
Failure of phagocytes to produce respiratory burst
Chediak-Higashi Syndrome
Neutrophils cannot degranulate
Host vs Graft
Host immune system rejects graft organ
Graft vs Host
Graft organ rejects host environment
Hypercholesterolemia
Presence of high levels of cholesterol in the blood
Atherosclerosis
Formation of fibrofatty lesions in the lining of the large arteries due to cholesterol
Small Vessel Vasculitis
Inflammatory injury and necrosis of small vessels
Medium Vessel Vasculitis (Polyarteritis Nodosa)
Inflammation of medium vessels
Large Vessel Vasculitis (Giant Cell)
Inflammation of large vessels
Acute Arteriole Occlusion
Interruption of arteriole flow
Atherosclerotic Occlusive Disease
Vessel occlusion caused by atherosclerotic plaques
Thromboangiitis Obliterans (Buerger Disease)
Inflammatory inflammatory disease causing thrombus formation
Raynaud's Disease
Arteriole occlusion of the digits
Aneurysm
Abnormal localized dilation of a blood vessel
Aortic Dissection
Rupture of arteriole wall forming a blood pocket
Vericose Veins
Impairment of venous blood flow
Chronic Venous Insufficiency
Long term impairment of venous blood flow
Venous Thrombosis
Presence of a thrombus in a vein that causes an inflammatory response
Primary Hypertension
High blood pressure with no identifiable cause
Secondary Hypertension
High blood pressure due to another disease or condition
Orthostatic Hypotension
Low blood pressure associated with a change in body position
Erythropoiesis
The production of red blood cells
Erythropoietin
Preceursor for RBC that is released from the liver and kidneys in response to low oxygen levels
Unconjugated bilirubin
Plasma insoluble product that results from indirect bilirubin degradation
Conjugated bilirubin
Plasma soluble product made by the liver that is attached to a gluconuride
Right shift on a hemoglobin binding curve
Decrease in pH
Increase in temperature
Increase in 2,3DPG
Left shift on a hemoglobin binding curve
Increase in pH
Decrease in temperature
Decrease in 2,3DPG
Mean corpuscular volume
Reflects the volume or size of the red blood cells

Decreases in microcytic anemia

Increases in macrocytic anemia
Mean corpuscular hemoglobin concentration
Reflects the concentration of hemoglobin in eaach cell

Hypochromic: lightly colored
Normochromic: normal colored
Anemia
A decrease in red blood cells or a decrease in hemoglobin

Manifestations: dyspnea, angina, cramps, pallow, heart failure and tachycardia
Acute Blood Loss Anemia
Bleeding due to trauma

Cells are normocytic and normochromic
Chronic Blood Loss Anemia
Slow blood loss over a long period of time

Cells are microcytic and hypochromic
Hemolytic Anemia
Premature destruction of red blood cells

Cells are normocytic and normochromic
Spherocytosis
Inherited hemolytic anemia caused by a mishaped RBC membrane (marble shaped instead of bioconcave)
Sickle Cell Anemia
Inherited hemolytic anemia caused by a glutamate to valine amino acid change

*More prevalent in African American populations
Thalacemia
Inherited hemolytic anemia caused by deficient synthesis of the hemoglobin alpha or beta chains

*More prevalent in Mediterannean populations
Reacting Antibodies Anemia
Acquired anemia

Warm (IgG max 37 degrees)
Cold (IgM max 4 degrees)
Iron Deficiency Anemia
Decreased formation of hemoglobin limits RBC formation

Cells are microcytic and hypochromic

Pica: desire to eat dirt
Megaloblastic Anemia
Vitamin B12 or folic acid deficiency
Aplastic Anemia
Stem cell disorder that results in a reduction of all three hematopoietic cell lines

Causes: neoplasia, chemical, infection or idiopathic
Chronic Disease Anemias
Anemia that occurs as a result of chronic infections, inflammation or cancer
Polycythemia
A high total red blood cell mass
Relative Polycythemia
A rise in hematocrit due to a loss of plasma volume
Absolute Polycythemia
A rise in hematocrit due to an increase in total red blood cell mass
Primary Polycythemia (Polycythemia Vera)
Neoplastic disease characterized by an absolute increase in RBC, WBC and platelet counts

Patients have thick blood

Treatment is bleeding
Secondary Polycythemia
An increase in the level of erythropoetin accompanied by a compensatory response to hypoxia
Acute Inflammation
Early reaction of local tissues and their blood vessels to injury
Cardinal Signs of Inflammation
Rubor (redness)
Calor (heat)
Tumor (swelling)
Dolor (pain)
Function laesa (loss of function)
Two Phases of Inflammation
1. Vascular: changes in small blood vessels at the site of injury

2. Cellular: changes in the lining of vasculature and movement of phagocytic cells into the area of injury of infection
Stages of Cellular Inflammation
1. Margination
2. Transmigration
3. Chemotaxis
4. Phagocytosis
Erythrocyte Segmentation Rate (ESR)
Looks at how much time is takes for erythrocytes to fall out of solution in a column

The faster they fall the more likely there is a problem
Serous Exudate
Watery fluids low in protein content (ex: water blister)
Hemorrhagic Exudate
Result of severe tissue injury that damages blood vessels (ex: blood blister)
Fibrinous Exudate
Contains large amounts of fibrinogen and forms a thick and sticky meshwork (seen in internal organs)
Membranous Exudate
Necrotic cells located on mucous membranes
Purulnt
Contains pus
Ulceration
Site of inflammation where an epithelial surface has become necrotic and eroded
Chronic Inflammation
Self perpetuating inflammation that may last for weeks, months or even years

Involves proliferation of fibroblasts instead of exudates
Nonspecific Chronic Inflammation
Diffuse accumulation of macrophages and lymphocytes at the site of injury
Granulomatous Chronic Inflammation
Confined mass of macrophages surrounded by lymphocytes
Systemic Manifestations of Inflammation
Increased ESR
Increased fibrinogen
Increased C reactive protein
Leukocytosis/Leukopenia
Muscle catabolism
Fever
Anorexia
Malaise
Parenchymal Tissue
Contains the functioning cells of an organ or body part
Stromal Tissue
Consists of supporting connective tissues, blood vessels extracellular matrix and nerve fibers
Tissue Regeneration
Replacement of injured tissue with functional tissue
Labile Cells
Cells continue to divide and replicate until death
Stable Cells
Cells stop dividing once growth ceases
Permanent Cells
Cells are unable to undergo mitotic division
Tissue Repair
Replacement of nonfunctional cells with connective tissue
Granulation Tissue
Bright red and moist connective tissue that contains newly formed capillaries, fibroblasts and residual inflammatory cells
Primary Intention
No tissue is lost
Secondary Intention
Tissue is lost
Phases of Wound Healing
1. Inflammatory: occurs at the time of injury and prepares the tissue for healing

2. Proliferative: focus is on building new tissue to fill the wound space

3. Remodeling: architecture of scar is reorientated to increase the strength of the wound
Keloids
Tumor like masses caused by excessive production of scar tissue that are produced during remodeling
Proud Flesh
Occurs when a wound keeps getting reopened while trying to heal
Factors that Influence Wound Healing
Malnutrition
Blood Flow
Oxygen Delivery
Infections
Medical Comorbidities
Hemostasis
Stoppage of blood flow
Stages of Hemostasis
1. Vessel spasm
2. Formation of platelet plug
3. Blood coagulation
4. Clot retraction
5. Clot dissolution
Antithrombin III
Anticoagulant that inactivates coagulation factors and neutralizes thrombin
Protein C
Anticoagulant that inactivates factors 5 and 8
Protein S
Anticoagulant that accelerates the action of protein C
Warfarin
Anticoagulant that decreases prothrombin and other procoagulation factors
Heparin
Anticoagulant that increases tha ability of antithrombin III to inactivate thrombin
Hemophilia A
Associated with a decrease in factor 8
Hemophilia B
Associated with a decrease in factor 9
Thrombocytosis
Increase in platelet count above 1,000,000/microliter

Primary: caused by bone marrow disorders

Secondary: caused by disease states
Inherited Hypercoagulation
Mutant factor 5a cannot be inactivated by protein C (affects 2 to 15% whites)
Acquired Hypercoagulation
Caused by prolonged immobility, MI, cancer, hyperestrogenic states, oral contraceptives, obesity, smoking, lupus and endothelial damage
Petechia
A pinpoint red or purple spot containing blood that appears in the skin or mucous membranes
Ecchymosis
Ruptured blood vessels marked by a livid black and blue or purple spot
Purpura
Patches of purple skin discolorations resulting from extravasation of blood into the skin and mucous membranes (bruise)
Hematoma
Clotted blood that forms in a tissue or organ (large bruise)
Thrombocytopenia
A decrease in platelet number less than 100,000/uL
Immune Thrombocytopenic Purpura
Excess destruction of platelets
Thrombotic Thrombocytopenic Purpura (TTP)
Combination of thrombocytopenia, hemolytic anemia, renal failure, fever and neurologic abnormalities

Causes: structurally weak blood vessels

Manifestations: ease of bruising, bleeding from gums, melina, arthralgia, myalgia and hypermenorrhea
Thrombocytopathia
Impaired platelet function

Causes: inherited, drugs (aspirin or NSAIDs), disease or surgery
von Willenbrand Disease
Caused by von Willebrand factor deficiency (not as severe as hemophilia)
Disseminated Intravasscular Coagulation
Widespread coagulation and bleeding in the vascular compartment
Totipotent Cell
Produced by the fertilization of an egg (can become any cell in the body)
Multipotent Cell
Gives rise to only a few other cell types
Unipotent Cell
Gives rise to only one cell type
Tumor
Swelling that can be caused by a number of conditions
Benign
Abnormal cell growth that is well encapsulated
Malignant
Widespread abnormal growth
Carcinoma
Functional and malignant
Sarcoma
Supportive and malignant
Growth Fraction
Ratio of dividing to non-dividing cells
Doubling Time
Length of time it takes for the total mass of cells in a tumor to double

30 before detection
35 before death
Proto-oncogenes
Normal genes that become oncogenes if mutated
Tumor suppressor genes
cancer results from these genes becoming less active
Epigenetic Mechanism
Changes in the pattern of gene expression not accompanied by changes in DNA
Phases of Cancer
1. Initiation: exposure of cells to carcinogens that make them susceptible to transformation

2. Promotion: beginning of unregulated growth in initiated cells

3. Progression: tumor cells acquire malignant phenotypic changes
Complete Carcinogen
Can initiate and promote neoplastic transformation (ex: sunlight)
Incomplete Carcinogen
Only causes initiation
Clinical Manifestations of Cancer
Cachexia
Anorexia
Fatigue & Sleep disorders
Wasting
Decreased tissue integrity
Paraneoplastic syndromes
Atrophy
Cells decrease in size
Hypertrophy
Cells increase in size and functioning tissue mass
Hyperplasia
Increase in cell number

Hormonal: breast enlargement due to pregnancy

Compensatory: wound healing

Nonphysiologic: BPH
Metaplasia
Reversible change from one adult cell type to another
Dysplasia
Deranged cell growth that results in cells that vary in size, shape and organization
Anaplasia
Cell reversion characterized by no distinct cell characteristics
Dystrophic Calcification
Macroscopic deposition of calcium salts in injured tissue
Metastatic Calcification
Calcification that occurs in normal tissue as a result of hypercalcemia (caused by renal failure)
Liquefaction Necrosis
Occurs when some cells die but thei catalytic enzymes are not destroyed (abscess)
Coagulation Necrosis
Acidosis develops and denatures structural proteins (MI)
Caseous Necrosis
Dead cells persist as soft cheeselike debris (TB)
Dry Gangrene
Related to an obstruction of arteriole blood flow

Common in diabetics

Generally no infections
Wet Gangrene
Related to an obstruction in venous blood flow

Vericose Veins

Associated with infections
Gas Gangrene
Results from infection of dead tissue

Common cause is dirty penetrating wounds

Very difficult to treat without amputation