Midterm Exam

Reversible and irreversible

Mild and transient

Severe and progressive

Cardiomegaly is a physiologic response while cardiomyopathy is a pathologic response

Cardiovascular exercise sees the enlargement of cardiac myocytes to compensate for the extra workload caused by physiological changes, while cardiovascular disease is compensating for the extra workload caused by cell death

Increase in cell size

Increase in cell number

Cardiac myocytes
Neurons

Renal tubular epithelium
Hepatocytes
Lung
Endocrine epithelium
Mesenchymal tissue
Connective tissue
Bone
Skeletal muscle

Bone marrow
Skin
Gastrointestinal
Genitourinary
Reproductive

Thyroid hypertrophy

Supplement iodine in diet (iodine table salt)

Decrease in use/workload
Loss of innervation
Decrease in blood supply
Decrease in nutrition
Loss of endocrine stimulation
Aging

Atrophy due to aging

Bones

Cell death causing inflammatory response

Programmed cell death causing non-inflammatory

Necrosis

Apoptosis

Pyknosis
Karyorrhexis
Karyolysis

Fragmentation into nucleosome-sized fragments

Nuclear shrinkage

Nuclear fragmentation

Nuclear fading

Genetic influences
Metabolic
Nervous
Somatic mutation

Inanimate factors
Animate factors

Force
Temperature
Humidity
Radiant energy
Electricity
Chemicals

Viruses
Rickettsia
Bacteria
Spirochetes
Fungi
Protozoa
Worms
Insects

Reactive oxygen species bind with lipoproteins and form holes in the cell membrane

Membrane damage

Release of cellular contents and cell death
Leaky cell causes edema

Breakdown and misfolding of proteins

Proteins won't function properly

Mutations

Changes function of the cell

Oxygen deprivation
Chemical agents
Immunologic reactions
Physical agents
Aging

Hypoxia
Ischemia

Air pollutants
Insecticides
Asbestos
Therapeutic drugs
Ethanol
Sterilization of implantable devices

Autoclave
Ethylene oxide

Trauma
Temperature extremes
Radiation
Electric shock
Extreme atmospheric pressure changes

Oxygen deficiency

Carbon monoxide
Cyanide

Loss of blood supply and/or nutrients

Oxygen deprivation

Oxygen deprivation

Pressure chamber used to sterilize equipment/supplies by subjecting them to high pressure saturated steam at 121.C for 15-20 minutes

Used for instruments that can't tolerate heat, moisture, or abrasive chemicals

Residual product of metabolism collecting in cardiomyocytes due to aging

Twisted protein fibers in brain collecting in neurons due to aging

Premature aging

Physiological

Physiological

Pathologic

Dystrophic calcification
Metastatic calcification

Focal deposition of calcium at sites of cell injury and necrosis

Dystrophic calcification reaction to tissue damage

Deposition of calcium salts in otherwise normal tissues

Dystrophic is focal while metastatic is located everywhere

Hyper acute

Acute

Subacute/Chronic

Edema

Neutrophils

Monocytes
Macrophages

Hyperacute
Acute
Subacute
Chronic

Rapid
Seconds to minutes to hours

Intermediate
Hours to a few days

Slow
Days

Edema

Neutrophils

Monocytes and macrophages

Increased blood flow
Leakage of plasma protein leads to edema
Neutrophil emigration

Steroids increase cell rigidity which causes the cells to not be able to divide or break open
Granules cannot be released and won't trigger inflammatory response

Cellular swelling
Fatty change

Hydropic change

Cellular swelling
Reversible

Free fatty acids result in lipid accumulation

Fatty change

Necrosis
Ultrastructural changes
Light microscope changes
Gross morphologic change

Coagulation
Gangrenous
Liquefactive
Caseous

Coagulation necrosis

Coagulation necrosis

Gangrenous necrosis

Liquefactive necrosis

Liquefactive necrosis

Caseous necrosis

Caseous necrosis

Algor mortis
Rigor mortis
Livor mortis

Reduction of body temperature following death

Stiffening of muscles after death due to no ATP available to release myosin

Settling of blood in the lower portion of the body

Spontaneous destruction of tissues by intracellular enzymes

The decomposition of organic matter (especially protein) by microorganisms that results in foul-smelling matter

Scalp

Skull

Dura mater

Subdural space

Arachnoid

Subarachnoid space with cerebral spinal fluid

Pia mater

Brain

Subarachnoid space

Pia mater

Redness
Swelling
Heat
Pain
Loss of function

Increased blood flow
Leakage of plasma proteins (edema)
Neutrophil inflammation

Antibodies/immunoglobulins
Complement cascade
Clotting cascade

IgG
IgE

Complement cascade

IgG

Allergic response

Toxin neutralizing
Agglutinating
Opsonizing
Bacteriolytic

Mediates changes in vascular permeability

Relating to immunity that involves antibodies secreted by B cells and circulating body fluids

Relating to immunity that involves cells within the body

Complement cascade
Leukocytes

Process by which a pathogen is marked for phagocytosis

Leukocytes is a broad term for white blood cells while lymphocytes is a type of leukocyte

Granulocytes
Lymphocytes

Polymorphonuclear and mononuclear

Neutrophils
Eosinophils
Basophils

Monocytes/macrophages

B cells
T cells

Neutrophil

Eosinophil

Basophil

Monocyte/Macrophage

Platelets

Lymphocytes
T-cells

Key cell in acute inflammation
First line of defense for phagocytosis

Acids and neutral proteases
Lysosomes

Defend against parasites and allergens

Reactive oxygen species
Elastase
Growth factors
Cytokines

Defend against allergens

Histamine (triggers inflammation response)
Heparin (increase clotting time)

Ingest foreign particles

Heparin
Histamine

Maintain homeostasis by plugging leaky blood vessels

Thymus

Tc
Td
Th
Ts

Recruits macrophages

CD8
Cytotoxic cell
Killer cell

Delayed hypersensitivity

T4
Helper cell

Recognizes antigens and secretes lymphokines that stimulate B cells and killer T cells (T8)

Works to suppress activation of immune system

Bone marrow

Neutrophils

Initial, rapid response to infections and tissue damage

Exudation of fluid and plasma proteins (edema)
Emigration of leukocytes (mainly neutrophils)

Minutes to hours

Vasodilation
Increased vascular permeability
Engorgement of small vessels
Blood leukocytes, mainly neutrophils, along endothelium

Histamine

Increase blood flow

Endothelial cell contraction
Endothelial cell injury
Transcytosis

Histamine
Bradykinin
Leukotrienes

Burns
Irradiation
UV radiation

Vascular endothelial growth factor (VEGF)

Extravascular fluid with low protein content and low specific gravity

Extravascular fluid with high protein content and high specific gravity

Acute inflammation

Acute inflammation

Acute inflammation

Right ventricular assist device

Chronic inflammation

Chronic inflammation

TB granuloma

Chronic-active inflammation

Active inflammation

Chronic inflammation
Granulation tissue encapsulation

Longer term inflammatory response

Lymphocytes
Macrophages
Proliferation of blood vessels
Fibrosis

Days

Chronic active inflammation (sustained)
Healing (resolving)

Proliferation of blood vessels

Macrophages
Leukocytes
Scattered neutrophils

Protection against infections

Collection of cells and molecules that are responsible for defending us against the countless pathogenic microbes in the environment

Mediated by cells and proteins that are always present, poised to react against infectious pathogens

Normally silent that responds to the presence of infectious microbes or implantable material by generating potent mechanisms for neutralizing and eliminating the pathogens

Inflammation

An immune response or intolerance that causes tissue injury and diseases

Type 1
Type 2
Type 3
Type 4

Immediate hypersensitivity

15-30 minutes

IgE
Mast cells
Eosinophils

Hay fever
Hives
Anaphylaxis
Asthma

Antibody mediated diseases

Minutes to hours

Antibodies

Erythroblastosis fetalis (Rh+ baby, Rh- mother)
Transplant rejection

Immune complex mediated

3-8 hours

Antibodies

Serum sickness

T cell mediated hypersensitivity
Delayed type hypersensitivity

48-72 hours

T-cells (CD4 and CD8)
Cytokines

Granulomatous inflammation
Contact dermatitis
Chemical sensitivity
Leprosy
Tuberculosis test

The initial tissue formed in the connective tissue after injury

Chronic inflammation with wall created by immune cells to keep infection contained

Healing

Chronic inflammation

Active process resulting from arteriolar dilation and increased blood flow

Passive process resulting from impaired outflow of venous blood from a tissue

Central vein and sinusoids are distended with blood
Necrosis of centrally located hepatocytes
Periportal hepatocytes (better oxygenated because of proximity to hepatic arterioles) experience less severe hypoxia but may develop fatty change

Centrilobular hepatocyte necrosis
Hemorrhage
Hemosiderin-laden macrophages

Normal lung tissue

Acute pulmonary congestion

Chronic pulmonary congestion

Acute hepatic congestion

Chronic passive congestion of liver

Reversible

Accumulation of fluid in body cavity

Hydrostatic pressure
Colloid osmotic pressure

Increased hydrostatic pressure
Decreased plasma osmotic pressure
Lymphatic obstruction
Sodium retention
Inflammation

Pitting edema

Non-pitting edema

Non-pitting edema has high protein content (exudate), while pitting edema has low protein content (transudate)

Extravasation of blood from vessels

Let or force a fluid out from the vessel that naturally contains it into the surrounding area

Accumulation of blood outside the vessel

Accumulation of blood within the vessel lumen

Blood in thoracic cavity

Blood in pericardium

Blood in peritoneal cavity

Blood in joints

Nose bleed

Coughing up blood

Blood in vomit

Black, tarry stool

Fresh blood in stool

Blood in urine

1-2 mm diameter hemorrhages

3-5 mm diameter hemorrhages

1-2 cm hemorrhages

20%

Can cause hemorrhagic shock

Net iron loss
Anemia

Precisely orchestrated process involving platelets, clotting factors, and endothelium that occurs at the site of a vascular injury and culminates in the formation of a blood clot

Formation of a blood clot within non-traumatized, intact vessels

Physiologic

Pathologic

Vasoconstriction
Platelet plug
Fibrin formation
Clot stabilization

Adhere to location of leakage by interacting with vWF
Change shape to increase affinity for fibrinogen
Secrete prostaglandin thromboxane A to induce platelet aggregation
Aggregate to form permanent plug

Series of amplifying enzymatic reactions that lead to the deposition of an insoluble fibrin clot

Belonging naturally

Not part of the essential nature or something coming/operating from outside

Negatively charge surface activates Factor 12

Vascular damage exposes Tissue Factor which initiates Factor VII

Factor 12 gets initiated into Factor 12a by a negatively charged surface
Factor 12a initiates Factor 11 into Factor 11a
Factor 11a initiates Factor 9 into Factor 9a
Factor 9a with Factor 8a initiates Factor 10 into Factor 10a
Factor 10a initiates prothrombin into thrombin
Thrombin initiates fibrinogen into fibrin

Factor 7 gets initiated into Factor 7a by exposed Tissue Factor caused by injury
Factor 7a initiates Factor 9 into Factor 9a
Factor 9a with Factor 8a initiates Factor 10 into Factor 10a
Factor 10a initiates prothrombin into thrombin
Thrombin initiates fibrinogen into fibrin

Endothelial injury
Abnormal blood flow
Hypercoagulability

Left Ventricular Assist Device Inflow Cannula:
-Endothelial injury when implanting it since it will touch the sides
-Abnormal blood flow in circulation changes due to turbulent flow caused by object protruding
-Hypercoagulability for implanting a foreign object in the space

Propagation
Embolization
Dissolution
Organization and recanalization

Detached intravascular solid, liquid, or gaseous mass that is carried by the blood from its point of origin to a distant site

Event where a thrombus dislodges and becomes embolic

Area of ischemic necrosis caused by occlusion of the vascular supply to the affected tissue

Deep vein thrombosis

Smaller emboli are clinically silent
Larger emboli can block major pulmonary artery and cause sudden death

Left ventricle infarcts
Dilated left atrium

Soft tissue injury or rupture of marrow vasculature sinusoids
Long bone fracture
Release microscopic fat globules into the circulation
Common after CPR

Pulmonary insufficiency
Neurologic symptoms
Anemia
Thrombocytopenia
Diffuse petechial rash

Caused by entry of amniotic fluid (and its contents) into maternal circulation via tears in placental membranes and/or uterine vein rupture

Pulmonary edema
Diffuse alveolar damage
Systemic fibrin thrombi generated by disseminated intravascular coagulation

Decompression sickness
Cassion disease
Death

Anatomy of vascular supply
Rate of occlusion
Tissue vulnerability to hypoxia

60-75%

Cardiogenic
Hypovolemic
Septic

Low cardiac output as a result of myocardial pump failure

Low cardiac output due to loss of blood or plasma volume

Microvascular thrombosis (DIC) leads to tissue ischemia
Tissue ischemia combined with immunosuppression, systemic effects, vasodilation, increased permeability, and decreased perfusion leads to multiorgan failure

Contamination with TSS bacteria

The thrombus becomes large enough with the addition of platelets and fibrin that it can cause vascular occlusion and embolization

Part or all of the thrombus is dislodged and transported elsewhere in the vasculature

If it is newly formed: Activation of fibrinolytic factors (plasmin) can lead to rapid shrinkage and complete dissolution
If it is an older thrombus: The more extensive fibrin polymerization leads it to have more resistance to plasmin-induced proteolysis

Their is ingrowth in the thrombus of endothelial cells, smooth muscle cells, and fibroblasts that overtime will lead to capillary channels forming throughout the length of the thrombus.

Formation of the platelet plug initiated by exposed vWF and collagen

Formation of fibrin initiated by the activation of Factor VII