Patho exam 1 Flashcards
1
Q
Simple Squamous epithelium
A
location: lining of ventral cavities, blood vessels, alveoli of lungs
function: reduces friction, controls vessel permeability, secretion
2
Q
Simple cubodial
A
location: glands and ducts
functions: secretion, absorption, limited protection
3
Q
Simple columnar
A
location: lining of stomach, intestine, esophagus, gallbladder
functions: protection, secretion, and absorption
4
Q
Transition epithelium
A
location: urinary bladder, renal pelvis of kidney, ureter
5
Q
Pseduostratified columnar
A
location: lining of nasal passage, trachea, bronchi
function: protection and secretion
6
Q
stratified squamous
A
location: skin, vagina, rectum, anus, mouth, throat
function: protection
7
Q
Types of hypoxia
A
- ischemia
- hypoxemia
- failure of oxidative phosphorylation
8
Q
Ischeima
A
- blood vessels and/or pumps do not work
- occlusion / pump failure
9
Q
Hypoxemia
A
- blood vessels and pumps work fine, but blood does not carry O2 properly
- failure to perfuse or ventilate lungs, lack of RBC, low O2 in blood stream, inability of hemoglobin to bind/release O2
10
Q
Failure of oxidative phosphorylation
A
- cells are not using O2 properly
- cyanide, carbon monoxide
11
Q
Patters of cell injury
A
- hypoxia
- poor nutrition
- infections agents
- chemical agents
- physical agents
- immune injury
12
Q
Sources of intracelluar accumulations
A
- triglycerides
- glycogen
- pigments
- calcium
13
Q
Dystrophic calcification
A
- “wrong place”
- calcium phosphate or calcium hydroxide create crystals which create masses
- Normal: pinal glands, airway cartilages, mitral valve, aortic valve
- abnormal: breast cancers, surgical scars, retained abortions
14
Q
Metastatic calcifications
A
- occur in abnormal places
- high levels of calcium and/or phosphate
- sites of pH gradients like small airways
15
Q
Coagulation necrosis
A
- usually due to ischemic hypoxia for free radical injury EXCEPT in the brain
- death of groups of cells
- DNA gets destroyed but cell membrane stays intact
- replaced by scar, destroyed, walled off, or healed
- has inflammatory response
16
Q
Liquefactive necrosis
A
- usually due to a bacterial infection
- death of groups of cells
- no inflammatory response
- results from hydrolysis via lysosomal or WBC enzymes
- cells disappear or leave gelatinous mass
17
Q
Casous necrosis
A
- also called saponification
- usually due to immune injury
- death of groups of cells
- crumbled, gross-pale, cheesy
- nucleus disappears, but the cells are not gone
18
Q
Apoptosis
A
- programmed cell death
- single cell death
- triggered by mitochondrial damage (leak caspase) or death receptors
- usually due to immune response
- cell membrane stays intact and remains are phagocytized by marcrophages
- no inflammatory response
19
Q
Dry gangrene
A
- caused by coagulation necrosis
- large scale death
- no infection
20
Q
Wet gangrene
A
- caused by liquefactive necrosis
- large scale death
- foul smelling
- infected
21
Q
Gas gangrene
A
- Clotridal gangrene
- flesh eating
22
Q
Atrophy
A
- decrease in cell size not cell number
- causes: loss of motor innervation, decreased blood supply, decreased hormonal stimulation, malnutrition
ex: breast after pregnancy, loss of muscle mass in a cast
23
Q
Hypertrophy
A
- increase in cell size not cell number
- causes: increased work load, increased hormonal stimulation, normal stress like HTN
- ex: muscle in weight lifters, heart in obese person, breast during pregnancy
24
Q
Hyperplaisa
A
- increase in number of cells not size of cells
- causes: compensatory, hormonal stimulation, genetic mutations
ex. female breast during puberty, lymph nodes close to infection, t-cells during infection, bone marrow after giving blood
25
Metaplasia
- adaptive substitution of one cell type for another
| - ex. pseudostratifed epithelium in airway changing to something more durable due to smoking
26
Dysplasia
- bad growth
- atypical hyperplasia
- loss of cell uniformity and orientation
- resembles cancer, but is not invasive yet
- results from genetic mutation to create a growth advantage
- anaplasia is when it invades
27
Roles of cells in inflammatory process
- neutrophils: infections caused by common bacteria
- lymphocytes: viral infections
- plasma cells: spirochete disease (syphilis and lyme disease)
- monocytes/macrophages: in TB and fungal infections
- eosinophils: infections caused by worms
28
Cardinal signs of acute inflammation
- vasodilation: increased blood flow
- neutorphil infiltration: margination, emigration, chemotaxis
- increased capillary permeability: leakage of fluids and proteins
29
Prostaglandins
- inflammatory mediators
- decrease vascular tone
- increase pain
30
Thromboxane A2
- a prostaglandin
- produced by platelets
- vasocontriction and platelet aggregation
31
Prostacyclin (PGI2)
- a prostaglandin
- produced by endothelial cells
- vasodilation, prevents platelet aggreation
32
Prostaglandin E2
- a prostaglandin
| - vasodilation, potentiates bradykinin, fever
33
Leukotrines
- inflammatory mediator
- smooth muscle contraction
- neutorphil chemotaxis
34
Leukotriene C4
- increases capillary permeability
- breaks down to LTD4 and LTE4
- causes smooth muscle contractions
35
Leukotriene B4
-neutrophil and monocyte chemotaxis
36
Define systemic inflammation
- SIRS
- systemic inflammatory response syndrome
- large production of inflammatory mediators that results in multisystem organ failure
- criteria (2 or more): temp >38 C or <36 C; HR >90bmp: RR >20/min: WBC >20,000 or <4, 000
37
Transudate edema
- salt water, little to no protein content leakage
- results from alterations in starling forces and lymphatic failure
- ex. heart failure, cirrhosis, liver failure
- caused by: excess total body water, salt/fluid overloading, excess aldosterone, kidney failure, lymphatic obstructions, many vein issues
38
Exudate edema
- protein rich salt water
- results from overly leaky capillaries
- loose proteins
- ex. inflammation, sepsis, burns
39
Mechanisms of shock
- hypovolemic shock
- cardiogenic shock
- distributive shock (warm)
- obstructive shock
40
Hypovolemic shock
-decrease in blood volume
41
Cardiogenic shock
-pump failure
42
Distributive shock
-profound vasodilation, lack of venous return
43
Obstructive shock
-external compression of heart or its outflow
44
Hypoxic injury mechanism
- lack of O2 stops oxidative phosphorlylation and electron transport chain (edema is early sign as water rushes into cells)
- anaerobic metabolism leads to lactic acid accumulation and pH drop
- Ca+2 ATPase fails
- Ca+2 entry is key step leading to cell death
45
Gaucher's disease
glucocerebroside
46
Tay-Sachs'
ganglioside
