Pathophysiology Exam 1 Study Materials - Inflammation and Healing

Leading cause of death (all)

heart disease

leading cause of death - 18-30 y/o

accidents

acute disease

short term, high intensity

chronic disease

long term, low intensity

etiology

cause of disease/pathology

pathogenesis

cellular mechanism that lead to dysfunction

pathophysiology

symptoms

sensitivity

ability for a test to be positive

specificity

ability of a test to be negative in the absence of disease

highly sensitive tests tend to have more false (negatives/positives)

positives

PSA test

not specific (high PSA does not tell you if the pt has prostate cancer)

LDH test

not specific (better for monitoring, not for diagnosis)

Troponins

very sensitive and specific (heart cells with damage/death)

continuously dividing cells

skin, GI, salivary glands, epithelial cells, etc

quiescent cells

halted division: liver, kidney, pancreas, smooth muscle

non-dividing cells

cardiac, neural, skeletal muscle

ischemia

decreased blood flow to a body part --> decreased oxygen

#1 cause of cell damage

ischemia

anoxia

good blood flow but oxygen not getting there

reperfusion injury

injury to tissue that occurs after blood flow is restored due to anaerobic metabolism and free radicals

what kind(s) of toxicant is lead?

neuro: ADHD and mental retardation

nephro: inhibits vitamin D activation

bone: can interfere with bone development and growth

blood: RBC production

what kind of toxicant is carbon monoxide?

blood

what kind of toxicant is cyanide?

blood (can't use O2 despite having it)

what kind of toxicant is ethanol?

hepatic

what kind of toxicant is elemental mercury?

neuro (vaporized and inhaled)

Organic mercury

ingested from fish (takes a lot), dermal absorption: very potent

thimerosal

antifungal, controversial paper with vaccines x autism

contusion vs hematoma

contusion = bruise

hematoma = swelling/lump

exotoxin

antibiotics work, secreted by viable living bacteria

endotoxin

fever spikes with antibiotics, ruptured cell wall --> release more endotoxin = increases sickness

ionized calcium

problems with accumulated Ca, cell works hard to maintain stores (mitochondria, ER, Ca binding proteins)

dystrophic calcification

RUPTURING

malignant calcification

high intensity, short period of time, increased in PTH abnormalities

saponification

lipases --> calcium soaps --> gritty

pyknosis

clumping of the nucleus (necrosis)

karyorrhexis

fragmentation of nucleus (necrosis)

karyolysis

nuclear dissolution and chromatin lysis

coagulative necrosis

protein denaturation (aerosol chemicals/huffing = cardiotoxins --> necrosis/pallor of cardiac muscle)

liquefactive necrosis

Neurons and glial cells of the brain

caseous necrosis

only TB infections

fat necrosis

activation of lipases ex: small dense breasts

Example of small dense breasts: dystrophic cells

could be cancer --> destroys cells --> dystrophic calcification precipitation

Example of small dense breasts: saponification

BENIGN: exercising/dieting (change of microenvironment) --> increases lipases

Common condition where gangrenous necrosis may occur?

diabetes (poor circulation --> abundance of glucose --> infection)

apoptosis

programmed cell death

energy to free radical ratio in young patients

energy > free radicals

energy to free radical ratio in aging patients

energy < free radicals

algor mortis

temperature decreases in death

livor mortis

blood pools after death (helpful to see if the body was moved)

rigor mortis

rigidity, at death = limp, 24 hours = ridgid, >24 hours = limp again

postmortem autolysis

bacteria in body breaks down

hypertrophy

increase in cell size

metaplasia

changing from one type of normal cell to another type of normal cell

atrophy

decrease in cell size

hyperplasia

increase in number of cells (never in permanent cells)

dysplasia

abnormal cell growth, NOT CANCER/PRECANCER

physiologic response

expected

pathologic response

unexpected/harmful response

innate resistance

first line of defense

second line of defense

inflammation

vascular response to inflammation

blood cells dilate, increased vascular permeability and leakage, WBC adhere to inner walls of vessels and migrate through the vessels

third line of defense

adaptive (acquired) immunity

goals of inflammation

limits and controls the inflammatory process, prevent and limit infection + further damage, interact with components of the adaptive immune system, prepare the areas of injury for healing

role of chemical mediators

increased vascular permeability

effect of emigration of leukocytes

margination, pavementing, diapedesis

role of neutrophil and macrophage activation

antigen destruction and phagocytosis

T or F: different parts of the body will have different inflammation steps

FALSE: will have the same pathogenic path, inflammation is inflammation

intracellular players of inflammation

WBC, PMN/neutrophils, lymphocyte, monocyte, eosinophil, basophil, platelets, plasma proteins (compliment, clotting, kinin)

extracellular players in inflammation

mast cells (first responder), macrophages, fibroblasts

Mast cells: (does/does not) migrate; located (inside/outside) the vessel

DOES NOT, OUTSIDE

role of macrophage

garbage pick up outside the cell

role of fibroblasts

secrete collagen

vascular factors players

histamine, serotonin, nitric oxide, kinin, complement, and coagulation factors

vascular factor effect

vasodilation and increased vascular permeability

acute inflammation players

neutrophils, platelets, mast cells

chronic inflammation players

macrophages, lymphocytes (B and T)

role of cytotoxic T cells

kill infected cells

role of helper T cells

secrete cytokines (B cells, macrophages, and neutrophils) and regulate inflammation (pro or anti)

role of B lymphocytes

produce antibodies (the studiers)

Pattern recognition receptors (PRRs)

receptor on the cell membrane, recognizes patterns (lactate dehydrogenase) in our own damaged cells

pathogen-associated molecular patterns (PAMPs)

recognize specific pathogen proteins

PRR vs PAMP

PRR: tissue damage, PAMP: pathogen detected

complement receptors

communicate to cells

neutrophils (granule status)

granules, 3 nuclei

eosinophils (granule status)

granules, red/orange

basophils (granule status)

granules, blue/purple

lymphocytes (granule status)

no granules, large nucleus

monocytes (granule status)

no granules, largest/rarest in blood

leukocyte mobility

very mobile, can squeeze between cells lining blood vessels by diapedesis and attack bacteria/debris

phagocytic WBCs

neutrophils, monocytes, and macrophages

role of eosinophils

allergic reactions and parasitic infections (also GERD, mono)

role of basophils

severe allergic reactions releasing histamine (promote inflammation) and heparin (blood clotting)

chronic inflammatory cells

lymphocytes, monocytes, macrophages, plasma cells (LyMMP)

acute inflammatory cells

neutrophils (PMNs, eosinophils for parasite)

where can mast cells be found?

loose connective tissue close to blood vessels --> everywhere

how are mast cells activated?

physical injury, chemical agents, immunologic processes, and receptor triggers

histamine degranulation

expels contents, exocytosis

histamine: synthesis of lipid-derived chemical mediators

takes time, not immediate response, the reason inflammation can last for days

Histamine

vasoactive amine that causes temporary, rapid dilation of blood vessels and postcapillary venules, binds to receptors

H1 receptors in blood vessels mechanism

receptors found on tunica media of blood vessels, when histamine is released from the mast cell (outside the vessel) → diffuse down towards blood vessel → binds to a receptor on the smooth muscle cells in the tunica media → relaxation → vasodilation and increased vascular permeability