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94 Cards in this Set
- Front
- Back
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PO2
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driving force for diffusion of O2 into tissue
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SaO2
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percent heme groups occupied by O2
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Cyanosis
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decreased O2 saturation (SaO2)
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O2 content
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1.34 x Hb x SaO2 + PaO2
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Oxygen
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electron acceptor in oxidative pathway
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Hypoxia
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inadequate O2 leads to ATP deletion
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Ischemia
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decreased arterial (or venous) blood flow
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Respiratory acidosis
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retention of CO2 always decreased PaO2
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Ventilation defect
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impaired delivery of O2 to alveoli; intrapulmonary shunting of blood (e.g., RDS)
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Perfusion defect
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absent blood flow to alveoli; increased alveolar dead space (e.g., pulmonary embolism)
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Diffusion defect
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O2 cannot cross alveolar-capilary interface
Interstitial lung disease (sarcoidosis) |
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Methemoglobin
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Decreased SaO2
Heme iron +3 Oxidizing agents (sulfur/ nitro drugs) Rx with IV methylene blue |
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Clinical methemoglobin
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Cyanosis not corrected by O2
Chocolate colored blood |
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Carbon monoxide
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Decreased SaO2
Left-shift O2 binding curve Inhibits cytochrome oxidase |
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Causes carbon monoxide poisoning
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Car exhaust
Space heaters Smoke inhalation |
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S/S Carbon monoxide poisoning
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Headache
Cherry Red color skin |
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Cyanide
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Inhibits cytochrome oxidase
Systemic asphyxiant |
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Carbon monoxide + cyanide poisoning
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House fires
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Left- shifted O2 curve
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Decreased 2,3 BPG
Carbon monoxide Alkalosis HbF Methemoglobin Hypothermia |
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Right- shifted O2 curve
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Increased 2,3 BPG
High Altitude Acidosis Fever |
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High altitude
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Respiratory alkalosis enhances glycolysis
Increased synthesis 2,3 BPG |
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Mitochondrial poisons
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Damages membrane and drains off protons
Alcohol Salicylates |
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Uncoupling agents in mitochondria
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Drain off protons
Dinitrophenol Thermogenin (brown fat) |
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Complication mitochondrial poisons/ uncoupling agents
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Hyperthermia
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Decreased ATP
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Impaired Na+/ K+ ATPase pump (cellular swelling)
Reversible |
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Anaerobic glycolysis
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ATP synthesis in hypoxia
Lactate decreased intracellular pH Denatures proteins |
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Irreversible injury hypoxia
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Increased cytosolic Ca2+ activates phospholipase, proteases, endonuclease
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Free radicals
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Unpaired electron in outer orbit
Damage cell membranes and DNA |
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Free radicals
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Superoxide
Hydroxyl Peroxide Drugs (acetaminophen) |
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Superoxide dismutase
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Neutralizes superoxide
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Glutathione
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Neutralizes peroxide
Drug FRs |
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Catalase
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Neutralizes peroxide
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Lipofuscin
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Indigestible lipid of lipid peroxidation
Brown pigment increased in atrophy and FR damage |
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Reperfusion injury in heart
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Superoxide FRs + calcium
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Mitochondrial injury
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Cytochrome C in cytosol initiates apoptosis
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SER hyperplasia
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Alcohol
Barbiturates Phenytoin |
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Complications SER hyperplasia
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Increases drug metabolism (e.g., oral contraceptives)
Decreased Vitamin D |
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Chediak- Higashi
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Membrane protein defect in transferring lysosomal enzymes to phagocytic vacuoles
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Chediak- Higashi
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AR
Giant lysosomes |
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I cell disease
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Absent enzyme marker in Golgi apparatus (mannose 6-phosphate)
Empty lysosomes |
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Rigor mortis
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Stiff muscles after death due to ATP depletion
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Fatty change in liver
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MCC alcohol (increase in NADH)
DHAP ---> G3P ---> TG |
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Fatty change in liver
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Increased VLDL pushes nucleus to side
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Causes fatty change
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Increased synthesis TG/ FAs
Decreased B-oxid FAs/ synthesis apoproteins/ release VLDL |
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Fatty change in kwashiokor
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Decreased synthesis of apoproteins
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Ferritin
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Primary iron storage protein
Soluble in blood Serum level reflects marrow storage iron |
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Hemosiderin
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Insoluble ferritin degradation product visible with Prussian blue stain
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Atrophy
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Reduction in cell/tissue mass by either loss or cell shrinkage
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Brain atrophy
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Ischemia
Alzheimer's |
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Exocrine gland atrophy in CF
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Duct obstruction by thick secretions
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Labile cells
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Stem cells
Skin, marrow, GI tract |
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Stable cells
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In Go phase (smooth muscle, hepatocytes)
Can enter cell cycle (growth factors, hormones) |
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Permanent cells
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Cannot replicate
Cardiac/ striated muscle Neurons |
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Hypertrophy
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Increase in cell size (structural components, DNA)
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LVH
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Increased preload (valve regurgitation)
Increased afterload (hypertension, aortic stenosis) |
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RVH
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Pulmonary hypertension
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Bladder smooth muscle hypertrophy
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Prostate hyperplasia constricts urethra
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Removal of kidney
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Hypertrophy of remaining kidney
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Hyperplasia
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Increase in number of cells
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Endometrial hyperplasia
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Unopposed estrogen (obesity, taking estrogen)
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RBC hyperplasia
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Increased EPO
Blood loss Ectopic secretion High altitude |
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Prostate hyperplasia
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Increased DHT
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Gynecomastia
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Hyperplasia of male breast tissue
Normal in newborn, adolescent, elderly |
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Metaplasia
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One adult cell type replaces another cell type
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Squamous metaplasia in bronchus
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Smoking
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Intestinal metaplasia in stomach
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Paneth cells
Goblet cells H. pylori chronic atrophic gastritis |
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Squamous metaplasia bladder
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Schistosoma hematobium infection
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Barrett's esophagus
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Glandular metaplasia of distal esophagus
Due to GERD |
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Dysplasia
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Atypical hyperplasia or metaplasia are precursors for cancer
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Squamous dysplasia in cervix
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Human papilloma virus
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Squamous dysplasia in bronchus
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Smoking
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Necrosis
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Death of groups of cells
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Coagulation necrosis
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Preservation of structural outline (due to increased lactic acid)
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Infarction
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Pale (e.g., heart, kidney)
Hemorrhagic (e.g., lung, small bowel) Dry gangrene |
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Liquefactive necrosis
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Brain infarct
Bacterial infections Wet gangrene |
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Caseous necrosis
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Variant coagulation necrosis
Granulomas due to TB/ systemic fungi |
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Granulomas
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Activated macrophages (epitheloid cells)
Multinucleated giant cells CD4 T cells |
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Epithelioid cells
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y- interferon released by CD4 T cells activates macrophages
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Multinucleated giant cells
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Fusion of epithelioid cells
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Granulomas
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Type IV hypersensitivity
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Enzymatic fat necrosis
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Associated with pancreatitis
Soap formation (Ca2+ + Fatty acids) |
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Fibrinoid necrosis
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Necrosis of immune reactions (immune vasculitis/ endocarditis)
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Postmortem necrosis
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Autolysis
No inflammatory reaction |
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Dystrophic calcification
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Calcification of damaged tissue
Normal serum calcium Pancreatitis Atherosclerotic plaque |
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Metastatic calcification
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Calcification of normal tissue
Increased serum calcium or phosphorous |
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Nephrocalcinous
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Metastatic calcification of collecting tube basement membranes
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S/S nephrocalcinous
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Polyuria due to nephrogenic diabetes insipidus
Renal failure |
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Apoptosis
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Gene regulated individual cell death
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Signals activating apoptosis
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Mullerian inhibitory factor
Tumor necrosis factor Hormone withdrawal |
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Signal Modulators of apoptosis
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TP53 suppressor gene
BCL-2 genes |
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BCL-2 genes
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Anti-apoptosis gene
Prevents cytochrome C from leaving mitochondria |
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Caspases
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Responsible for enzymatic cell death in apoptosis
Proteases and endonucleases |
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Markers of apoptosis
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Eosinophilic cytoplasm
Pyknotic (ink dot) nucleus |
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Apoptosis
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Loss of Mullerian epithelium in male fetus
Thymus involution Killing cancer cells |
