Peripancreatic fat (saponification via lipase)

Gangrenous NecrosisDryWetWhere?

Dry: Ischemic CoagulativeWet: BacteriaLimbs and GI tract

Reversible Cell InjuryWhat is required?PathoPhysHisto

Oxygen↓ ATP synthesis, ↓ GlycogenSwelling (impaired Na/K pump), Chromatic clumping, Fatty Change, Ribosomal detachment

Irreversible Cell InjuryPathwayWhat happens to the cell?Histo

Ca influx –> caspase activationPlasma membrane damage, Lysosomal Rupture, Mito PermeabilityPyknosis, Karyolysis, Karyorrhexis

Location of Kidney susceptible to ischemic injury

Straight segment of PT in medullaThick Ascending Limb in medulla

Red InfarctsWhat kind of infarct?What kind of tissue?Organs?When?

"Red = Reperfusion"HemorrhagicTissue with collateralsLiver, Lungs, IntestinesFollowing reperfusion

Medicine /USMLE - Pathology Part 1

USMLE - Pathology Part 1

Medicine100 CardsCreated 4 days ago

Apoptosis is programmed cell death that occurs in a controlled, energy-dependent manner, requiring ATP and mediated by caspases. It is characterized histologically by cell shrinkage, nuclear fragmentation, and formation of apoptotic bodies without triggering inflammation. Dead cells are cleared by phagocytosis.

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Apoptosis
What is it?
What is required?
Phys
Inflammation
Histo
Clean up?

Programmed cell death

ATP required

Cytosolic caspases mediate cellular breakdown

No inflammation

Shrinkage, Pyknosis (nuc shrinkage), Basophilia, Blebbing, Nuclear Fragmentation (karyorrhexis), Apoptotic bodies

Phagocytosis

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Key Terms

Term

Definition

Apoptosis

What is it?

What is required?

Phys

Inflammation

Histo

Clean up?

Programmed cell death

ATP required

Cytosolic caspases mediate cellular breakdown

No inflammation

Shrinkage, Pyknosis (nuc s...

Intrinsic Apoptosis Pathway

What process is it involved with?

Mechanism

Mito involvement

Tissue remodeling in embryogenesis and after exposure to injurious stimuli

Growth factor withdrawn from proliferating cells

Changes in ...

Extrinsic Apoptosis Pathways

Fas ligand binding to Fas Receptor (CD95)

Tc cells release Perforin and Granzyme B

Necrosis

What causes it?

Process?

Inflammation?

Exogenous injury

Enzymatic degradation and protein denaturation –> Intracellular components extravasate

Inflammation

Coagulative Necrosis

Heart, Liver, Kidney

Liquefactive Necrosis

Brain, Bacterial Abscess, Pleural Effusion

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USMLE - Pathology Part 1

Term	Definition
Apoptosis What is it? What is required? Phys Inflammation Histo Clean up?	Programmed cell death ATP required Cytosolic caspases mediate cellular breakdown No inflammation Shrinkage, Pyknosis (nuc shrinkage), Basophilia, Blebbing, Nuclear Fragmentation (karyorrhexis), Apoptotic bodies Phagocytosis
Intrinsic Apoptosis Pathway What process is it involved with? Mechanism Mito involvement	Tissue remodeling in embryogenesis and after exposure to injurious stimuli Growth factor withdrawn from proliferating cells Changes in proportions of anti and pro apoptotic factors lead to ↑ mito permeability and ctyochrome c release
Extrinsic Apoptosis Pathways	Fas ligand binding to Fas Receptor (CD95) Tc cells release Perforin and Granzyme B
Necrosis What causes it? Process? Inflammation?	Exogenous injury Enzymatic degradation and protein denaturation –> Intracellular components extravasate Inflammation
Coagulative Necrosis	Heart, Liver, Kidney
Liquefactive Necrosis	Brain, Bacterial Abscess, Pleural Effusion
Caseous Necrosis	TB, Systemic Fungi
Fatty Necrosis	Peripancreatic fat (saponification via lipase)
Fibrinoid Necrosis	Blood vessels
Gangrenous Necrosis Dry Wet Where?	Dry: Ischemic Coagulative Wet: Bacteria Limbs and GI tract
Reversible Cell Injury What is required? PathoPhys Histo	Oxygen ↓ ATP synthesis, ↓ Glycogen Swelling (impaired Na/K pump), Chromatic clumping, Fatty Change, Ribosomal detachment
Pro-apoptotic Mito protein	Bax
Anti-apoptotic Mito Protein	Bcl-2
Irreversible Cell Injury Pathway What happens to the cell? Histo	Ca influx –> caspase activation Plasma membrane damage, Lysosomal Rupture, Mito Permeability Pyknosis, Karyolysis, Karyorrhexis
Location of Brain susceptible to ischemic injury	ACA/MCA/PCA boundary area
Location of Heart susceptible to ischemic injury	Subendocardium of LV
Location of Kidney susceptible to ischemic injury	Straight segment of PT in medulla Thick Ascending Limb in medulla
Location of Liver susceptible to ischemic injury	Central Vein (zone III)
Location of Colon susceptible to ischemic injury	Splenic Flexure and Rectum
Red Infarcts What kind of infarct? What kind of tissue? Organs? When?	"Red = Reperfusion" Hemorrhagic Tissue with collaterals Liver, Lungs, Intestines Following reperfusion
Hypoxic Ischemic Encephalopathy affects what kind of cells?	Pyramidal Cells of Hippocampus and Purkinje cells
Pale Infarcts What kind of tissue? Organs?	Solid tissues with a single blood supply Heart, Kidney, Spleen
Reperfusion injury is due to…	Free Radicals
Hypovolemic Shock Output TPR Presentation	Low output ↑ TPR Cold and Clammy
Cardiogenic Shock Output TPR Presentation	Low output ↑ TPR Cold and Clammy
Septic Shock Output TPR Vasculature Presentation	High output ↓ TPR Dilated arterioles, High venous return Hot
Atrophy What is it? Possible causes?	Reduction in size or # of cells ↓ hormones, innervation, blood flow nutrients ↑ pressure Occlusion of secretory ducts
Characteristics of Inflammation	Redness, Heat, Swelling, Loss of Function
Vascular component of inflammation	↑ vascular permeability, vasodilation, endothelial injury
Cellular component of inflammation	Neutrophil mediated
Acute component of inflammation Mediators Onset Duration Possible outcomes	Neutrophils, Eosinophils, Abs Seconds to minutes Minute to days Resolution, Abscess, Chronic inflammation
Chronic component of inflammation Mediators Characteristic Associated with... Outcomes	Mononuclear cells Persistent destruction and repair Blood vessel proliferation. Fibrosis Scarring, Amyloidosis
Granuloma Histo Pathway	Nodular collection of Epithelioid Macrophages and Giant Cells Th1 secretes IFNγ which activates Macs which secrete TNFα
Leukocyte Extravasation \| Steps w/ mediators	1.Rolling: Vasculature: E and P selectins. Leukocyte: Sialyl-Lewis Tight Binding V: ICAM. L: LFA1 (integrin) Diapedesis (between endothelial cells) V: PECAM. L: PECAM Migration
Leukocyte (neutrophil) chemotactic factors	"CLIK" \| C5a, LTB4, IL8, Kallikrein
How do free radicals damage cells?	Membrane lipid peroxidation Protein modifications DNA breakage
Free Radicals What causes them? How are they eliminated?	Radiation, Metabolism of drugs, Redox rxns, Nitric Oxide (NO), Transition metals, Leukocyte oxidative burst Enzymes (Catalase, SOD, Glutathione Peroxidase), Decay, Antioxidants (A, C, E)
Free Radical Diseases	ROP, Bronchopulmonary Dysplasia, CCl4 --> liver necrosis (fatty change), Acetominophen OD, Hemochromatosis, Reperfusion
Would Healing Phases	Inflammatory, Proliferative, Remodeling
Would Healing Inflammatory Phase When? Mediators What happens?	Immediate Platelets, Neutrophils, Macrophages Clot formation and ↑ permeability
Would Healing Proliferative Phase When? Mediators What happens?	2-3 days after injury Fibroblasts, Myofibroblasts, Endothelial cells, Keratinocytes, Macrophages Deposition of granulation tissue and collagen. Angiogenesis, Epithelial cell proliferation, Dissolution of clot, Wound contraction (via myofibroblasts)
Would Healing Remodeling Phase When? Mediators What happens?	1 week Fibroblasts Collagen III replaces Collagen I --> ↑ tensile strength of tissue
Granulomatous Diseases	TB Fungal Infections (Histoplasmosis, Coccidioidomycosis) Treponema Pallidum (Syphilis) M Leprae (Leprosy) Bartonella Henselae (cat scratch disease) Sarcoidosis, Crohn's Disease, Wegener's, Churg Strauss Berylliosis, Silicosis
Transudate Cellularity? Protein? Specific gravity Causes	Hypocellular Low protein Less than 1.012 ↑ hydrostatic pressure, ↓ oncotic pressure, Na retention
Exudate Cellularity? Protein? Specific gravity Causes	Cellular Protein rich Greater than 1.02 Lymphatic obstruction or Inflammation
Iron Poisoning MoA Acute Chronic	Peroxidation of membrane lipids Acute gastric bleeding Chronic: Metabolic acidosis, Scarring --> GI obstruction
Amyloidosis What is it? What does it cause? Appearance of tissue?	Abnormal aggregation of proteins into β-pleated sheets Cell damage and apoptosis Waxy appearance
AL Amyloidosis What kind of protein? What disorders present with it? Organ systems affected	Ig Light chains Plasma cell disorder or Multiple Myeloma Renal (nephrotic), Cardiac (failure, arrhythmia), Hematologic (easy bruising), Hepatomegaly, Neuropathy
AA Amyloidosis What kind of protein? What diseases? Systems involved?	Amyloid A fibrils RA, IBD, Spondyloarthropathy, Chronic Infections Multiple systems like in AL
Dialysis Related Amyloidosis What kind of protein? What kind of pt? Presentation	β2 microglobulin ESRD on long term dialysis Carpal tunnel syndrome and other joint issues
Heritable Amyloidosis Genetics Disease	Transthyretin (TTR or prealbumin) gene mutation \| ATTR neurologic/cardiac amyloidosis
Age-Related (Senile) Amyloidosis What kind of protein? Organs affected Progression	wt TTR Systemic: deposited in myocardium and other sites Slower progression of cardiac dysfunction vs AL
Organ Specific Amyloidosis What is affected? Example with protein	A single organ \| Alzheimer's Disease due to deposition of amyloid-β protein from APP
Anaplasia	Abnormal cells lacking differentiation
Desmoplasia	Fibrous tissue formation in response to neoplasm
Tumor Grade	Degree of cellular differentiation
Tumor Stage \| TNM	Degree of localization/spread based on site and size Tumor Size Node Involvement Metastases
Tumor stage vs grade re prognostic value	Stage has more prognostic value
Epithelium tumor names Benign Malignant	Adenoma, Papilloma \| Adenocarcinoma, Papillary carcinoma
Tumor of Blood Vessels Benign Malignant	Hemangioma \| Angiosarcoma
Tumor of Smooth Muscle Benign Malignant	Leiomyoma \| Leiomyosarcoma
Tumor of Striated Muscle Benign Malignant	Rhabdomyoma \| Rhabdomyosarcoma
Tumor of Connective Tissue Benign Malignant	Fibroma \| Fibrosarcoma
Tumor of Bone Benign Malignant	Osteoma \| Osteosarcoma
Tumor of Fat Benign Malignant	Lipoma \| Liposarcoma
Cachexia Presentation Disease with it? Mediated by	Wt loss, Muscle atrophy, Fatigue Cancer, AIDS, Heart Failure, TB TNFα, IFNγ, IL6
Neoplasm of Down Syndrome	ALL, AML
Neoplasm of Xeroderma Pigmentosum or Albinism	Melanoma, Basal Cell Carcinoma, Squamous Cell Carcinoma of the Skin
Neoplasm of Chronic Gastritis, Pernicious Anemia, Postsurgical Gastric Remnant	Gastric Adenocarcinoma
Neoplasm of Tuberous Sclerosis	Giant Cell Astrocytoma, Renal Angiomyolipoma, Cardiac Rhabdomyoma
Neoplasm of Actinic Keratosis	Squamous cell carcinoma of the skin
Neoplasm of Barrett's Esophagus	Esophageal adenocarcinoma
Neoplasm of PVS	Squamous cell carcinoma of the esophagus
Neoplasm of Paget's Disease of Bone	Osteosarcoma, Fibrosarcoma
Neoplasm of Immunodeficiency States	Malignant Lymphomas
Neoplasm of AIDS	Malignant Lymphomas and Kaposi Sarcoma
Neoplasm of autoimmune disease	Lymphoma
Neoplasm of Acanthosis Nigricans	Visceral Malignancy (Stomach, Lung, Uterus)
Neoplasm of Dysplastic Nevus	Malignant Melanoma
Neoplasm of Radiation Exposure	Leukemia, Sarcoma, Papillary Thyroid Cancer, Breast Cancer
abl What kind of protein? Tumor Product	Oncogene CML Tyrosine Kinase
c-myc What kind of protein? Tumor Product	Oncogene Burkitt's Lymphoma Transcription factor
bcl2 What kind of protein? Tumor Product	Oncogene Follicular and undifferentiated lymphoma Anti-apoptotic molecule
HER2/neu (c-erbB2) What kind of protein? Tumor Product	Oncogene Breast, Ovarian, Gastric Carcinoma Tyrosine Kinase
ras What kind of protein? Tumor Product	Oncogene Colon Carcinoma GTPase
L-myc What kind of protein? Tumor Product	Oncogene Lung Tumor Transcription Factor
N-myc What kind of protein? Tumor Product	Oncogene Neuroblastoma Transcription Factor
ret What kind of protein? Tumor Product	Oncogene MEN 2A and 2B Tyrosine Kinase
c-kit What kind of protein? Tumor Product	Oncogene GI stromal tumor Cytokine Receptor
Rb What kind of protein? Tumor Product	Tummor Suppressor Retinoblastoma, Osteosarcoma Normally inhibits E2F thus blocking G1 --> S transition
p53 What kind of protein? Tumor Product	Tummor Suppressor Most human cancers, Li-Fraumeni Syndrome Transcription factor for p21. Normally blocks G1 --> S transition
BRCA1 and BRCA2 What kind of protein? Tumor Product	Tummor Suppressor Breast and Ovarian Cancer DNA repair protein
p16 What kind of protein? Cancer	Tummor Suppressor \| Melanoma
BRAF What kind of protein? Tumor Product	Tummor Suppressor Melanoma B-raf
APC What kind of protein? Cancer?	Tummor Suppressor \| Colorectal cancer
WT1 What kind of protein? Tumor	Tummor Suppressor \| Wilm's Tumor (Neuroblastoma)
NF1 What kind of protein? Tumor Product	Tummor Suppressor Neurofibromatosis type 1 RAS GTPase activating protein (RAS GAP)
NF2 What kind of protein? Tumor Product	Tummor Suppressor Neurofibromatosis type 2 Merlin (Schwannomin) protein
DPC4 What kind of protein? Tumor Product	Tummor Suppressor Pancreatic Cancer "Deleted in Pancreatic Cancer"
DCC What kind of protein? Tumor Product	Tummor Suppressor Colon Cancer "Deleted in Colon Cancer"

USMLE - Pathology Part 1

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Apoptosis
What is it?
What is required?
Phys
Inflammation
Histo
Clean up?

Key Terms

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USMLE - Pathology Part 1

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ApoptosisWhat is it?What is required?PhysInflammationHistoClean up?

Key Terms

Related Flashcard Decks

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Apoptosis
What is it?
What is required?
Phys
Inflammation
Histo
Clean up?