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exam 1 patho study guide, Study Guides, Projects, Research of Pathophysiology

University of Central Florida (UCF)Pathophysiology

study guide for exam 1 pathophysiology

Typology: Study Guides, Projects, Research

2020/2021

Uploaded on 06/02/2023

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ariadna-perez-mirabal 🇺🇸

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Exam Patho 1
Cell Injury
-The most likely cause can be trauma and ischemia
-Lack of blood flow & oxygen, you’ll have depleted ATP
Impaired calcium homeostasis- cytosolic calcium levels are kept low by energetic
mechanisms
Ionizing radiation- creates free radicals that destabilize electrons & interrupt cell
replication. Creates radiation injury
Pathologic calcification- abnormal tissue deposition of calcium salts together with
smaller amounts of iron, magnesium & other minerals
Denervation atrophy- not using that certain part so it loses function/muscle get smaller
Metastatic calcification- calcium deposits in previously normal tissue
Dystrophic calcification- calcium deposits in previously damaged tissue
Stenosis- narrowing
Thrombosis- formation of blood clot inside vessel
Hypoxic cell injury can lead to edema
-Hypoxic cell injury can cause acute cellular swelling + hypoxic cell injury
ROS Formation: free radicals have an unpaired electron that causes them to be unstable
& highly reactive
-Can cause free radicals damage cell membranes, inactive enzymes & damage DNA
1. Lipid peroxidation
2. Oxidative
Necrosis- irreversible cell death
Apoptosis
-Extrinsic pathway: the endotoxin found in the outer membrane of a gram neg bacteria
acts as a signaling molecule that activates the extrinsic pathway
-Intrinsic pathway: activated by conditions such as DNA damage, ROS, hypoxia,
decreased ATP levels
Stress
Anterior pituitary- ACTH
Hypothalamus- CRH
Adrenal cortex- cortisol
Posterior pituitary- ADH/vasopressin
Adrenal medulla- epi, norepi/ HPA Axis
** hypotensive stress = fluid volume loss **
Glucocorticoid Hormones
1. Potentiates the actions of epinephrine & glucagon
2. Inhibits the release/actions of reproductive hormones & TSH
3. Produces a decrease in immune cells & inflammatory mediators
Mineralocorticoid hormones
1. Increase sodium absorption by kidneys
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Exam Patho 1

Cell Injury

  • The most likely cause can be trauma and ischemia
  • Lack of blood flow & oxygen, you’ll have depleted ATP  Impaired calcium homeostasis- cytosolic calcium levels are kept low by energetic mechanisms  Ionizing radiation- creates free radicals that destabilize electrons & interrupt cell replication. Creates radiation injury  Pathologic calcification- abnormal tissue deposition of calcium salts together with smaller amounts of iron, magnesium & other minerals  Denervation atrophy- not using that certain part so it loses function/muscle get smaller  Metastatic calcification- calcium deposits in previously normal tissue  Dystrophic calcification- calcium deposits in previously damaged tissue  Stenosis- narrowing  Thrombosis- formation of blood clot inside vessel  Hypoxic cell injury can lead to edema
  • Hypoxic cell injury can cause acute cellular swelling + hypoxic cell injury  ROS Formation : free radicals have an unpaired electron that causes them to be unstable & highly reactive
  • Can cause free radicals damage cell membranes, inactive enzymes & damage DNA
  1. Lipid peroxidation
  2. Oxidative  Necrosis - irreversible cell death  Apoptosis
  • Extrinsic pathway: the endotoxin found in the outer membrane of a gram neg bacteria acts as a signaling molecule that activates the extrinsic pathway
  • Intrinsic pathway: activated by conditions such as DNA damage, ROS, hypoxia, decreased ATP levels  Stress  Anterior pituitary- ACTH  Hypothalamus- CRH  Adrenal cortex- cortisol  Posterior pituitary- ADH/vasopressin  Adrenal medulla- epi, norepi/ HPA Axis ** hypotensive stress = fluid volume loss ** Glucocorticoid Hormones
  1. Potentiates the actions of epinephrine & glucagon
  2. Inhibits the release/actions of reproductive hormones & TSH
  3. Produces a decrease in immune cells & inflammatory mediators Mineralocorticoid hormones
  4. Increase sodium absorption by kidneys

Cortisol

  1. Adrenal cortex (neuroendocrine response to stress)
  • Decreases immune response
  • Shut off during resistance stage
  • Increase fat metabolism
  • Increase glucose metabolism & inhibit insulin serum RAAS
  1. Response to low BP or low sodium
  2. Mediates a peripheral increase in vascular tone and renal retention of sodium & water Liver produces angiotensinogen  kidney produces renin  angiotensinogen + renin = angiotensin 1  lungs release ACE  angiotensin 2  adrenal glands create aldosterone Aldosterone : increases reabsorption of sodium = higher BP Angiotensin 2 (in kidney) : vasoconstriction in arterioles = higher BP GAS
  3. Alarm stage: general stimulation of SNS & HPA axis, the release of catecholamines and cortisol
  4. Resistance stage: body selects most effective defense & cortisol levels drop
  5. Exhaustion stage: resources are depleted, systemic damage occurs Corticotropin-releasing factor
  • Stimulates ACTH release from the anterior pituitary & increased activity of the LC neurons
  • ACTH: stimulates release of cortisol  Gangrene
  • tissue death due to interrupted blood supply
  1. Wet : In moist or wet gangrene, the area is cold, swollen, and pulseless. The skin is moist, black, and under tension. Blebs form on the surface, liquefaction occurs, and a foul odor is caused by bacterial action.
  2. Dry : Dry gangrene is confined almost exclusively to the extremities, but moist gangrene may affect the internal organs or the extremities. If bacteria invade the necrotic tissue, dry gangrene may be converted to wet gangrene.
  • Adenocarcinoma: malignant tumor of glandular epithelial tissue
  • Carcinoma: malignant tumor of epithelial tissue
  • Adenoma: benign tumor of glandular epithelial tissue
  • Sarcoma: malignant tumor of mesenchymal region
  • Papilloma: benign microscopic or microscopic finger-like projections growing on a surface
  • AFP: liver cancers
  • CEA: colorectal, pancreas, lung cancers
  • PSA: prostate cancer  Parenchymal: functional components of an organ  Supporting tissue: includes the extracellular matrix & connective tissue  Integumentary TABLE 52-1 Primary and Secondary Skin Lesions Lesion Description Examples Primary Lesions Macule, patch Flat, nonpalpable skin color change (color may be brown, white, tan, purple, red)  Macul e: < cm; circu mscri bed border  Patch : > cm; may Freckles, flat moles, petechiae, rubella, vitiligo, port-wine stains, ecchymosis

Lesion Description Examples have irregul ar border Papule, plaque Elevated, palpable, solid mass with a circumscribed border Plaque may be coalesced papules with flat top.  Papul e: <0. 5 cm  Plaqu e: >0. 5 cm Papules: Ele vated nevi, warts, lichen planus Plaques: Ps oriasis, actinic keratosis Nodule, tumor Elevated, palpable, solid mass that extends deeper into the dermis than does a papule  Nodul e: 0.

cm; circu mscri bed  Tumo r: >1– Nodules: Li poma, squamous cell carcinoma, poorly absorbed injection, dermatofibro ma Tumors: Lar ger lipoma, carcinoma

Lesion Description Examples fluid in a cavity ( e.g. , as a vesicle does) Pustule Pus-filled vesicle or bulla Acne, impetigo, furuncles, carbuncles Cyst Encapsulated fluid-filled or semisolid mass in the subcutaneous tissue or dermis Sebaceous cyst, epidermoid cysts Secondary Lesions Erosion Loss of superficial epidermis that does not extend to dermis; depressed, moist area Ruptured vesicles, scratch marks Ulcer Skin loss extending past epidermis; necrotic tissue loss; bleeding and scarring Stasis ulcer of venous insufficiency , pressure ulcer

Lesion Description Examples possible Fissure Linear crack in the skin that may extend to dermis Chapped lips or hands, tinea pedis Scales Flakes secondary to desquamated, dead epithelium that may adhere to skin surface; color varies (silvery, white); texture varies (thick, fine) Dandruff, psoriasis, dry skin, pityriasis rosea Crust Dried residue of serum, blood, or pus on skin surface Large, adherent crust is a scab Residue left after vesicle rupture: impetigo, herpes, eczema

Lesion Description Examples the epidermis; loss of surface markings; secondary to loss of collagen and elastin; underlying vessels may be visible Lichenification Thickening and roughening of the skin or accentuated skin markings that may be secondary to repeated rubbing, irritation, scratching Contact dermatitis