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Pharmacy School Fall P1 > Pathophysiology and Drug Action Exam 4 > Flashcards

Pathophysiology and Drug Action Exam 4 Flashcards

1
Q

What is the first stage of healing after tissue injury?

A

-Hemostasis
-occurs in minutes

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2
Q

What is the second stage of healing after tissue injury?

A

-inflammation
-driven by platelet-derived mediators (redness, swelling, pain)
-occurs in hours

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3
Q

What is the third stage of healing after tissue injury?

A

-PROLIFERATION fibroblast secreted mediators signal cell proliferation to regenerate lost tissue; laying down type III collagen
-occurs over days

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4
Q

What is the fourth and final stage of healing after tissue injury?

A

-REMODELING type III collagen is replaced with type I collagen and tensile strength of the new tissue is increased
-occurs over weeks to months

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5
Q

What is the difference between tissue regeneration and tissue repair?

A

-tissue regeneration occurs when cells lost by injury are replaced by cells of the exact same type and function
-tissue repair occurs when regeneration is not possible and is replaced by cells that are not the same as the ones lost in injury. this results in scarring or fibrosis.

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6
Q

What are the factors that determine whether a tissue gets regenerated versus repaired?

A

-depends on the nature of the cells injured, extent of the injury, presence of ongoing inflammation, and the co-existence of underlying disease

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7
Q

What are the common outcomes of various signal transduction pathways of growth factors?

A

-change in gene expression

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8
Q

What are the two forms of the Extra-cellular Matrix and their key components?

A

-extracellular matrix and interstitial matrix
-integrins hold the epithelium to the basement membrane; serve as a reservoir for growth factors
-fibroblasts are connected to the ECM and work in fibrosis

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9
Q

What are the three key growth factors that regulate fibrosis?

A

PDGF (Platelet-derived growth factor)
TGFB (transforming growth factor)
FGF-2 (Fibroblast growth factor)

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10
Q

What are the three key elements of shock?

A

-life threatening condition
-circulatory failure
-inadequate oxygenation

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11
Q

What are the four main types of shock and their causes associated with them?

A

-distributive shock (sepsis, Anaphylaxis, Neurogenic)
-hypovolemic shock (Hemorrhage, Severe burns, severe vomiting, diarrhea)
-cariogenic shock (myocardial infarction, ventricular arrhythmia, cardiac myopathy, valvular disease)
-obstructive shock (cardiac tamponade, Pulmonary embolism, Pneumothorax)

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12
Q

What is the component of gram-negative bacteria that mediates septic shock?

A

endotoxin (LPS)

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13
Q

What is the role of adrenomedullin in modulating vascular function?

A

-when in the intravascular space, it enhances the endothelial barrier and reduces the movement of solutes out of the vascular space
-when in the interstitial space, it mediates the relaxation in vascular smooth muscle and causes vasodilation

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14
Q

what does edema mean?

A

-accumulation of fluid in interstitial space of body tissues

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15
Q

What are the primary drivers of fluid in and out of the vascular space?

A

hydrostatic and colloid osmotic pressure

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16
Q

Describe the mechanisms and common clinical causes of edema

A

-increased capillary permeability (cellulitis, sepsis, hypersensitivity reactions)
-Increased capillary hydrostatic pressure (compartment syndrome, chronic venous insufficiency, heart failure, renal failure, pregnancy)
-Decreased capillary oncotic pressure (protein deficient states, nephrotic syndrome, cirrhosis)
-Lymphatic obstruction (lymphedema) tumor, trauma, infection (filariasis)

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17
Q

What type of shock is associated with the triad symptoms of hypothermia, coagulopathy, and acidosis?

A

-Hypovolemic Shock

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18
Q

How do vascular changes at the site of inflammation lead to the classical local signs of acute inflammation?

A

A. changes in vascular diameter and flow that result in reduced blood velocity
vasodilation -diameter increases, fluid velocity decreases
increased viscosity - due to fluid loss to tissues
B. Increased vascular permeability

19
Q

What are the two major components of inflammation?

A

-eliminating infection and repairing

20
Q

What are the five mechanisms underlying increased vascular permeability during acute inflammation?

A

1.endothelial cell contraction/retraction leading to intercellular gaps that leak fluid
2.direct endothelial injury (trauma)
3.leukocyte-dependent endothelial cell damage/death due to release of toxic mediators by leukocytes
4.increased fluid flow through endothelial cells
5. leakage from new blood vessels that form at the site of injury

21
Q

What events occur during white blood cell migration? What do adhesion molecules and enzymes do in this process?

A
  1. Margination and rolling
  2. Adhesion (Sialyl-Lewis X-modified glycoproteins on leukocytes is main attractor; selectins tell leukocytes where to bind)
  3. Firm Adhesion (Integrins on the leukocytes act as receptors; ICAM-1 and VCAM-1 act as ligands)
22
Q

What is the mechanisms of phagocytosis and degranulation? What is the definition of opsonin and how does it work?

A

Phagocytosis- leukocyes that bind and ingest microorganisms and dead cells through surface receptors or host proteins aka opsonins which coat microbes and target them for phagocytosis (opsonization)
Degranulation- fusion of the phagosome with a lysosome which forms a phagolysosome and causes the destruction of the phagosome contents by the contents of the lysosome

23
Q

What are the two general classes of local mediators and plasma mediators and the major role of them? (nitric oxide, TNF, IL1, ROS)

A

TNF, IL-1 (cytokines; local endothelial activation)
Nitric Oxide, ROS (killing of microbes)
Nitric Oxide (Vascular smooth muscle relaxation, phagocytosis, lysosomal degradation)
Plasma mediators-liver
local mediators-Cell-derived (preformed mediators and Newly synthesized)

24
Q

What is the metabolism of arachidonic acid in inflammation and the molecular targets of listed drugs?

A

COX 1/2 and 5-lipoxygenase
NSAIDS(COX 1/2 inhibitor) -aspirin, ibuprofen, naproxen, celebrex, Vioxx
Singulair-leukotriene receptor antagonist

25
Q

What are the four major effects of TNF/IL-1?

A

Endothelial effects, fibroblast effects, systemic effects, leukocyte effects

26
Q

What are the outcomes of acute inflammation?

A

-chronic inflammation
-resolution
-fibrosis

27
Q

What is the relationship and differences between acute and chronic inflammation?

A

acute- characterized by vascular changes, edema, and a predominantly neutophilic infiltrate
chronic- infiltration with mononuclear cells: macrophages, lymphocytes and plasma cells, tissue destruction, repair (angiogeneisis and fibrosis) results due to viral infectio; persistent microbial infection; prolonged exposure to toxic agents; and autoimmune diseases

28
Q

Why could anti-PD-1 and anti-CTLA-4 antibodies be useful for chronic HBC infection?

A

they can block interactions between T Cells and antigen presenting cells that lead to T Cell exhaustion

29
Q

What are the normal defense mechanisms against pathogens?

A

Physical and Chemical Barriers, Innate/Adaptive Immunity

30
Q

What are the common routes of infections and how pathogens break the normal defenses?

A

Skin- pathogens break by replease of enzymes to break the barrier, cuts, wounds, burns, IV catheters
Respiratory Tract-expressing molecules allow pathogen ti adhere to the respiratory tract
Intestinal Tract- bacteria release enterotoxins or exotoxins, damage internal mucosa and lamina propria and then pass through the mucosa. noneveloped viruses are resistant to bile/digestive enzymes. immuncompromised hosts fungi. Intestinal protozoan use cysts and helminthes cause obstruction of the gut
Urongenital tract- difference between male and femaile urogenital tract; antibiotic kill lactobacilli, microorganisms can attach to vaginal and cervical mucosa during sexual intercourse

31
Q

How are pathogens disseminated into various organs/tissues?

A

through the lymph into the bloodstream

32
Q

What are the four major mechanisms by which microbes can evade immune defense?

A
  1. Remaining inaccessible to the host immune system
  2. Constantly changing antigenic repertoires (Influenza, HIV)
  3. Inactivating antibodies or complement, resisting phagocytosis, or growing within phagocytes from ingestion
  4. Suppressing the host adaptive immune response, by inhibiting MHC expression and antigen presentation
33
Q

What are the mechanisms of viral entry?

A
  1. Host-cell receptors for a particular virus
  2. Cell-type speccific transcription factors that recognize viral enhancer and promoter sequences
  3. Physical barriers
34
Q

What are the mechanisms of bacterial injury?

A
  1. The ability of bacteria to cause disease (virulence)
  2. Bacterial adherence to host cells
  3. Virulence of intracellular bacteria
  4. Bacterial endotoxin (LPS)
  5. Bacterial exotoxins (proteases, hyaluronidase,coagulases,fibrinolysins)
35
Q

How does the diphtheria toxin inhibit protein synthesis?

A

The frament A of the toxin catalyzes the transfer of ADP-ribose from NAD to the EF-2, thus inactivating it and can kill a cell by ADP-ribosylating more than 10^6 EF-2 molecules

36
Q

What are the mechanisms of viral injury?

A
  1. Lysis of host cells
  2. Immune cell-mediated killing
  3. Alteration of apoptosis pathways
  4. Induction of cell proliferation and transformation, resulting in cancer
  5. Inhibition of his cell DNA, RNA, or protein synthesis
  6. Damage to plasma membrane
  7. Damage to cells involved in antimicrobial defense, leading to secondary infections
37
Q

How do cells respond to injury?

A
  1. Homeostasis
  2. Adaptation
  3. Cell Injury
  4. Cell death
38
Q

What are the five major cellular adaptations in response to injury or stimuli?

A
  1. Hypertrophy (size)
  2. Hyperplasia (number)
  3. Atrophy (size)
  4. Metaplasia (form)
  5. Dysplasia (organization)
39
Q

What are the 8 causes of cell injury and examples?

A
  1. Oxygen Deprivation (hypoxia; ischemia)
  2. Chemical agents (poisons, air pollutants, CO, asbestos)
  3. Infectious agents (viruses, bacteria, fungi, parasites)
  4. Immunological reactions (autoimmune diseases)
  5. Genetic defects (sickle cell anemia, familial hypercholesterolemia)
  6. Physical agents (trauma, heat, cold, electric shock)
  7. Nutritional imbalances-typically indirect causes of injury (too little calories/vitamins, excess nutrition, diabetes, atherosclerosis)
  8. Aging (accumulation of damage by ROS, loss of telomerase function)
40
Q

What are the characteristics of reversible versus irreversible cell injury?

A

Reversible injury
1. Cellular swelling
2. Fatty change
Irreversible injury
1. mitochondrial dysfunction
2. membrane dysfunction

41
Q

What are the mechanisms of cell injury (ATP depletion, mitochondria damage, membrane damage, calcium influx, increased ROS)?

A

ATP depletion (due to ischemia/hypoxia)
Damage to mitochondria (increase cytosolic Ca2+, ROS, lipid peroxidation)
Influx of Calcium (leads to activation of various enzymes)
Increased oxidative stress (lipid peroxidation of membranes, DNA fragmentation, Protein oxidation and cross-linking)
Defects in membrane permeability (mitochondrial membrane damage, plasma membrane damage, lysosomal membrane damage)

42
Q

What are the two apoptotic pathways and their causes?

A

Mitochondrial (intrinsic) pathway and Death receptor (extrinsic) pathway
Physiological causes: programmed destruction of cells during embryogenesis; Involution of Hormone-dependent tissues upon hormone deprivation; Cell loss in proliferating cell populations; Elimination of potentially harmful self-reactive lymphocytes; Cell death induced by cytotoxic T lymphocytes
Pathological causes: DNA damage, misfolded proteins, cell injury in certain infection, pathological atrophy in parenchymal organs after duct obstruction

43
Q

What is the difference between apoptosis and necrosis?

A

Necrosis- cell side is enlarged, plasma membrane is disrupted, leakage of cellular contents, frequent inflammation, and pathologic
Apoptosis- reduced cell size, Nucleus is fragmented into nucleosome sized fragments, Plasma membrane is intact bit altered structured as well as cellular contents, no inflammation and is often physiologic and may be pathologic

44
Q

What is the role of major players in the two apoptotic pathways (Bcl-2, Bax, caspase-3,7,9, cytochrome C) and DNA fragmentation?

A

Bax, Bak increase mitochondrial membrane permeability (pro-apoptotic)
Bcl-2 bind Bax and inhibit their function (anti-apoptopic)
cytochrome C activates caspase-9 which initiates the caspase cascade
Caspase 3 and 7 are excutioner capsases

Pharmacy School Fall P1 (30 decks)

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