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DUSON Summer '18 > Patho/Pharm 2 > Flashcards

Patho/Pharm 2 Flashcards

1
Q

When presented with a challenge, cells….(3)

A
  • Withstand and return to normal (reversible)
  • Adapt (generally reversible)
  • Die (irreversible)
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2
Q

Types of reversible cell injury

A

Hydropic, cellular accumulations

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3
Q

Types of generally reversible cell injury

A

Atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia (this is least reversible)

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4
Q

Types of irreversible cell injury

A

Necrosis, apoptosis

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5
Q

Hydropic cell injury

A

Due to accumulation of water. Results from malfunction of Na-K pumps (Na ions in cell bring water in). First manifestation of most forms of reversible cell injury.

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6
Q

-megaly

A

Generalized swelling in the cells of particular organs. Increase in size and wait.

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7
Q

Intracellular Accumulations

A
  • Excessive amounts of normal intracellular substances (lipids, carbs, glycogen).
  • Accumulation of abnormal substances produced by cell b/c of issues (underlying issue, glucose)
  • Accumulation of pigments and particles that cell is unable to degrade (bilirubin - jaundice)
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8
Q

Cellular adaptations to increases or decreases in functional demand

A
  • Atrophy: cells shrink and reduce their function
  • Hypertrophy: cells increase in mass, augmented functional capacity
  • Hyperplasia: increase in the number of cells by biotic division to meet the physiologic demands as a result of injury.
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9
Q

Cellular adaptations to persistent injury

A
  • Metaplasia: replacement of one differentiated cell type with another
  • Dysplasia: abnormal appearance of cells d/t abnormal variations in shape, she, and arrangement. Disorderly growth. Significant probability of cancer developing.
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10
Q

Necrosis

A

Results from ischemia or toxic injury. Breakdown of plasma membrane. Cells rupture and spill their contents -> inflammation. Changes in WBC, fever, systemic signs (malaise, loss of appetite).

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11
Q

Apoptosis

A

Doesn’t directly kill the cell, but activates a chain of events that leads to cellular death. Cell membrane stays intact but blebs off, becomes phagocytize. No damage to surrounding cells, no inflammation. Intracellular triggers tell cell it’s time to die. Normal process of self regulation (except in heart failure/dementia).

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12
Q

Etiology of cellular injury

A 
Ischemia and hypoxia
Nutritional
Infectious and immunologic
Chemical
Physical and mechanical
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13
Q

Hypoxia

A

Poor oxygenation

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14
Q

Ischemia

A

Interruption of blood flow, worse than hypoxia alone because cells can adapt to hypoxia.

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15
Q

Hypoxia and Ischemia Mechanisms

A
  • ATP production in cell stalls
  • ATP dependent pumps fail
  • Na accumulates and brings water inside cell
  • Excess Ca in the mitochondria interferes
  • Glycogen stores are depleted
  • Lactate is produced
  • pH falls, cellular components are more dysfunctional
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16
Q

Calcium Overload

A

Increased concentration of Ca that crosses the cell membrane. Presence of extra calcium can trigger apoptosis. Can continue to have cell death after reintroduction of O2 due to excess Ca2+.

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17
Q

Formation of reactive oxygen molecules

A

Free radicals have an unpaired electron that is looking for a partner. They steal electrons from molecules, where they steal from is where the damage is.

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18
Q

Steps of Reperfusion Injury and Reactive Oxygen Species

A
  1. Calcium Overload
  2. Formation of reactive oxygen molecules
  3. Inflammation
  4. Complement activation
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19
Q

Nutritional Cellular Injuries

A

Deficiencies (iron, malabsorption), Excess (obesity)

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20
Q

Chemical Cellular Injuries

A

Free radicals, heavy metals (pregnancy, lead in children), toxic gases (ozone, carbon monoxide poisoning)

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21
Q

Physical and Mechanical Cellular Injuries

A 
Temperature extremes
Abrupt changes in atmospheric pressure (the bends)
Abrasion - trauma
Electrical
Radiation
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22
Q

Infectious and Immunologic Cellular Injuries

A

Bacteria (endotoxins, exotoxins), Viruses, and indirect immunologic response.

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23
Q

Tolerance

A

State in which a larger dose is required to produce the same response as before on a smaller dose. Can develop tolerance to the sedation adn respiratory depression, but not to the constipation.

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24
Q

Physical Dependence

A

State in which an abstinence syndrome will occur if drug use is abruptly stopped. This is physiologic.

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25
Addiction
Condition manifesting as uncontrollable cravings, inability to control drug use, compulsive drug use, and use despite doing harm to oneself or others. Behavioral.
26
Apirin
1st gen NSAID. Inflammation suppression, analgesia, antipyretic, prevention of platelet aggregation. Don't use in peds! Reye's.
27
Mu vs Kappa receptors
Mu has more. Both have analgesia, sedation, decreased GI motility. Mu also has respiratory depression, physicall dependence, euphoria
28
Physiology at birth
Increased systemic vascular resistance Decreased pulmonary vascular resistance Closure of ductus arterioles, foramen vale, ductus venous
29
Pathogenicity
Ability to cause a disease
30
Virulence
How severe a disease is
31
Most common parasite locations
Skin, GI
32
Infections caused by fungi are called....
mycoses
33
Cell wall synthesis inhibiting drugs
``` Amoxicillin Amoxicilin + Clavulanic Acid Piperacillin + Tazobactam Cephalexin Cephtriaxone ```
34
Amoxicillin
Cell wall synthesis. Broad spectrum, oral, renally eliminated. G+ and G-.
35
Amoxicilin + Clavulanic Acid
Cell wall synthesis. G+, G-, extends spectrum to organisms that produce beta-lactamase
36
Piperacillin + Tazobactam
Cell wall synthesis. Broad spectrum G+ G- anaerobes. Not oral.
37
Cephalexin.
Cell wall synthesis. 1st gen cephalosporin, mainly G+ (skin flora). Renally eliminated.
38
Cephtriaxone.
Cell wall synthesis. 3rd gen cephalosporin. IM/IV. Some G+ and G-, excellent CNS penetration. Don't use in neonates!
39
Protein Synthesis Inhibition
Doxycycline | Azithromycin
40
Doxycycline
Protein synthesis inhibition. G+, G-, can't be taken with dairy or antacids within 2 hours. Phototoxicity! Don't use in pregnancy or children because of tooth discoloration.
41
Azithromycin
Protein synthesis inhibition. Covers atypical organisms like chlamydia and mycoplasm.
42
DNA Synthesis Inhibition
Metronidazole
43
Metronidazole
DNA synthesis inhibition. Protozoa (trick, giardiasis, systemic amebiasis), and anaerobic bacteria. Interactions with CYP 34A substrate (warpharin, phenobarbital)
44
Fluconazole
Antifungal. Inhibits CYP 450 dependent synthesis of ergosterol, resulting in damage to cytoplasmic membrane and accumulation of ergosterol precursors. Mostly used for candida.
45
Pernicious anemia
Lack of vitamin B -> altered DNA synthesis
46
Folate deficiency anemia
Leads to premature cell death
47
Iron deficiency anemia
Lack of hemoglobin
48
Thalassemia
Congenital. Impaired synthesis of hemoglobin chain
49
Aplastic anemia
Bone marrow suppression -> decreased RBC production
50
Sickle cell anemia
Congenital. Abnormal hemoglobin molecule
51
Post hemorrhage anemia
Blood loss -> insufficient RBCs
52
Anemia of chronic disease
Chronic infection/inflammation/malignancy -> increased demand or suppression
53
Hemolytic disease of newborn
Maternal antibodies cause destruction fo fetal cells
54
Petechia
Flat pinpoints
55
Purpura
Groups/patches of petichia. Itchier.
56
Echymosis
Bruising
57
Hemarthrosis
Blood at joint
58
Hematoma
Blood collection in tissue
59
Hematochezia
Blood from the anus
60
Epistaxis
Nose bleeds
61
Hemoptysis
Coughing up blood
62
Platelet count nml values
150,000 - 450,000
63
INR
0.9 - 1.1
64
APTT
Activated partial thromboplastin time. Evaluates intrinsic pathway of coagulation.
65
CBC
Determines if anemia is present, # of platelets, morphology of platelets.
66
Thrombocytopenia
Small # of platelets. Common cause of generalized bleeding. Decreased production or increased consumption of platelets. Assessment: petechiae, purpura, decreased platelet counts, bleeding. Treat or remove the cause!
67
Virchow's Triad
Endothelia/Vessel wall injury Circulatory stasis Hypercoagulable conditions
68
DVT Treatment
- Thrombolytic to break down the clot | - Anticoagulant to reduce further clot formation
69
Unfractionated/low molecular weight Heparin
Enoxaparin. Binds to factor Xa, does NOT bind to thrombin. Sub-q. More predictable bioavailability, doesn't require labs to be checked. Antidote: protamine sulfate
70
Heparin antidote
Protamine sulfate
71
Unfractionated Heparin
"hugs" both factor Xa and thrombin, so that prothrombin cannot convert to thrombin so no clotting. Must check APTT labs. IV or sub-q.
72
Warfarin
Oral anticoagulant. Vitamin K antagonist. Suppresses production of Factors 2, 7, 9, 10. Must monitor INR and PT labs. Long half life, delayed onset, LOTS of drug/food interactions. Antidote: Phytonadione (Vitamin K)
73
Warfarin antidote
Phytonadione (Vitamin K)
74
DOACs
Dabigatran | Rivaroxaban
75
Dabigatran
Thrombin inhibitor. No labs. Some drug interactions, increased bleeding risk. Can have GI effects, abdominal pain. Antidote: Idarucizumab
76
Dabigatran antidote
Idarucizumab
77
Rivaroxaban
Factor Xa inhibitor. NO antidote. Active less immediately, fewer drug interactions than warfarin.
78
Rivaroxaban antidote
NONE
79
Cyanocobalamin
Vitamin B12, for anemia
80
Iron Dextran
Parenteral iron for iron deficiency anemia

DUSON Summer '18 (8 decks)

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