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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
Q

Addiction

A

Condition manifesting as uncontrollable cravings, inability to control drug use, compulsive drug use, and use despite doing harm to oneself or others. Behavioral.

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26
Q

Apirin

A

1st gen NSAID. Inflammation suppression, analgesia, antipyretic, prevention of platelet aggregation.

Don’t use in peds! Reye’s.

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27
Q

Mu vs Kappa receptors

A

Mu has more. Both have analgesia, sedation, decreased GI motility. Mu also has respiratory depression, physicall dependence, euphoria

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28
Q

Physiology at birth

A

Increased systemic vascular resistance
Decreased pulmonary vascular resistance
Closure of ductus arterioles, foramen vale, ductus venous

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29
Q

Pathogenicity

A

Ability to cause a disease

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30
Q

Virulence

A

How severe a disease is

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31
Q

Most common parasite locations

A

Skin, GI

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32
Q

Infections caused by fungi are called….

A

mycoses

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33
Q

Cell wall synthesis inhibiting drugs

A 
Amoxicillin
Amoxicilin + Clavulanic Acid
Piperacillin + Tazobactam
Cephalexin
Cephtriaxone
34
Q

Amoxicillin

A

Cell wall synthesis. Broad spectrum, oral, renally eliminated. G+ and G-.

35
Q

Amoxicilin + Clavulanic Acid

A

Cell wall synthesis. G+, G-, extends spectrum to organisms that produce beta-lactamase

36
Q

Piperacillin + Tazobactam

A

Cell wall synthesis. Broad spectrum G+ G- anaerobes. Not oral.

37
Q

Cephalexin.

A

Cell wall synthesis. 1st gen cephalosporin, mainly G+ (skin flora). Renally eliminated.

38
Q

Cephtriaxone.

A

Cell wall synthesis. 3rd gen cephalosporin. IM/IV. Some G+ and G-, excellent CNS penetration.

Don’t use in neonates!

39
Q

Protein Synthesis Inhibition

A

Doxycycline

Azithromycin

40
Q

Doxycycline

A

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
Q

Azithromycin

A

Protein synthesis inhibition. Covers atypical organisms like chlamydia and mycoplasm.

42
Q

DNA Synthesis Inhibition

A

Metronidazole

43
Q

Metronidazole

A

DNA synthesis inhibition. Protozoa (trick, giardiasis, systemic amebiasis), and anaerobic bacteria. Interactions with CYP 34A substrate (warpharin, phenobarbital)

44
Q

Fluconazole

A

Antifungal. Inhibits CYP 450 dependent synthesis of ergosterol, resulting in damage to cytoplasmic membrane and accumulation of ergosterol precursors. Mostly used for candida.

45
Q

Pernicious anemia

A

Lack of vitamin B -> altered DNA synthesis

46
Q

Folate deficiency anemia

A

Leads to premature cell death

47
Q

Iron deficiency anemia

A

Lack of hemoglobin

48
Q

Thalassemia

A

Congenital. Impaired synthesis of hemoglobin chain

49
Q

Aplastic anemia

A

Bone marrow suppression -> decreased RBC production

50
Q

Sickle cell anemia

A

Congenital. Abnormal hemoglobin molecule

51
Q

Post hemorrhage anemia

A

Blood loss -> insufficient RBCs

52
Q

Anemia of chronic disease

A

Chronic infection/inflammation/malignancy -> increased demand or suppression

53
Q

Hemolytic disease of newborn

A

Maternal antibodies cause destruction fo fetal cells

54
Q

Petechia

A

Flat pinpoints

55
Q

Purpura

A

Groups/patches of petichia. Itchier.

56
Q

Echymosis

A

Bruising

57
Q

Hemarthrosis

A

Blood at joint

58
Q

Hematoma

A

Blood collection in tissue

59
Q

Hematochezia

A

Blood from the anus

60
Q

Epistaxis

A

Nose bleeds

61
Q

Hemoptysis

A

Coughing up blood

62
Q

Platelet count nml values

A

150,000 - 450,000

63
Q

INR

A

0.9 - 1.1

64
Q

APTT

A

Activated partial thromboplastin time. Evaluates intrinsic pathway of coagulation.

65
Q

CBC

A

Determines if anemia is present, # of platelets, morphology of platelets.

66
Q

Thrombocytopenia

A

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
Q

Virchow’s Triad

A

Endothelia/Vessel wall injury

Circulatory stasis

Hypercoagulable conditions

68
Q

DVT Treatment

A
  • Thrombolytic to break down the clot

- Anticoagulant to reduce further clot formation

69
Q

Unfractionated/low molecular weight Heparin

A

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
Q

Heparin antidote

A

Protamine sulfate

71
Q

Unfractionated Heparin

A

“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
Q

Warfarin

A

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
Q

Warfarin antidote

A

Phytonadione (Vitamin K)

74
Q

DOACs

A

Dabigatran

Rivaroxaban

75
Q

Dabigatran

A

Thrombin inhibitor. No labs. Some drug interactions, increased bleeding risk. Can have GI effects, abdominal pain.

Antidote: Idarucizumab

76
Q

Dabigatran antidote

A

Idarucizumab

77
Q

Rivaroxaban

A

Factor Xa inhibitor. NO antidote. Active less immediately, fewer drug interactions than warfarin.

78
Q

Rivaroxaban antidote

A

NONE

79
Q

Cyanocobalamin

A

Vitamin B12, for anemia

80
Q

Iron Dextran

A

Parenteral iron for iron deficiency anemia

DUSON Summer '18 (8 decks)

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