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APhA reviewer FPGEE > Chapter 26 Clinical Pathophysiology > Flashcards

Chapter 26 Clinical Pathophysiology Flashcards

1
Q
  • reaction of vascularized tissue in the body to local injury or insult.
  • Protective attempt to remove harmful stimuli
A

Inflammation

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2
Q

Chemical irritants or toxins
Mechanical or physical trauma
Altered or damaged cells
Microorganisms

A

Causes of inflammation

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3
Q

Redness
Fever
Swelling

A

Signs and symptoms of ACUTE INFLAMMATION

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4
Q

long-term damage

as in Cancer and lung disease

A

Signs and symptoms of CHRONIC INFLAMMATION

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5
Q

Vascular and Cellular

A

Components of inflammatory response

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6
Q

component of inflammatory response that causes
Dilation of the microvasculature
allowing increased permeability of macromolecules into the tissue space
may cause EDEMA

A

VASCULAR component

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7
Q

component of inflammatory response that causes

MARGINATION

A

CELLULAR component

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8
Q

Leukocytes relocate to the endothelium wall

A

Margination

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9
Q

white blood cells

A

Leukocytes

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10
Q

mast cells-release produces vasodilation/increased permeability

A

Histamine

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11
Q
  • inactive form in plasma

- activation leads to different inflammatory cascades

A

Factor XII(Hageman factor)

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12
Q

cascade that causes THROMBIN FORMATION-FIBRINOGEN TO FIBRIN

A

coagulation cascade

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13
Q

peptide=VASCULAR DILATION/INCREASED PERMEABILITY

A

BRADYKININ

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14
Q

cascade that causes BRADYKININ production

A

Kinin cascade

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15
Q

cascade that causes PLASMIN production

A

Fibrinolytic cascade

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16
Q

cascade that causes

MEMBRANE ATTACK/inflammatory mediators=chemotaxis,phagocytosis, histamine release

A

complement cascade

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17
Q

fatty acid-precursor to COX and LOX

A

Arachidonic acid

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18
Q

pathway that

Prostaglandins and thromboxanes

A

Cyclooxygenase pathway

COX pathway

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19
Q

pathway that produces

LEUKOTRIENES

A

Lipoxygenase pathway

LOX pathway

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20
Q

COX product that promotes

VASODILATION/INCREASED PERMEABILITY

A

Prostaglandin

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21
Q

COX product that promotes PLATELET AGGREGATION(repair)

A

Thromboxanes

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22
Q

LOX product that promotes

CHEMOTAXIS-VASODILATION-INCRESED PERMEABILITY

A

Leukotrienes

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23
Q

fluid in interstitial spaces

A

Edema

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24
Q

composes 50-60% body weight

A

BODY WATER

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25
Q

2/3 of body water

A

Intracellular component

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26
Q

1/3 of body water

-interstitial space separated by capillary wall

A

Extracellular component

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27
Q

controls normal exchange in the compartments

A

hydrostatic and osmotic pressure

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28
Q

regulate hydrostatic and osmotic pressure

A

plasma proteins

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29
Q

__________hydrostatic pressure causes EDEMA

A

INCREASED

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30
Q

__________osmotic pressure

causes EDEMA

A

DECREASED

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31
Q

increased blood volume

A

Congestion and hyperemia

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32
Q

passive-drainage is interrupted EX: VALVULAR STENOSIS

A

Congestion

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33
Q

active-Increased blood flow EX:ACUTE INFLAMMATION

A

Hyperemia

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34
Q

blood out of the circulatory system

A

Hemorrhage

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35
Q

trauma;
vascular wall damage resulting from disease;
or malfunction of the body’s normal mechanism to maintain hemostasis(CLOTTING)

A

CAUSES OF HEMORRHAGE

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36
Q

accumulation of blood bruise to subdural hematoma

A

Hematoma

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37
Q

<0.3 cm

A

Petechiae

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38
Q

0.3 and 1 cm

A

Purpuras

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39
Q

> =1 cm

A

Ecchymoses

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40
Q

pathologic process of blood clotting

A

Thrombosis

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41
Q

formed clot

A

Thrombus

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42
Q

Virchow’s triad

A

Decreased blood flow
Injury
Coagulation changes

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43
Q
  • movement of dislodged mass/embolus

- most common-deep veins

A

Embolism

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44
Q

emboli from blood clots

A

Thromboemboli

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45
Q

ischemic necrosis

A

Infarction

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46
Q

lack of adequate blood supply

A

Ischemia

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47
Q

thickening of the arterial wall by lipid plaques

A

Atherosclerosis

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48
Q

inadequate blood flow=decreased perfusion

A

Shock

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49
Q

-cold, mottled skin; mental status changes; and oliguria

A

SIGNS and SYMPTOMS of SHOCK

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50
Q

SHOCK from hemorrhage or trauma

A

Hypovolemic Shock

51
Q

SHOCK from low volume produced by body

A

Distributive Shock

52
Q

SHOCK from INFECTION

A

Septic shock

53
Q

SHOCK from ANAPHYLAXIS

A

Anaphylactic

54
Q

SHOCK from MEDICATIONS

A

Neurogenic

55
Q

SHOCK from cardiac malfunction-commonly caused by myocardial infarction or cardiac arrhythmias

A

Cardiogenic Shock

56
Q

SHOCK from blood flow that is interrupted or obstructed

A

Obstructive shock

57
Q

GOAL OF THERAPY for shock

A

restore blood flow

58
Q

STAGE OF SHOCK where

body feedback mechs are activated

A

Nonprogressive stage

59
Q

STAGE OF SHOCK where

damage/less compensation

A

Progressive stage

damage/ mababa bayad pa, progressive palang

60
Q

STAGE OF SHOCK where

sustained injury beyond repair

A

Irreversible stage

61
Q

CAUSES OF DEVELOPMENTAL DEFECTS

A 
DD GEMI
Genetic or chromosomal abnormality
Environment
Multifactorial
Idiopathic
62
Q

intrinsic cause

A

Malformations

MALIC

63
Q
  • defects in the form, shape, or position of a body part

- abnormal mechanical forces placed on the fetus during development.

A 
Deformations
FORM
SHAPE
POSITION
MECHANICAL FORCES
64
Q

defect in cellular organization or arrangement.

A

Dysplasias

65
Q

extrinsic exposures

A

Disruptions

ex ex disrupt

66
Q

missing or extra chromosomes commonly from NONDISJUNCTION

A

aneuploidy

67
Q
  • most common numerical abnormality
  • Error in cell division/meiotic segregation
  • less commonly caused by MOSAICISM and Robertsonian translocation of Chrom 21/14
A

DOWN SYNDROME-Trisomy 21

68
Q

-missing or additional genetic material

A

Structural abnormalities

MA/Structural

69
Q
  • translocation of chromosomes 9 and 22 occurs

- chronic myelogenous leukemia

A

Philadelphia chromosomes

70
Q

environmental agents

A

Teratogens

Tera sa environment

71
Q

infection-cat feces-undercooked meats

A

Toxoplasma gondii

72
Q

growth and mental retardation

A

Radiation

ILAWAN MO ANG UTAK MO

73
Q

deformities such as limb abnormalities and congenital heart defects

A

DM/HTN while pregnant

74
Q

overgrowth or abnormal proliferation of cells

A

Neoplasia NEOVERGROWTH

75
Q

Carcinogens alter/mutate DNA

A

Neoplasm ALTERASM

76
Q

failure of organ formation during embryo development

A

Agenesis

FAILURE EMBRYO AGENT

77
Q

failure of organ or tissue development

A

Aplasia

PLAISURE of org/tiss development

78
Q

enlargement or overgrowth of an organ or tissue because of an increase in CELL SIZE

A

Hypertrophy

79
Q

enlargement in the size of an organ or tissue because of cellular PROLIFERATION

A

Hyperplasia

80
Q

BREAKDOWN of a given body tissue or organ.

A

Atrophy

81
Q

CHANGE IN CELL TYPE

A

Metaplasia

82
Q

ABNORMAL MATURATION/ORGANIZATION/ARRANGEMENT or DIFFERENTIATION of cells

A

Dysplasia

83
Q

slower growing non-invasive

A

Benign neoplasm

84
Q

rapid invading disrupting

A

Malignant neoplasm

85
Q

Invasion into surrounding tissue/distant sites

A

Metastasis

86
Q

physical or chemical agents capable of causing genetic mutations

A

Carcinogens

87
Q

Carcinogens

A 
Tobacco and tobacco smoke
Radiation (e.g., ultraviolet rays from the sun)
Viruses (e.g., human papillomavirus)
Asbestos
Certain pesticides
Certain heavy metals (e.g., lead)
88
Q

codes for proteins that control cell proliferation, differentiation, and elimination

A

Proto-oncogenes

89
Q

defective and mutated POG

A

Oncogenes

90
Q

is a single nucleotide change in the DNA sequence that results in a change in a single amino acid in a protein

A

Point mutation

91
Q

overexpression of the encoded protein.

A

Gene amplification

92
Q

inappropriate expression of the gene.

A

Chromosomal translocation

93
Q

recessive-Mutation of both alleles=inactivation of the protein

A

Tumor suppressor genes

94
Q

corrects errors during cell duplication

A

DNA repair genes

95
Q

wasting syndrome loss of body fat and mass~often by malignancy
-generalized weakness, weight loss, anorexia, and fever

A

Cachexia

96
Q

Hypertension

A

> 130/80mmHg

97
Q

no cause identified-more common HTN

A

Primary HTN

98
Q

known cause-HTN

Renal artery stenosis, chronic renal disease, and hyperaldosteronism

A

Secondary HTN

99
Q
  • JG cells of the kidney converts Angiotensinogen to Angiotensin 1 in
    • RESPONSE TO decreased renal arteriolar pressure or blood flow
A

RENIN

100
Q

Angiotensin I to II

A

ANGIOTENSIN CONVERTING ENZYME

101
Q

potent direct vasoconstrictor

-stimulates aldosterone

A

ANGIOTENSIN II

102
Q

responsible for sodium and water retention=INCREASED BLOOD VOLUME&VASCULAR RESISTANCE

A

ALDOSTERONE

103
Q

Sympathetic NS regulation mechanism

A

CATHECOLAMINES

104
Q
  • secreted by the atria of the heart in response to increased blood flow.
    • increases urinary excretion of sodium and water
    • decrease in blood pressure
A

ATRIAL NATRIURETIC PEPTIDE

105
Q

potent vasodilator

A

NITRIC OXIDE

106
Q

VASOCONSTRICTOR=HYPERTENSION

A

ENDOTHELIN

107
Q

PRODUCTION OR USE of insulin is IMPAIRED

A

Diabetes mellitus

108
Q

transport of glucose

	- beta cells of the islets of Langerhans of the pancreas
	- release~serum glucose levels
A

INSULIN

109
Q

DM TYPE

IMMUNE-mediated *idiopathic-most common in children/adolescent

A

DM TYPE 1

110
Q

DM TYPE

insulin resistance & secretion deficiency

A

DM TYPE 2

111
Q 
Gestational diabetes
Drug-induced
Genetic defects
Exocrine pancreas disease 
Endocrinopathies
Infections
A

Secondary DM types

112
Q

SYMPTOMS

ACUTE DM

A 
polyuria-increases urine output
polydipsia-thirst from dehydration
polyphagia-hunger caused by calorie and glucose loss in urine
fatigue
weight loss
113
Q

most commonly seen in type 1 disease

A

DKA

114
Q

free fatty acids from lipid breakdown~KETONE BODIES-ACIDOTIC STATE

A

lipolysis

115
Q

CHRONIC DM TYPE of complication with HIGHER RISK OF-hypertension,myocardial infarction, stroke, and coagulopathies

A

MACROVASCULAR

116
Q

CHRONIC DM TYPE of complication where there is
Formation of advanced glycosylation end products
Sorbitol formation in cells through the polyol pathway
Oxidative stress as a result of hyperglycemia

A

MICROVASCULAR

117
Q

fat elevation in the blood

A

Hyperlipidemia

118
Q

ormed and secreted by the liver. They are rich in triglycerides and are eventually converted to lowdensity
lipoproteins.

A

VLDLs

119
Q

formed by catabolism of VLDLs

major transporters of cholesterol from the liver to tissue.

A

LDLs

120
Q

“good cholesterol”

A

secreted by the liver and intestine into the blood,
where they take up cholesterol and transport it back to the liver; there it
is excreted into bile

121
Q

-formed from exogenous fat sources and solubilized in
the intestinal epithelium
-carry lipids to muscle and adipose tissue.

A

Chylomicrons

122
Q

chronic airway inflammatory disorder
attacks
bronchospasms,
mucus hypersecretion, and inflammation

A

ASTHMA

123
Q

allergic irritant

release of histamine and leukotrienes from mast cells

A

ASTHMA

124
Q

ASTHMA TREATMENT

A

ACUTE:SABA

MAINTENANCE/CHRONIC:ICS

APhA reviewer FPGEE (15 decks)

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