Chapter 26 Clinical Pathophysiology Flashcards
(124 cards)
1
Q
- reaction of vascularized tissue in the body to local injury or insult.
- Protective attempt to remove harmful stimuli
A
Inflammation
2
Q
Chemical irritants or toxins
Mechanical or physical trauma
Altered or damaged cells
Microorganisms
A
Causes of inflammation
3
Q
Redness
Fever
Swelling
A
Signs and symptoms of ACUTE INFLAMMATION
4
Q
long-term damage
as in Cancer and lung disease
A
Signs and symptoms of CHRONIC INFLAMMATION
5
Q
Vascular and Cellular
A
Components of inflammatory response
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
7
Q
component of inflammatory response that causes
MARGINATION
A
CELLULAR component
8
Q
Leukocytes relocate to the endothelium wall
A
Margination
9
Q
white blood cells
A
Leukocytes
10
Q
mast cells-release produces vasodilation/increased permeability
A
Histamine
11
Q
- inactive form in plasma
- activation leads to different inflammatory cascades
A
Factor XII(Hageman factor)
12
Q
cascade that causes THROMBIN FORMATION-FIBRINOGEN TO FIBRIN
A
coagulation cascade
13
Q
peptide=VASCULAR DILATION/INCREASED PERMEABILITY
A
BRADYKININ
14
Q
cascade that causes BRADYKININ production
A
Kinin cascade
15
Q
cascade that causes PLASMIN production
A
Fibrinolytic cascade
16
Q
cascade that causes
MEMBRANE ATTACK/inflammatory mediators=chemotaxis,phagocytosis, histamine release
A
complement cascade
17
Q
fatty acid-precursor to COX and LOX
A
Arachidonic acid
18
Q
pathway that
Prostaglandins and thromboxanes
A
Cyclooxygenase pathway
COX pathway
19
Q
pathway that produces
LEUKOTRIENES
A
Lipoxygenase pathway
LOX pathway
20
Q
COX product that promotes
VASODILATION/INCREASED PERMEABILITY
A
Prostaglandin
21
Q
COX product that promotes PLATELET AGGREGATION(repair)
A
Thromboxanes
22
Q
LOX product that promotes
CHEMOTAXIS-VASODILATION-INCRESED PERMEABILITY
A
Leukotrienes
23
Q
fluid in interstitial spaces
A
Edema
24
Q
composes 50-60% body weight
A
BODY WATER
25
2/3 of body water
Intracellular component
26
1/3 of body water
| -interstitial space separated by capillary wall
Extracellular component
27
controls normal exchange in the compartments
hydrostatic and osmotic pressure
28
regulate hydrostatic and osmotic pressure
plasma proteins
29
__________hydrostatic pressure causes EDEMA
INCREASED
30
__________osmotic pressure
| causes EDEMA
DECREASED
31
increased blood volume
Congestion and hyperemia
32
passive-drainage is interrupted EX: VALVULAR STENOSIS
Congestion
33
active-Increased blood flow EX:ACUTE INFLAMMATION
Hyperemia
34
blood out of the circulatory system
Hemorrhage
35
trauma;
vascular wall damage resulting from disease;
or malfunction of the body’s normal mechanism to maintain hemostasis(CLOTTING)
CAUSES OF HEMORRHAGE
36
accumulation of blood bruise to subdural hematoma
Hematoma
37
<0.3 cm
Petechiae
38
0.3 and 1 cm
Purpuras
39
>=1 cm
Ecchymoses
40
pathologic process of blood clotting
Thrombosis
41
formed clot
Thrombus
42
Virchow's triad
Decreased blood flow
Injury
Coagulation changes
43
- movement of dislodged mass/embolus
| - most common-deep veins
Embolism
44
emboli from blood clots
Thromboemboli
45
ischemic necrosis
Infarction
46
lack of adequate blood supply
Ischemia
47
thickening of the arterial wall by lipid plaques
Atherosclerosis
48
inadequate blood flow=decreased perfusion
Shock
49
-cold, mottled skin; mental status changes; and oliguria
SIGNS and SYMPTOMS of SHOCK
50
SHOCK from hemorrhage or trauma
Hypovolemic Shock
51
SHOCK from low volume produced by body
Distributive Shock
52
SHOCK from INFECTION
Septic shock
53
SHOCK from ANAPHYLAXIS
Anaphylactic
54
SHOCK from MEDICATIONS
Neurogenic
55
SHOCK from cardiac malfunction-commonly caused by myocardial infarction or cardiac arrhythmias
Cardiogenic Shock
56
SHOCK from blood flow that is interrupted or obstructed
Obstructive shock
57
GOAL OF THERAPY for shock
restore blood flow
58
STAGE OF SHOCK where
| body feedback mechs are activated
Nonprogressive stage
59
STAGE OF SHOCK where
| damage/less compensation
Progressive stage
damage/ mababa bayad pa, progressive palang
60
STAGE OF SHOCK where
| sustained injury beyond repair
Irreversible stage
61
CAUSES OF DEVELOPMENTAL DEFECTS
```
DD GEMI
Genetic or chromosomal abnormality
Environment
Multifactorial
Idiopathic
```
62
intrinsic cause
Malformations
| MALIC
63
- defects in the form, shape, or position of a body part
| - abnormal mechanical forces placed on the fetus during development.
```
Deformations
FORM
SHAPE
POSITION
MECHANICAL FORCES
```
64
defect in cellular organization or arrangement.
Dysplasias
65
extrinsic exposures
Disruptions
| ex ex disrupt
66
missing or extra chromosomes commonly from NONDISJUNCTION
aneuploidy
67
- most common numerical abnormality
- Error in cell division/meiotic segregation
- less commonly caused by MOSAICISM and Robertsonian translocation of Chrom 21/14
DOWN SYNDROME-Trisomy 21
68
-missing or additional genetic material
Structural abnormalities
MA/Structural
69
- translocation of chromosomes 9 and 22 occurs
| - chronic myelogenous leukemia
Philadelphia chromosomes
70
environmental agents
Teratogens
| Tera sa environment
71
infection-cat feces-undercooked meats
Toxoplasma gondii
72
growth and mental retardation
Radiation
| ILAWAN MO ANG UTAK MO
73
deformities such as limb abnormalities and congenital heart defects
DM/HTN while pregnant
74
overgrowth or abnormal proliferation of cells
Neoplasia NEOVERGROWTH
75
Carcinogens alter/mutate DNA
Neoplasm ALTERASM
76
failure of organ formation during embryo development
Agenesis
| FAILURE EMBRYO AGENT
77
failure of organ or tissue development
Aplasia
| PLAISURE of org/tiss development
78
enlargement or overgrowth of an organ or tissue because of an increase in CELL SIZE
Hypertrophy
79
enlargement in the size of an organ or tissue because of cellular PROLIFERATION
Hyperplasia
80
BREAKDOWN of a given body tissue or organ.
Atrophy
81
CHANGE IN CELL TYPE
Metaplasia
82
ABNORMAL MATURATION/ORGANIZATION/ARRANGEMENT or DIFFERENTIATION of cells
Dysplasia
83
slower growing non-invasive
Benign neoplasm
84
rapid invading disrupting
Malignant neoplasm
85
Invasion into surrounding tissue/distant sites
Metastasis
86
physical or chemical agents capable of causing genetic mutations
Carcinogens
87
Carcinogens
```
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
codes for proteins that control cell proliferation, differentiation, and elimination
Proto-oncogenes
89
defective and mutated POG
Oncogenes
90
is a single nucleotide change in the DNA sequence that results in a change in a single amino acid in a protein
Point mutation
91
overexpression of the encoded protein.
Gene amplification
92
inappropriate expression of the gene.
Chromosomal translocation
93
recessive-Mutation of both alleles=inactivation of the protein
Tumor suppressor genes
94
corrects errors during cell duplication
DNA repair genes
95
wasting syndrome loss of body fat and mass~often by malignancy
-generalized weakness, weight loss, anorexia, and fever
Cachexia
96
Hypertension
>130/80mmHg
97
no cause identified-more common HTN
Primary HTN
98
known cause-HTN
| Renal artery stenosis, chronic renal disease, and hyperaldosteronism
Secondary HTN
99
- JG cells of the kidney converts Angiotensinogen to Angiotensin 1 in
- RESPONSE TO decreased renal arteriolar pressure or blood flow
RENIN
100
Angiotensin I to II
ANGIOTENSIN CONVERTING ENZYME
101
potent direct vasoconstrictor
| -stimulates aldosterone
ANGIOTENSIN II
102
responsible for sodium and water retention=INCREASED BLOOD VOLUME&VASCULAR RESISTANCE
ALDOSTERONE
103
Sympathetic NS regulation mechanism
CATHECOLAMINES
104
- secreted by the atria of the heart in response to increased blood flow.
- increases urinary excretion of sodium and water
- decrease in blood pressure
ATRIAL NATRIURETIC PEPTIDE
105
potent vasodilator
NITRIC OXIDE
106
VASOCONSTRICTOR=HYPERTENSION
ENDOTHELIN
107
PRODUCTION OR USE of insulin is IMPAIRED
Diabetes mellitus
108
transport of glucose
- beta cells of the islets of Langerhans of the pancreas
- release~serum glucose levels
INSULIN
109
DM TYPE
| IMMUNE-mediated *idiopathic-most common in children/adolescent
DM TYPE 1
110
DM TYPE
| insulin resistance & secretion deficiency
DM TYPE 2
111
```
Gestational diabetes
Drug-induced
Genetic defects
Exocrine pancreas disease
Endocrinopathies
Infections
```
Secondary DM types
112
SYMPTOMS
| ACUTE DM
```
polyuria-increases urine output
polydipsia-thirst from dehydration
polyphagia-hunger caused by calorie and glucose loss in urine
fatigue
weight loss
```
113
most commonly seen in type 1 disease
DKA
114
free fatty acids from lipid breakdown~KETONE BODIES-ACIDOTIC STATE
lipolysis
115
CHRONIC DM TYPE of complication with HIGHER RISK OF-hypertension,myocardial infarction, stroke, and coagulopathies
MACROVASCULAR
116
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
MICROVASCULAR
117
fat elevation in the blood
Hyperlipidemia
118
ormed and secreted by the liver. They are rich in triglycerides and are eventually converted to lowdensity
lipoproteins.
VLDLs
119
formed by catabolism of VLDLs
| major transporters of cholesterol from the liver to tissue.
LDLs
120
“good cholesterol"
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
-formed from exogenous fat sources and solubilized in
the intestinal epithelium
-carry lipids to muscle and adipose tissue.
Chylomicrons
122
chronic airway inflammatory disorder
attacks
bronchospasms,
mucus hypersecretion, and inflammation
ASTHMA
123
allergic irritant
| release of histamine and leukotrienes from mast cells
ASTHMA
124
ASTHMA TREATMENT
ACUTE:SABA
| MAINTENANCE/CHRONIC:ICS
