Cardiovascular/CAD/PAD/Pulmonnary Flashcards

Flash cards for exam 3

1
Q

Blood flows from the RA thru the __ valve

A

Tricuspid

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2
Q

Blood flows from the LA thru the __ valve

A

Mitral

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3
Q

Blood flows from the RV thru the __ valve

A

Pulmonary

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4
Q

Blood flows from the LV thru the __ valve

A

Aortic

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5
Q

Heart valves in order of flow:

A

Tricuspid
Pulmonary
Mitral
Aortic

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6
Q

Average stroke volume:

A

70mL/Beat

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7
Q

Cardiac output is determined by:

A

SV X BPM

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8
Q

Ability of the heart muscle to pump effectively!

A

Cantractility

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9
Q

Volume of blood in ventricles before contraction

A

Preload

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10
Q

Pulmonary vascular Resistance

A

RV afterload

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11
Q

Systemic vascular resistance

A

LV afterload

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12
Q

RV afterload can cause

A

right sided heart failure

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13
Q

LV after load can be too high due to:

A

HTN or atherosclerosis/arteriosclerosis

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14
Q

RV afterload can be caused by

A

atherosclerosis/arteriosclerosis of pulmonary vessels; stiff, noncompliant lung tissue

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15
Q

Normal preload value:

A

~4-6 L/min

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16
Q

Blood flow back to the heart

A

venous return

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17
Q

Most venous disorders occur in:

A

the legs

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18
Q

CVI

A

chronic venous insufficiency

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19
Q

DVT

A

deep vein thrombosis

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20
Q

CVI & DVT are usually related to problems pertaining to:

A

maintaining forward flow

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21
Q

AKA “valve incompetence”

A

Venous insufficiency

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22
Q

Pooling of blood due to venous insufficiency

A

venous congestion

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23
Q

Factors contributing to venous congestion

A

Gravity (standing for long periods)

Valve incompetence

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24
Q

Worn out, “floppy” valves in leg veins

A

Venous insufficiency

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25
Blood pooling due to worn out, floppy leg vein valves
Venous stasis
26
Venous stasis causes an increase in:
hydrostatic pressure
27
Increased hydrostatic pressure can result in:
fluid shifting into the legs > edema
28
Mini concept map for Venous stasis ulcers
Venous stasis > increased hydro. pressure > fluid shift into tissue > edema > improperly functioning skin cells due to pressure > skin breaks easily > venous stasis ulcers
29
Another possible sequela to Venous insufficiency caused by increased hydrostatic pressure
Varicose veins
30
Contributing factors to CVI
``` Aging Genetics Obesity Pregnancy Job functions (standing) Immobility ```
31
Pathologic clot that forms in walls of veins, especially in veins of thighs & calves
deep vein thrombosis
32
Inflamed tissue around a DVT
thrombophlebitis
33
S/S of DVT
SHEP Usually occurs unilaterally May be extreme or discrete May have no S/S
34
Risk factors of DVT are called:
Virchow's Triad
35
Virchow's triad consists of:
Injury to venous endothelium Stasis of blood flow (due to immobility or venous insufficiency) States of hyper-coagulability (dehydration, individual tendencies to clot easily)
36
Individual tendency to clot easily is called
coagulopathy
37
Potentially deadly sequela of DVT
Pulmonary embolism
38
Mini concept map of PE
DVT > thrombus or part breaks loose & travels > embolus > embolus travels to/thru the heart > embolism lodges into pulmonary arterioles
39
Oxygenated blood blocked from entering the pulmonary capillaries due to an embolism can cause:
SOB, chest pain
40
Hemoptysis as a S/S of PE is caused by:
inflammation of alveolar tissue causing leakage of blood/fluids into the alveolar space
41
S/S of PE include:
SOB, chest pain, shock, hemoptysis, death
42
Treatment/prevention of PE includes:
Encouraging mobility & hydration Elevating feet & legs Monitor skin for breakdown & stasis ulcers Anticoagulants
43
Ability of arteries to work efficiently is determined by
vasomotor tone | State of the lumen
44
__ can be determined by vasomotor tone
BP
45
Normal, healthy arterial lumens should be
smooth and patent (free of any sort of blockage)
46
Delivery of O2 & nutrients to tissue beds via the arterial system
perfusion
47
Good perfusion results in:
adequate delivery of O2 & nutrients Normal pulses & BP Normal cap refill Normal organ function
48
Strength & quality of pulses are indicative of:
state of the lumen & vasomotor tone
49
AKA "arterial disease"
arterial insufficiency
50
Common to all arterial disorders is:
ischemia
51
Arterial dz is almost always due to
athero/arteriosclerosis
52
Atherosclerosis=
stiffening of arteries & buildup of fat & other substances in arterial walls
53
Chronic dz of arterial system usually related to aging, where arterial walls become thick & hard
arteriosclerosis
54
Etiology of arteriosclerosis is caused by vessel damage from:
``` HTN smoking diabetes infection high cholesterol aging genetics free radicals ```
55
Mini concept map of arteriosclerosis
tunica intima microscopically damage > collagen fibers enter vessel wall > stiffening of vessel wall > decreased elasticity & arterial compliance
56
Atherosclerosis develops from:
atherous involvement of arteriosclerosis
57
"fatty deposits"
Athero
58
Atherosclerotic walls have deposits of:
collagen as well as LDLs
59
Fatty deposits in arterial walls cause:
irritation | inflammatory & coagulation responses
60
Formation of a fibrous capsule with a fatty middle section
Plaque
61
Formation of plaque is caused by:
stiff arteries, fat deposits, and inflammatory & clotting responses
62
Sequela of plaque growing & protruding into the lumen
Ischemia
63
Buildup of blockage in/along arterial walls results in:
loss of vasomotor tone and non-patent lumen
64
If arterial pathology exists in one area...
it is usually occurring system-wide
65
Narrowed, stiff, atheromatous arteries often result in:
compromised perfusion > ischemia
66
Characteristics of ischemic pain:
increased with exacerbation decreases with rest present in tissue distal to the plaque or narrowed arteries
67
S/S of ischemia seen in the periphery
diminished/absent pulses delayed cap refill pale, cool skin/mucous membranes delayed healing
68
Specific S/S of ischemia in the heart
Altered function | decreased cardiac output
69
Specific S/S of ischemia in the brain
Altered LOC
70
Specific S/S of ischemia in the kidneys
Decreased urine output
71
Non-modifiable risk factors of arterial dz
``` Family HX (tendency to atherosclerosis &hypercholesterolemia) Advanced age > stiffer arteries ```
72
Modifiable risk factors for arterial dz
Diet, obesity, sedentary lifestyle Alcohol consumption DM2 Cigarettes/nicotine
73
Characteristic of DM2, increased circulating LDLs
lipodystrophy
74
Nicotine is a powerful ___
vasoconstrictor
75
Cardiovascular dz can be described as ___
atherosclerosis of coronary arteries
76
Venous insufficiency is often due to ___ and results in ___
bad valves in leg veins; venous congestion & peripheral edema
77
Arterial insufficiency is almost always due to ___ and results in ___
atherosclerosis; ischemia
78
PAD =
Peripheral artery disease
79
PAD is a dz of ___
any arterial vessels outside the heart, but most commonly refers to arterial problems of the legs
80
PAD usually manifests as __ due to __
problems of ischemia; narrowed peripheral arteries
81
S/S of PAD
``` Intermittent claudication Cool, pale feet Diminished pulses & delayed cap refill No hair growth on legs (shiny skin) Ischemic skin ulcers ```
82
5 Ps of PAD
``` Pain Pallor Paresthesias Pulselessness Poikilothermia ```
83
Poikilothermia =
cold, pale feet
84
Arterial thrombi form where __
flow is sluggish, and/or where there is narrowing/injury to vessel walls
85
Veinous thrombi block blood flow ___, causing ___
to the heart; congestion distal to the blockage
86
Arterial blockage results in ___
ischemia to distal tissue
87
If narrowing/injury/atherosclerosis occurs at an arterial bifurcation:
a thrombus might form
88
Emoboli of a bifurcation thrombus would travel to:
distal arteries &arterioles
89
Hypertension is ___
consistent elevation of systemic arterial BP over 140/90
90
2 categories of HTN
primary & secondary
91
Secondary HTN is caused by ___
altered hemodynamics associated with a dz process
92
Primary HTN, AKA ___, is caused by ___
Essential HTN; a complex set of factors
93
__% of hypertensives have primary HTN
92-95
94
Non-modifiable Risk factors of HTN
``` Family HX (inherited tendency) advanced agin ```
95
Modifiable risk factors of HTN
Diet, obesity, sedentary lifestyle Heavy alcohol consumption DM2 Cigarette smoking/nicotine intake
96
Certain conditions usually present in HTN to come degree:
Atherosclerosis | Overactivity of SNS & RAAS
97
Atherosclerosis contributes to HTN due to __
decreased elasticity of vessels
98
__ is consistently released by intracardiac nerve fibers, causing over stimulation of ___ to increase __ & __
Epinephrine beta receptors HR & contractility
99
Mini concept map of increased HR & contractility due to SNS overactivity
greater cardiac output & ejection pressure > pathologically larger volume of blood & pressure > sustained increase in BP
100
RAAS is usually a ___ triggered by ___
compensatory mechanism; drop in BP
101
For unknown reasons the RAAS sometimes becomes ___ causing ___
chronically activated; chronically high BP & blood volume
102
Vicious cycle of chronic HTN
arterial walls stimulated to strengthen via hypertrophy & hyperplasia > decreased lumen size > HTNn increases even more
103
Chronic HTN damages the __
tunica intima
104
S/S of HTN are often __
secondary to years of vascular damage
105
3 systems most often affected by HTN
Neuro Renal Cardiovascular
106
Neurological effects of HTN on the brain
Strokes due to ischemia from narrowed vessels
107
Effects of HTN on the eyes
ischemia & infarcts of parts of retina, vision changes
108
Effects of HTN on the renal system
High pressures & vessel damage can cause spilling of blood & protein into urine > eventually kidney failure
109
Effects of HTN on the cardiovascular system
increased workload ejecting blood against narrowed, stiff arteries; Multiple problems including MI
110
Local dilation or out pouching of arterial vessel walls
Aneurysms
111
Pathology of aneurysms
Atherosclerosis & HTN cause weakness in arterial walls which can cause bulges in certain areas; Minute injuries to intimal lining accumulate & allow blood to seep into muscle & tissue layers of arteries, which increase the size & chances of rupture
112
Areas of typical aneurysms
brain & aorta
113
The aorta is susceptible to aneurysms due to:
constant stress, especially from higher pressure of HTN
114
S/S of AAA
pulsatile, palpable mass inn abdomen; abdominal pain
115
S/S of thoracic aortic aneurysm
S/S usually resemble that of MI (chest pain, diminished pulses unilaterally)
116
Educational aspects of nursing implications for managing HTN
managing stress, smoking cessation, moderation of alcohol intake
117
Dietary aspects of managing HTN
low LDL intake; high intake of HDL & omega-3 fats
118
Desired daily intake of HDL:
40 mg/dL
119
Medicinal approaches for overactivity of SNS
beta & Ca channel blockers
120
Medicinal approaches for overactivity or RAAS
ACE inhibitors or angiotensin receptor blockers
121
Symbolizes ventricular repolarization on an EKG
T wave
122
Symbolizes ventricular depolarization on an EKG
QRS complex
123
Consistent, regular pattern or PQRST
sinus rhythm
124
Good CO is linked with ___
S/S of good perfusion
125
S/S of good perfusion
normal BP, pulses, cap refill, mentation, and skin color/ and warmth
126
SV is affected by:
contractility preload afterload
127
CO can improve or deteriorate based on:
changes in HR/rhythm; changes in SV
128
Definition: how well cardiomyocytes responds to electrical impulses
contractility
129
The effect of different factors on contractility
Inotropic
130
Some thing that enhances contractility
Positive inotropic effect
131
Something that decreases contractility
Negative inotropic effect
132
Amount or volume of blood in the ventricles before contraction
Preload
133
Any form of resistance to ejection of blood from any heart chamber
afterload
134
Normal after load exists when the receiving arteries have:
good vasomotor tone; smooth, patent lumens
135
Normal RV after load is called:
pulmonary vascular resistance
136
Normal LV after load is called:
systemic vascular resistance
137
HR >100BPM
tachycardia
138
Describe the neurohormonal effect on the SNS during physical exertion or stress:
Epinephrine binds to beta receptors, causing HR to increase
139
Hypopolarization causes cardiomyocytes to ___
contract more quickly
140
The PNS effect on HR involves the release of ___ by the ___
acetylcholine; vagus nerve
141
Interference in impulse conduction due to ischemic or infarcted cardiac tissue causes:
dysrhythmias
142
Chaotic electrical impulses in the atria that cause atrial "quivering"
Afib
143
Percentage of elderly that have Afib
~3%
144
Afib can cause a small, but sometimes significant ___
decrease in CO
145
Arterial thrombi in the LA that break loose can cause:
stroke
146
Arterial thrombi in the RA that break loose can cause:
PE
147
Increased preload, pathologically, relates to:
increased blood volume/fluid volume overload
148
Decreased preload, pathologically, relates to:
decreased blood volume/fluid volume deficit
149
Fluid volume deficit eventually leads to:
decreased BP & CO
150
Pathologically increased after load in the RV can be caused by:
atherosclerosis of pulmonary arteries, or chronic disorders such as bronchitis
151
Pathologically increased after load in the LV can be caused by:
Atherosclerosis of the aorta & systemic arteries; peripheral vasoconstriction; HTN; pathologically high blood volume
152
Pathologically decreased afterload in the LV is usually due to:
massive peripheral vasodilation/shock
153
A disorder in which the coronary arteries are narrowed or occluded
Coronary artery disease
154
Risk for CAD increases with high serum levels of:
hemocysteine
155
Risk of CAD is linked with ___ due to inflammatory process of plaque formation
elevated CRP
156
Cardiac cell ischemia has a ___ effect, leading to ___
negative inotropic; decreased CO
157
If not reversed, CAD can lead to:
cell death/necrosis
158
Most common symptom of CAD
angina
159
Ischemic pain in the heart muscle tissue
Angina
160
Classification of CAD is based on:
degree of coronary artery occlusion & ischemia
161
2 categories of CAD, based on symptoms
Stable Angina; Acute coronary syndrome
162
___ is established thru arteriogenesis to compensate for slow development of plaque
Collateral circulation
163
Acute coronary syndrome manifests as __ or __
Unstable angina or MI
164
Necrosis of myocardial cells
MI
165
2 enzymes that indicate MI upon lab testing
Creatine kinase; troponin
166
2 internal compensatory mechanisms of CAD patients
Collateral circulation; hypertrophy of cardiac muscle cells
167
A heart murmur is caused by ___ or ___
cardiac valve stenosis (valvular prolapse/ insufficiency) or regurgitation (back flow)
168
Right sided heart valves
Tricuspid, Pulmonary
169
Left sided heart valves
mitral, aortic
170
Valve malfunction may be caused by autoimmune disorders, such as:
rheumatic fever
171
Stenosis impedes blood flow because of:
narrowed or constricted valve orifices
172
A state of incompetent, floppy valves is called:
valvular prolapse valve insufficiency regurgitation
173
General term used to describe types of cardiac dysfunction secondary to failure of the heart to effectively propel blood forward
Heart failure
174
3 aspects of the pathology of HF
``` weakened contractility (pump problem) increased afterload (resistance) Increased preload (fluid volume overload) ```
175
One sequela of HF pertaining to the kidneys is:
Diminished CO stimulates the kidneys to secrete Renin as part of the RAAS, causing retention of fluids, making the problem worse instead of better
176
4 sequela of venous insufficiency
localized edema local skin breakdown Local skin discoloration Varicose veins
177
Renin stimulates:
secretion of angiotensin I
178
Angiotensin 2 stimulates:
peripheral vasoconstriction, secretion of Aldosterone from Adrenal glands
179
Effects of Aldosterone:
causes distal convoluted tubules to reabsorb Na > increases tonicity > water is shifted from tissues into blood > increased UO
180
Increased systemic tonicity triggers release of __ which aids in fluid retention
ADH
181
Most common type of hypertension
Primary/Essential
182
Factors contributing to left heart failure
Weekend LV w/ decreased contractility and/or High afterload
183
High afterload can be due to:
HTN and/or pathologically increased arterial vasoconstriction and/or narrowed/blocked systemic arteries
184
Common sequela of LHF
Fluid overload overwhelms the LV, causing fluid to backup in the lungs > pulmonary edema
185
Weakened LV contractility can be caused by:
``` Ischemia/MI and/or Electrolyte imbalance and/or HR/rhythm problems And/Or High afterload ```
186
Sequela of RHF
RV overwhelmed by fluid overload (high preload) > fluid buildup in systemic veins > peripheral edema
187
RAAS complication of RHF
Aldosterone secreted by adrenal glands causes retention of Na+ > H2O retention > further increased preload
188
General S/S of decreased CO
``` Fatigue, weakness mentation changes hypotension dyspnea delayed cap refill Oliguria ```
189
S/S of pulmonary Edema (fluid backup)
``` Fluid congestion in lungs Crackles on auscultation Pink, frothy sputum Orthopnea Increased RR Decreased SpO2 ```
190
S/S of peripheral Edema
JVD Pedal edema Liver congestion/enlargement Ascites (abdominal edema)
191
Definition: when RHF is caused by pathologically increased pulmonary vascular resistance
Cor pulmonale
192
Lung congestion is caused by ___ But Lung congestion causes __
LHF; RHF
193
Fluid volume overload triggers the __
NPS
194
NPS causes the kidneys to ___, > ___
excrete more Na+ > water follows
195
In volume overload, the ventricles secrete ___ and the atria secrete ___
BNP; ANP
196
The gold-standard for confirmation/quantification of level of HF is ___
serum level BNP
197
Healthy male serum BNP level:
50pg/mL
198
S/S of cariogenic shock are generally related to ___
decreased perfusion + compensatory responnses
199
``` Normal ABG values pH: pO2: sO2: pCo2: HCO3: ```
``` 7.35-7.45 80-100mmHg 97-100% 34-45mmHg 22-26mEq/mL ```
200
If pCO2 is abnormal, the pH imbalance is ___ in nature | if HCO3 is abnormal, the pH imbalance is ___ in nature
respiratory | metabolic
201
Respiratory acidosis is a state of ___
low pH caused by inhibition of normal breathing pattern
202
Decreased RR causes:
hypercapnia (retention of CO2
203
Respiratory acidosis is typically caused by some degree of __
hypoventilation
204
Typical ABG findings of respiratory acidosis
low pH low pO2 high pCO2 normal HCO3
205
Increased depth or rate of breathing causes:
CO2 blow off > alkalosis
206
The kidneys attempt to compensate for respiratory alkalosis by:
decreasing HCO3 production or increasing excretion os HCO3
207
State of low pH caused by accumulation of acids in the body
metabolic acidosis
208
HCO3 levels will be ___ in metabolic acidosis
low
209
Normal breathing should be ___
passive
210
Subjective feeling of not getting enough air
dyspnea
211
DOE
dyspnea on exertion
212
dyspnea upon lying down
orthopnea
213
Usually related to increased preload when lying down + compromised LV unable to pump effectively
Orthopnea
214
Waking suddenly and feeling SOB
paroxysmal nocturnal dyspnea (PND)
215
RR < 12/min
hypoventilation
216
RR > 20/min
tachypnea/hyperventilation
217
Shallow breathing
hypopnea
218
increased depth of breathing
hyperpnea
219
absence of breathing
apnea
220
Purulent sputum usually indicates ___
infection
221
Accessory muscle use during exhalation due to difficulty breathing =
respiratory distress
222
When a PT can no longer breathe adequately on their own
respiratory failure
223
Restrictive lung dz generally refers to dz processes related to ___
difficulty w/ inhalation
224
V/Q ratio means:
liters of air breathed in per minute/# liters of blood available for gas exchange in one minute
225
Normal V/Q ratio:
0.8 (4/5)
226
Low VQ disorders are caused by
inability to get the normal amount of air from the atmosphere to the blood
227
High VQ disorders are caused by:
difficulty w/ perfusion
228
In low VQ disorders, low V=
less ventilation (can't get air from atmosphere to blood)
229
Low VQ disorders include restrictions in the: (4)
chest wall airway Pleura lung tissue
230
Chest wall restrictions can include:
physical deformity or neuromuscular weakness
231
airway restrictions can include:
foreign bodies, tumors | inflammation
232
Most dz that cause inflammation of the larynx and bronchi are caused by:
viruses
233
Inflammation of the larynx, trachea, and bronchi typically seen inn young children
croup
234
Pleural restrictions include:
pleural effusion, pneumothorax
235
irritation/inflammation of the pleural space that causes fluid buildup
pleural effusion
236
S/S of pleural effusion
chills, fever (infection related) pleuritic pain w/ movement shallow respirations
237
Presence of air in pleural space caused bay rupture in pleura
pneumothorax
238
Pneumothorax disrupts the ___
normal negative pressure environment
239
Pneumothorax caused by outside trauma
open pneumothorax
240
Pneumothorax caused by internal trauma
closed pneumo
241
Lung tissue restriction is caused by __
pneumonia
242
Pneumonia is an infection of the ___
lower respiratory tract
243
Pneumonia can be caused by:
viruses bacteria parasites fungi
244
3 types of pneumonia
Community acquired Hospital acquired (nosocomial) Aspiration
245
Organisms that cause CAP are usually ___
less virulent
246
Nosocomial pneumonia is typically caused by __
virulent microbes like pseudomonas
247
Inhalation of foreign substance into lungs that results in inflammation of lung tissue
aspiration pneumonia
248
Aspiration pneumonia usually effects:
ppl with debilitations or depressed/absent gag, cough, or swallowing reflexes
249
Collapse of portions of lung tissue
atelectasis
250
Atelectasis is caused by:
accumulation of inflammatory/infectious debris that accumulates in alveoli
251
Excess water in alveoli
pulmonary edema
252
Noncardiogenic pulmonary edema is caused by:
injury to capillary endothelium from external sources
253
Pathology of pulmonary edema:
capillary endothelium injured by external source > increased capillary permeability, disruption of surfactant production > fluids/proteins shift from capillaries into alveoli
254
S/S of pulmonary edema
pink, frothy sputum inspiratory crackles hypoxemia Dyspnea
255
Lung cancer arises from __
respiratory epithelium
256
Pathology of lung cancer
carcinogens from smoking cause genetic abnormalities in bronchial cells > carcinoma in situ > invasive carcinoma
257
High VQ disorders involve restriction of:
blood vessels in the lungs
258
Most common cause of High VQ ratio
pulmonary embolism
259
Virchow's triad:
``` endothelial injury Hypercoagulability Venous stasis (DVT) ```
260
High VQ ratio in PE is caused by:
lower O2 saturation of blood returning to the LV
261
Obstructive pulmonary dz results in:
difficulty w/ exhalation
262
S/S of obstructive pulmonary disorders
Accessory muscle use Prolonged expiratory phase Dyspnea
263
Common types of obstructive pulmonary dz
Asthma Bronchitis and Emphysema Cystic fibrosis
264
Chronic inflammatory disorder caused by bronchial hypersensitivity to stimuli
Asthma
265
Pathology of asthma
Inhaled irritants > inflammatory mediators > vasodilation and swelling spasm and constriction of bronchi
266
Collective term for emphysema and chronic bronchitis
COPD
267
S/S of COPD
prolonged expiration accessory muscle use chronically low PF made worse by exacerbation
268
Basic pathology of emphysema
Inhalation of irritants > airway inflammation > alveolocapillary membrane and walls between clusters destroyed > alveoli stiff and hyper inflated > loss of elastic recoil > air becomes trapped in alveoli and exhalation becomes harder
269
Emphysemics live in a chronic state of ___
hyperventilation > respiratory alkalosis
270
Hypersecretion of mucous and chronic productive cough for > 3 months for > 2 consecutive years
chronic bronchitis
271
Hypoxemia in chronic bronchitis is caused by:
mucous plugs in bronchial walls
272
PTs with chronic bronchitis are typically in a state of chronic ___ due to ___
hypercapnia (>45); inability to exchange gases
273
Enlargement of the prostate gland tissues
Benign prostatic hyperplasia
274
S/S of BPH
Varying degrees of urinary flow obstruction Urgency, delayed start of flow Decreased flow Urine retention
275
TX for BPH
TURP | Transurethral resection of prostate
276
Malignant neoplasm of the prostate
prostate cancer
277
Risk factors for Prostate cancer
Age >50 family Hx diet high in saturated fat high T levels
278
Cancer most common in males age 15-35
testicular cancer
279
Inflammation of the a. prostate b. urethra
prostatitis | urethritis
280
Female flow related problems of the uterus
dysmenorrhea, amenorrhea, endometriosis
281
More painful, higher than normal volume of bleeding than normal menstruation
dysmenorrhea
282
Absence of menses (can be sign of start of menopause)
amenorrhea
283
Presence of functioning endometrium outside of the uterus
Endometriosis
284
pathology of Endometriosis
sloughed off endometrium travels to the abdominal cavity thru the Fallopian tube > tissue reacts to menstrual hormones by proliferating & bleeding as if still in the uterus
285
S/S of endometriosis
dyspareunia,dysmenorrhea, pelvic pain
286
#1 cause of cancer deaths in females
ovarian cancer
287
early S/S of ovarian cancer
bloating, mild abdominal pain, constipation
288
S/S of abdominal metastasis ovarian cancer
abdominal pain, ascites, dyspepsia, committing, alterations in BMs
289
Infection of the female reproductive tract
pelvic inflammatory disease
290
PID can cause:
infertility
291
UTIs are most commonly caused by __
E. coli
292
UTI involving the urinary bladder
cystitis
293
UTI involving only the kidneys
pyelonephritis
294
STI that causes urethritis in males, PID in females
Chalmydia
295
STI that is easily treated in early stages, but left untreated may become systemic and evolve
Syphilis
296
Not an STI: | HSV1 - HSV2
HSV1
297
STI that invades the genital area and spreads to the perineum and anus
HSV2 "genital herpes"
298
Anything that interferes with flow of urine from the kidneys to the urethral meatus
Obstructive disorders of the urological system
299
Enlargement of and pressure on the renal pelvis due to pathologic accumulation of fluid
hydronephrosis
300
Hydronephrosis is caused by:
retrograde flow of urine that cannot get past an obstruction
301
Hydronephrosis can lead to:
infection and fibrosis within the kidney; decline in nephron function
302
Types of urological obstructions (not gender specific)
Tumors scarring from past problems Neurogenic problems (paralysis) Kidney stones
303
Presence of kidney stones
lithiasis
304
Risk factors for lithiasis
``` male gender Gout Dehydration Dietary factors Hypercalcemia caused by dz state ```
305
Kidney stones form when urine becomes super saturated with:
calcium, uric acid, and other ions
306
Volume of fluid filtered from the glomerular capillaries into the Bowmans capsule per minute
Glomerular filtration Rate (GFR)
307
Clinically speaking, decreased GFR = ___
decreased UO
308
Decreases in GFR increases the risk of ___
accumulation of wastes and water in the body
309
Abbrupt (<48 hrs) oliguria and/or jump in serum creatinine
acute kidney injury
310
2 possible outcomes of AKI
full recovery if caught and corrected early | Some degree of residual kidney problem if not caught early enough
311
3 categories of AKI based on location
Prerenal AKI Intrarenal AKI Postrenal AKI
312
Intrarenal AKI can lead to ___
acute tubular necrosis (ATN)
313
S/S of prerenal AKI
S/S of decreased preload: dry mucous membranes, dry mouth and oliguria
314
Causative factors of Prerenal AKI
decreased arterial blood flow to kidneys due to arterial vasoconstriction or trauma to aorta/renal arteries and hypotension/hypovolemia
315
Occurs when a blockage occurs between the kidneys and the urethral meatus
post renal AKI
316
Factors that can cause Postrenal AKI
obstruction from BPH Uterine prolapse Ureteral obstruction/calculi
317
Intrarenal AKI can occur when:
post- or prerenal AKI are not fixed | Acutely diminished kidney function due to direct kidney tissue injury
318
Pathology of infrarenal AKI
ischemia to nephron blood supply > tubule cells slough off and block urine flow > retrograde flow > hydronephrosis > ischemia, necrosis, malfunction
319
Causative agents of ATN
direct trauma to nephrons by: | ischemia, hydronephrosis, nephrotoxic drugs, poison/toxins, renal infections
320
S/S of intrarenal AKI
acute oliguria high serum creatinine Casts in urine
321
Slow, negative effect on renal function from a slow, insidious problem or genetic disorder
Chronic kidney dz (CKD)
322
Congenital Disorders that can cause CKD
PKD
323
Acquired dz that can cause CKD
unresolved AKI Atherosclerosis diabetes mellitus HTN
324
Autoimmune dz that can cause CKD
glomerulonephritis
325
2 divisions of CKD
fluid/solute balance impairment | Metabolic function impairment
326
Pathology of glomerulonephritis
inflammatory process > glomerular capillaries become leaky > substances allowed into urine that aren't supposed to be (RBCs, protein)
327
post infectious glomerulonephritis is caused by
autoantibodies attached to the glomerular membrane, causing inflammation & leakiness
328
high BUN and serum creatinine
Azotemia
329
___ is almost always associated with renal dysfunction
high serum creatinine
330
serum creatinine levels are high in renal dysfunction due to:
inability of impaired kidneys to excrete the normal amount into urine
331
Azotemia + other S/S is called ___
uremia
332
Precipitation of urea on skin, causing itching
pruritis
333
Hyperkalemia/hypernatremia in CKD is due to:
unresponsiveness of DCT to aldosterone
334
Sequela of Na+ and H2O retention in CKD
peripheral/pulmonary edema, HTN
335
Neurological changes from toxic levels of urea in the blood
Uremic encephalopathy
336
Inability to activate vitamin D in CKD is caused by
hypocalcemia
337
because CKD PTs will usually be hypocalcemic, they will also be:
hyperphosphatemic
338
pH imbalance seen in CKD
metabolic acidosis
339
Dietary restriction for CKD patients should include
restrictions of Na, K, and H2O intake
340
Dietary supplements that should be given to CKD patients:
vitamin D and calcium, phosphate-binding antacids, erythropoeietin
341
Medications given to CKD patients should include
antihypertensives and non-potassium sparing diuretics
342
___ is converted from ammonia by the liver
urea nitrogen
343
Pathology of hyperkalemia/hypernatremia in CKD
DCT unresponsive to aldosterone > pathologic retention of solutes > increase in serum K+ and Na+