Respiratory and Cardiovascular diseases Flashcards
(50 cards)
1
Q
Eupnea
A
normal breathing
2
Q
Dyspnea
A
shortness of breath
3
Q
orthopnea
A
shortness of breath while laying down
4
Q
Hyperventilation
A
over ventilate, blow off excessive bicarbinate
above metabolic demands
5
Q
Hypoventilation
A
low ventilation, become acidic, below metabolic demands
6
Q
Hypercapnia
A
high CO2 in blood
7
Q
Hypocapnia
A
low CO2 in blood
8
Q
Hemoptysis
A
coughing blood
9
Q
cyanosis
A
bluish coloring, low oxygen
10
Q
Hypoxemia
A
decreased oxygen of arterial blood
11
Q
Hypoxia
A
low oxygen to the tissues
12
Q
ischemia
A
low blood supply to tissues
13
Q
atelectasis
A
lung collapse due to inadequate expansion
- inability to expand to full capacity
- reduction in oxygen
- inefficient gas exchange, low oxygen in blood to tissues
14
Q
Types of atelectasis
A
Resorption-usually due to obstruction, in airways, prevented from reaching distal branches, alveoli collapse
Compression-accumulation of blood, fluid, or air, heart not pumping, air backing up into lungs, or chest cavity compromised, pressure inside same as outside
contraction-fibrotic changes, prevents lungs from expanding, hampers elasticity
15
Q
Obstructive pulmonary diseases
A
worse with exhalation reduced airflow due to partial/complete blockage emphysema chronic bronchitis asthma bronchiectasis
16
Q
Empysema
A
Loss of surface area
Alveolar enlargement
Loss of elastic recoil
17
Q
Types of Emphysema
A
Centriacinar -Most common -From smoking -In upper lungs, mostly respiratory branches Panacinar -Alpha-1-antritrypsinase deficiency •Inhibits elastase normally -Lower lungs, alveoli/bronchi
18
Q
Pathogenesis of emphysema
A
Two causes: Protease-antiprotease inbalance -Neutrophils activate elastase • Breakdown elastic fibers in lungs • Alpha-1-AT either deficient or shut down -Panacinar Oxidant-antioxidant imbalance -Tobacco -Reactive oxygen species -Centracinar
19
Q
Clinical features of emphysema
A
Dyspnea Hunched over breathing -Pursed lips Barrel-chest Weight loss over time
20
Q
Chronic bronchitis
A
Larger airways -mucus, inflammation of epithelium -lose respiratory elevator usually mixed with emphysema 90% smokers persistant, productive cough for 3 months for 2 consecutive years
21
Q
Types of chronic bronchitis
A
o Simple Mucus, airflow not restricted o Chronic Asthmatic Bronchiospasms Excessive mucus obstructs airway o Chronic obstructive Lots of thick mucus Blocks airways
22
Q
Pathogenesis of chronic bronchitis
A
loss of PCCE
Trigger of mucin gene->hypertrophy of submucosal glands
begins in large airways, progresses to smaller
infection often follows
23
Q
Clinical manifestations of chronic bronchitis
A
Blue bloaters
Cough with sputum
Dyspnea with exertion
24
Q
Asthma
A
• Bronchial asthma • 2 Types o Extrinsic Outside body Allergic reaction (IgE) Smoking, ozone, allergens, obesity (GERD), protective o Intrinsic Within body No allergic reaction, no IgE Exercise Stress (bronchioconstriction)
25
Bronchiectasis
permanent dilation of bronchiole due to obstruction or infection
• Features
o Sputum (copius, purulent, bad smelling)
Because not moving, infection, necrosis
o Dyspnea
o Cough
o Increased risk for infection
26
Restrictive Pulmoary Disorders
problems on inhalation
reduced expansion->reduced lung capactiy
chest wall disorders, pleural disorders
27
Acute respiratory distress syndrome
Lung shock
Direct: immediate fluid buildup in lungs (breathing it in)
Indirect: trauma->fluid buildup
White-out on x-rays
diffuse alveolar damage
dyspnea, tachypnea, cyanosis, hypoxemia, edema
28
Pneumonia
Bacterial most common (typical)
Viral and fungal possible, but less common (atypical)
Nosocomial (hospital)
29
Bronchial pneumona
in larger airways (bronchi)
gray hepatization
-because oxygen not all the way out to tissues, they gray out
30
Lobar pneumonia
lower lung, alveoli
hemorrhage in lobes
red hepatization
31
Preload
muscle length of myocytes before the contract
venous return (inc. VR-> inc. EDV -> inc. preload)
right side of heart
32
Afterload
pressure left side of heart has to generate to open the aortic valve and send blood to body
33
Congestive heart failure
```
usually systolic (prob on contraction events), can be diastolic)
CO decreased
```
34
Etiology of CHF
endocarditis-inflammatory disease of endocardium
| Abnormal load-hypertension
35
How does the heart compensate for CHF
Hypertrophy
• Muscle buildup
Increases NE releaseincreased contractility (heart beats more forcefully)
• Because of increased pressure in systemic
o Heart has to work harder to pump blood
• Vascular resistance
• Over time peripheral resistance increases, VR decreases, less blood in, less blood out
o Short-term solution
Lose water through urine, decrease blood pressure
Renin-angiotensin-aldosterone activation
• Antidiuretic system
• Increase blood pressure by retaining water
• Increases venous returnincrease stroke volume->increase cardiac output
ANP (atrial naturetic peptide) release
• Causes diuresis
• Fewer side effects
36
Left-sided CHF
Causes: ischemic heart disease, systemic hypertension, mitral or aortic valve disease, primary myocardial disease
Morphology: hypertrophy, dilated ventrical, pulmonary congestion and edema
biggest impact on pulmonery circui
37
Right-sided CHF
typical cause is left-sided CHF
-also lung diseases
biggest impact on systemic circuit
38
Left-sided heart failure may lead to right sided heart failure owing to
a. Excessive volume retention
b. Poor perfusion of right coronary artery
c. Increased right ventricular afterload
d. Arterial hypotension
c. Increased right ventricular afterload
| - because lungs back up with fluid, increasing afterload of right side
39
Arteriosclerosis
blood vessel injury
inflammatory response
two types: arteriolosclerosis, artherosclerosis
treatments: angiogram, angioplasty, stent therapy
40
Arteriolosclerosis
```
type of arteriosclerosis
Narrowing over time in response to hypertension
Loss of anti-thrombotic agents
Inability to clot
Smooth muscle cells migrate into intima
-Create a growth
-Lumen narrows
Loss of recoil
Increase blood pressure
Blood vessel injury
Inflammation in a vessel
```
41
Artherosclerosis
```
type of ateriosclerosis
formation of plaque
Inflammatory response to chronic injury
Foam cells
-Fatty streak
Macrophages, inflammatory cells gather in vessel
Leads to hypertension
Lipid buildup
```
42
Ischemic heart disease
imbalance between perfusion and demand
| Artherosclerosis major cause
43
Pathogenesis of IHD
chest pain (angina pectoris)
acute myocardial infarction
chronic IHD
sudden cardiac death
44
Stable angina
pain when exerting self
| most common
45
Prinzmetal/variable angina
pain at rest at night
46
Unstable/crescendo angina
usually disrupted plaque lodged in coronary vessels
| pain gets worse over time
47
____ angina occurs because of vasospasms of one of more coronary arteries and often during sleep
Prinzmetal
48
Acute myocardial infarction
quick, short period of time
can withstand 20 minutes of ischemia
Subendocardial-wavefront, starts in endothelium, moves to outerwall
Transmural-all the way through the wall
49
Leaked myocardial proteins
```
Troponin I (TnI) and Troponin T (TnT)
-unlinks from tropomyosin
-appears 2-4 hours
-peaks at 24
-stay elevated for a week-10 days
Creatine kinase myocardial bound (CK-MB)
-2-4, peaks 24-48, gone 72
-marks damage to heart itself
Lactic dehydrogenase (LDH)
-indicates heart trying to use glycolysis as energy source
```
50
Compications from MI
```
Arrhythmias-disrupt e signal
Contractile dyfunction
myocardial aneurysm or rupture
mural thrombus
progressive heart failure
```
