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Pathology (BIO 320) > Respiratory and Cardiovascular diseases > Flashcards

Respiratory and Cardiovascular diseases Flashcards

1
Q

Eupnea

A

normal breathing

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2
Q

Dyspnea

A

shortness of breath

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3
Q

orthopnea

A

shortness of breath while laying down

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4
Q

Hyperventilation

A

over ventilate, blow off excessive bicarbinate

above metabolic demands

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5
Q

Hypoventilation

A

low ventilation, become acidic, below metabolic demands

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6
Q

Hypercapnia

A

high CO2 in blood

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7
Q

Hypocapnia

A

low CO2 in blood

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8
Q

Hemoptysis

A

coughing blood

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9
Q

cyanosis

A

bluish coloring, low oxygen

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10
Q

Hypoxemia

A

decreased oxygen of arterial blood

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11
Q

Hypoxia

A

low oxygen to the tissues

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12
Q

ischemia

A

low blood supply to tissues

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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
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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

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15
Q

Obstructive pulmonary diseases

A 
worse with exhalation
reduced airflow due to partial/complete blockage
emphysema
chronic bronchitis
asthma
bronchiectasis
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16
Q

Empysema

A

Loss of surface area
Alveolar enlargement
Loss of elastic recoil

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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
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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
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19
Q

Clinical features of emphysema

A 
Dyspnea
Hunched over breathing
-Pursed lips
Barrel-chest
Weight loss over time
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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
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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
Q

Bronchiectasis

A

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
Q

Restrictive Pulmoary Disorders

A

problems on inhalation
reduced expansion->reduced lung capactiy
chest wall disorders, pleural disorders

27
Q

Acute respiratory distress syndrome

A

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
Q

Pneumonia

A

Bacterial most common (typical)
Viral and fungal possible, but less common (atypical)
Nosocomial (hospital)

29
Q

Bronchial pneumona

A

in larger airways (bronchi)
gray hepatization
-because oxygen not all the way out to tissues, they gray out

30
Q

Lobar pneumonia

A

lower lung, alveoli
hemorrhage in lobes
red hepatization

31
Q

Preload

A

muscle length of myocytes before the contract
venous return (inc. VR-> inc. EDV -> inc. preload)
right side of heart

32
Q

Afterload

A

pressure left side of heart has to generate to open the aortic valve and send blood to body

33
Q

Congestive heart failure

A 
usually systolic (prob on contraction events), can be diastolic)
CO decreased
34
Q

Etiology of CHF

A

endocarditis-inflammatory disease of endocardium

Abnormal load-hypertension

35
Q

How does the heart compensate for CHF

A

Hypertrophy
• Muscle buildup
Increases NE releaseincreased 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 returnincrease stroke volume->increase cardiac output
ANP (atrial naturetic peptide) release
• Causes diuresis
• Fewer side effects

36
Q

Left-sided CHF

A

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
Q

Right-sided CHF

A

typical cause is left-sided CHF
-also lung diseases
biggest impact on systemic circuit

38
Q

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

A

c. Increased right ventricular afterload

- because lungs back up with fluid, increasing afterload of right side

39
Q

Arteriosclerosis

A

blood vessel injury
inflammatory response
two types: arteriolosclerosis, artherosclerosis
treatments: angiogram, angioplasty, stent therapy

40
Q

Arteriolosclerosis

A 
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
Q

Artherosclerosis

A 
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
Q

Ischemic heart disease

A

imbalance between perfusion and demand

Artherosclerosis major cause

43
Q

Pathogenesis of IHD

A

chest pain (angina pectoris)
acute myocardial infarction
chronic IHD
sudden cardiac death

44
Q

Stable angina

A

pain when exerting self

most common

45
Q

Prinzmetal/variable angina

A

pain at rest at night

46
Q

Unstable/crescendo angina

A

usually disrupted plaque lodged in coronary vessels

pain gets worse over time

47
Q

____ angina occurs because of vasospasms of one of more coronary arteries and often during sleep

A

Prinzmetal

48
Q

Acute myocardial infarction

A

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
Q

Leaked myocardial proteins

A 
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
Q

Compications from MI

A 
Arrhythmias-disrupt e signal 
Contractile dyfunction 
myocardial aneurysm or rupture
mural thrombus
progressive heart failure

Pathology (BIO 320) (8 decks)

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