Midterm Flashcards
(141 cards)
1
Q
What are the symptoms that are considered alarm findings that increase clinical concern when paired with chest pain?
A
Productive cough, syncope, evidence of systemic inflammation (joint pain, night sweats, significant wt loss)
2
Q
Alarm findings: what are the signs that increase clinical concern when paired with chest pain?
A
fever, hypotension, tachycardia/tachypnea, pleural/pericardial friction rubs, rales/crackles, asymmetric lung sounds, absent lung sounds
3
Q
What is the chest pain called that is made worse by taking a deep breath?
A
respirophasic
4
Q
Is there a relationship b/t typical angina and exertion?
A
Yes. Classically exercise induced
5
Q
What is exercise-induced transient abdominal pain AKA?
A
side stitch
6
Q
What is believed to cause a side stitch?
A
stretching of ligaments that extend from diaphragm to internal organs (esp. liver)
7
Q
If your chest is sore upon palpation, what is the most likely origin of the pain?
A
muscle/ribs/cartilage
8
Q
What are the three characteristics of pleuritic pain?
A
- localized to distribution of intercostal nerve 2. NOT made worse by palpation 3. may or may not be respirophasic
9
Q
What is direct pleuritic pain?
A
inflammation of parietal pleura
10
Q
What are the three main characteristics of direct pleuritic pain?
A
- NOT made worse by palpation 2. is made worse by taking a deep breath 3. usually made worse by lateral flexion away from the involved side
11
Q
What is indirect pleuritic pain?
A
Inflammation in the vicinity of the parietal pleura
12
Q
What is indirect pleuritic pain most often associated with?
A
lung diseases
13
Q
Which type of pleuritic pain is more likely to have alarm findings?
A
indirect
14
Q
How often does pleuritic chest pain accompany myocardial infarction?
A
About 14%
15
Q
How do you DDx musculoskeletal “mimics” from pleuritic pain?
A
pain is localized or made worse by palpation
16
Q
What is the first step in plaque progression?
A
endothelial activation
17
Q
What occurs during endothelial activation?
A
Endothelium becomes more permeable, which allows leukocytes and macrophages to migrate into tunica intima
18
Q
What can be used to conservatively intervene with pts between 45 and 79 suffering from endothelial activation?
A
aspirin (also some Rx ACE-inhibitors)
19
Q
T/F: decreased arterial stress is a major pathophysiologic problem
A
TRUE (normal laminar flow through normal artery => high arterial wall stress)
20
Q
Why is decreased arterial stress a bad thing?
A
endothelium will favor vasoconstriction and platelet aggregation
21
Q
Test question:
A
Most people with a strong family Hx of heart dz also have one or more of the other risk factors for CV dz. Therefore it’s even more important to treat and control any other risk factors they have.
22
Q
Can elevated BP be reversed?
A
Yes, partially but there is a residual risk.
23
Q
What do sudden or abrupt increases in BP result in?
A
vasconstriction and inhibition of platelet reactivity
24
Q
What is a healthy endothelium’s response to sudden increases in BP?
A
release of nitrous oxide and prostacyclin
25
What does a damage endothelium favor?
vasconstriction and thrombus formation
26
What also induces endothelial release of vasoactive substances?
hypoxia
27
What does a pt with CV dz HAVE to avoid?
Anything that would cause a sudden spike in blood pressure
28
What can diabetes and insulin resistance lead to?
1. basement membrane thickening 2. increased permeability 3. endothelial activation/dysfunction (can occur in absence of plaque)
29
What vasculature does diabetes have more of an impact on?
capillaries and smaller arterioles
30
What does nicotine stimulate?
stimulates adrenal medulla to increase release of epinephrine => increased BP, HR, RR, and blood glucose levels
31
T/F: aggressive management of BP in diabetic pt is just as important as tight glycemic control
True
32
What is considered a strong independent risk factor for CV dz?
Tobacco smoking
33
What is the risk of CV dz proportional to (in regards to tobacco)?
proportional to number of cigarettes smoked and how deeply the smoker inhales
34
What substance increases plasma cholesterol, triglycerides, and fibrinogen?
Cigarette smoke
35
What substance enhances thromboxane producton and platelet aggregation?
Cigarette smoke
36
What effect does cigarette smoke have on HDL?
Decreases HDL
37
What effect does chronic exposure to epinephrine and norepinephrine have?
Toxic to cardiac myocytes
38
What are the most notable chemical by-products found in cigarette smoke?
carbon monoxide, various nitrogen oxides, various hydrogen cyanides, and ammonia
39
How many components of cigarette smoke are known to be carcinogenic?
About 70
40
How long does it take to fully reverse the effects of long-term smoking?
Up to 15 years
41
What are 3 independent risk factors that can lead to hypertriglyceridemia?
1. poorly controlled diabetes 2. obesity 3. excessive alcohol consumption
42
What is the purpose of aspirin in decreasing risk of CVD?
Decreases risk of thrombus formation
43
When are "uninhibited" platelets normally activated?
When they contact exposed collagen
44
How does aspirin decrease risk of thrombus formation?
irreversibly suppresses "activation" for life-span of platelet
45
How does aspirin suppress platelet activation?
competes for receptor sites
46
What is the primary concern with aspirin use?
hemorrhagic stroke
47
What are the 2 kinds of stroke?
1. hemorrhagic stroke 2. ischemic stroke
48
What percentage of strokes are hemorragic?
20%
49
What percentage of strokes are ischemic?
80%
50
What is the second concern with aspirin use?
Upper GI bleeding
51
Why is aspirin recommended for men?
decreased risk of myocardial infarction
52
Why is aspirin recommended for women?
decreased risk of ischemic stroke
53
What age group should be encouraged to use aspirin?
45-79
54
When should aspirin be recommended?
When benefit of MI/stroke reduction outweighs potential harm
55
How long should patients with existing CHD remain on aspirin therapy?
life-long
56
T/F: aspirin does not reduce mortality risk DURING an MI
FALSE
57
What dosage of aspirin should be given to a patient during an MI?
full-dose; 325 mg
58
How should the patient take aspirin during an MI?
chew the tablet
59
What is defined as "diffuse thickening of the tunica intima and deposition of extra-cellular lipids"?
Type IV atheroma
60
Do type IV atheromas result in clinical symptoms?
May or may not
61
What type of angina might type IV atheromas be associated with?
typical
62
Why is risk factor management so important?
type IV atheromas are unpredictable
63
Are type IV atheromas stable?
may or may not be
64
What is defined as "a fibrous cap that forms over an atheroma"?
Type V lesion - the fibroatheroma
65
Will type V atheromas result in symptoms?
May or may not
66
Are type V atheromas stable?
may or may not be
67
What is the ultimate goal with atheroma management?
keeping stable plaques stable
68
What is the first step in destabilizing type IV and V lesions?
oxidize excess LDLs
69
What is the second step in destabilizing type IV and V atheromas?
inflammation and cell "activation"
70
What is the third step in destabilizing type IV and V atheromas?
break down fibrous cap
71
What is defined as "surface defects in the fibrous cap"?
type VI "complicated" fibroatheroma
72
Why are type VI atheromas a bad thing?
much greater chance of hemorrhage, formation of thrombi, and subsequent ACS or MI
73
What is considered a key element in the disruption of stable plaque?
inflammation
74
What percentage of people who go to the ER with chest pain are actually having a heart attack?
10-15%
75
What percentage of people who are considered "low risk" and are sent home are actually having heart attacks?
4%
76
How soon within onset of symptoms do 60% of people with heart attacks die?
within 2 hours
77
What does chest pain of visceral origin imply?
cardiac ischemia
78
Is visceral pain made worse by taking a deep breath?
no
79
Is visceral pain made worse by changes in body position?
no
80
Is visceral pain made worse by palpation?
no
81
What percentage of MI cases present with pleuritic chest pain?
14%
82
What does "activation" of the sympathetic nervous system manifest in? (4)
diaphoresis, pallor, elevated resting HR, elevations in BP
83
What causes endogenous sympathetic activation?
response to the release of epinephrine/norephinephrine
84
When is endogenous sympathetic activation often seen?
in response to heart failure and/or hypoxia
85
What causes exogenous sympathetic activation?
response to various Rx, OTC, and recreational stimulants
86
What is an important differential for systemic activation of sympathetic nervous system?
Pain
87
What is the first clinical indication of an MI in 1/3 of male pts?
sudden cardiac death
88
T/F: the plaque responsible for ACS is often NOT critical before it rapidly evolves into an acutely threatening lesion
TRUE
89
Does the onset of acute coronary syndrome (ACS) cause symptoms before rupture?
may not
90
What do a large fraction of ACS cases appear to be triggered by?
external factors or conditions
91
What percentage of MI patients do not have chest pain?
33%
92
What is the problem with the physical exam in ACS pts?
results may be normal
93
What 2 factors increase the likelihood of ACS?
1. history 2. presence of cardiac "markers"
94
What is defined as "an abnormal localized collection of blood within soft tissue space or an organ"?
hematoma
95
What most often initiates hematoma formation?
a break or tear in a vessel's tunica intima
96
Which is more common, frank rupture of the abdominal aorta or an aortic dissection?
aortic dissection
97
What disease is classically associated with dissecting aneurysm?
Marfan's syndrome
98
What is the most important contributing risk factor for dissecting aneurysm?
hypertension
99
What percentage of pericarditis cases are idiopathic?
26-86%
100
What is the cardinal symptom of pericarditis?
chest pain
101
What usually makes pericarditis chest pain worse?
lying down flat
102
What usually makes pericarditis chest pain better?
sitting up and leaning forward
103
What sign is considered pathognomonic for acute pericarditis, even though it is not always present?
pericardial friction rub
104
What patient position is the best way to hear a friction rub?
sitting up and leaning forward
105
What is the primary factor in determining O2 consumption?
myocyte contraction
106
T/F: cardiac ischemia usually leads to frank/overt pain
FALSE
107
What is the most common trigger of typical angina?
exertion/exercise
108
What is the quality of pain in a typical angina?
poorly-localized and visceral
109
Is the location of a typical angina the same in each patient?
No - varies from pt to pt
110
Is a given individual's angina location the same every time?
Yes, usually predictable and unvarying
111
What does "umbilicus to eyebrows" mean?
suspect angina when a pt with CV risk factors describes any exercise induced, rest relieved discomfort above the waist or below the eyebrows
112
What causes dysfunctional intramyocardials?
occlusion of the "microcirculation"
113
are atypical anginas consistently precipitated by exertion and relieved by rest?
No
114
What demographics are more likely to experience atypical angina? (3)
1. older pts 2. females 3. diabetics
115
What is a Prinzmetal angina?
vasospasm in absence of plaque
116
What percentage of MI are accounted for by prinzmetal anginas?
1%
117
Why are women at high risk for heart disease? (3)
1. atypical angina more common 2. atypical chest pain more common 3. more likely to have comorbid condition (diabetes)
118
What is the leading cause of death in US women?
coronary artery dz
119
What type of chest pain might be "respirophasic", might be made worse by taking a deep breath, and is localized/dermatomal but NOT made worse by palpation?
inflammation of parietal pleura
120
What important question should you ask a pt with any lung dz?
Ask if pt is a smoker
121
How is pleurisy pain usually described?
sharp/stabbing and well-localized (course of intercostal nn.)
122
What life-threatening dzs can pleurisy be associated with? (4)
1. pneumonia 2. pulmonary emboli 3. pneumothorax 4. MI
123
Which type of pneumonia is often preceded by viral dzs such as influenza?
typical pneumonia
124
What type of pneumonia is found in a non-hospitalized, non-immunosuppressed person?
community-acquired
125
What type of pneumonia is acquired in the hospital?
nosocomial
126
What are 2 general clinical indications of lobar pneumonia in a pt with a cough and fever?
1. rales/crackles 2. bronchial breath sound
127
What is the positive LR of rales/crackles in a pt with cough and fever?
2
128
What is the positive LR of bronchial breath sound in a pt with cough and fever?
3.3
129
What is the 6th leading cause of death in the US?
pneumonia
130
What is considered "classic" lobar pneumonia history?
history of cold followed by sudden abrupt onset of fever
131
What is the time frame for early consolidation and red hepatization in lobar pneumonia?
days 3-4
132
What is the time frame for late consolidation and white hepatization in lobar pneumonia?
days 4-6
133
What is the "classic" association with a pancoast tumor?
rapid onset of shoulder/arm/brachial plexus symptoms in a middle age male smoker
134
Pulmonary emboli can arise from DVT where in the body?
anywhere
135
What is the second most common cause of sudden death?
massive pulmonary embolism
136
What type of pts is the highest incidence of PE seen in?
hospitalized pts
137
Why is the clinical presentation of PE misleading?
Sx usually sudden onset
138
What is the classic triad of PE Sx?
1. dyspnea 2. hemoptysis 3. chest pain
139
What is defined as "free air in the intra-pleural space"?
pneumothorax
140
How does tension pneumothorax present?
sudden onset of respiratory distress
141
What is "compressive atelectasis"?
collapse of previously expanded lung tissue d/t massive fluid accumulation in the intra-pleural space
