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path 2 exam 1 Flashcards

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1
Q

what is pulm sequestration?

A

a segment of lung tissue with no connection to the airway and has systemic circulatory supply (which is not pulm)

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2
Q

what are the 3 types of atelectasis?

A

resorption (reversible) –> complete obstruction of airway, air in the dependent lung is resorbed causing collapse of lung, mediastinum will shift TOWARD the affected lung

compression (reversible) –> when there is air, tumor, or fluid compressing the lung and preventing it from expanding, mediastinum will shift AWAY from the affected lung

contraction (irreversible) –> pulm or pleural fibrosis that prevents the lung from expanding

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3
Q

what are the heart failure cells?

A

hemosiderin laden macrophages

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4
Q

what is the pathogenesis of ALI?

A
  1. endothelial activation = mediated by inflammatory cytokines, either local or systemic
  2. accumulation and activation of neutrophils = degranulation and releasing additional inflammatory cytokines, proteases, etc
  3. accumulation of intra-alveolar fluid and hyaline membranes
  4. resolution of injury
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5
Q

what are the preventions of PE?

A

early mobilization, elastic stockings, graduated compression stockings, and anticoagulants

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6
Q

what are lung abscesses?

A

local suppurative process producing necrosis of lung tissue

-aspiration of infective material
- antecedent primary lung infection = postpneumo abscess usually associated with S. aureus, K. pneumonia, and S. pneumococcus
- septic embolism = IE
- neoplasia = primary or metastatic malignancy may obstruct a bronchopulmonary segment, leading to infection

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7
Q

what are the 3 types of chronic pneumonia?

A

histoplasmosis
blastomycosis
coccidiomycosis

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8
Q

MRI head is important for…

A

accessing infections, tumors, demyelinating diseases, etc.

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9
Q

CTA and MRA are needed to access…

A

vessels for dissection and aneurysms

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10
Q

Non contrast CT for…

A

stroke and head trauma ALWAYS to assess for hemorrhage

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11
Q

CT non contrast head is good for…

A

stroke, hemorrhage, trauma, hydrocephalus

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12
Q

if fev1/fvc is < 0.7 then…

A

there is an obstructive lung disease causing difficulty blowing air out

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13
Q

what are the obstructive lung diseases?

A

emphysema
chronic bronchitis
asthma
bronchiecstasis

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14
Q

COPD includes…

A

emphysema and chronic bronchitis

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15
Q

explain alpha 1 antitrypsin

A

deficient in panacinar emphysema

potent antiprotease (especially inhibits elastase), encoded by Pi locus on chr 14
Pi locus is dimorphic –> homozygotes for Z allele have significant decrease in alpha 1 antitrypsin and PiZZ will develop panacinar emphysema that is accelerated and more severe with smoking

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16
Q

what are the categories of chronic diffuse interstitial lung diseases?

A

fibrosing
granulomatous
eosinophilic
smoking related
other

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17
Q

what are the diseases that can occur in the hilar lymph nodes?

A

primary TB

silicosis (fibrosing)

sarcoidosis (granulomatous)

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18
Q

which diseases involve caseating necrosis?

A

histoplasmosis
TB
hypersensitivity pneumonitis

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19
Q

what are the chronic diffuse interstitial diseases that are smoking related?

A

desquamative interstitial pneumonia
respiratory bronchiolitis-associated interstitial lung disease

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20
Q

what are the chronic diffuse interstitial diseases that are others?

A

pulmonary langerhan’s cel histiocytosis
pulm alveolar proteinosis

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21
Q

what are the chronic diffuse interstitial diseases that are granulomatous diseases?

A

sarcoidosis
hypersensitivity pneumonitis

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22
Q

what are the chronic diffuse interstitial diseases that are fibrosing diseases?

A

idiopath pulm fibrosis
nonspecific interstitial pneumonia
COP
pneumoconioses
coal worker’s lung disease
silicosis
asbestos-related pulm disease

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23
Q

most carcinomas are between…with peak…

A

most carcinomas are between 40-70s, with peak incidence in 50-60s

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24
Q

some people may be genetically susceptible to tobacco smoke because…

A

polymorphisms of cytochrome P459 mono-oxygenase

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25
what are the environmental exposures that can cause carcinoma?
asbestos, uranium, and vinyl chloride
26
what are the major types of lung carcinoma?
squamous cell carcinoma (common) adenocarcinoma (common) small cell carcinoma large cell carcinoma
27
where can metastatic lung carcinoma spread to?
to pleural space hematogenously or in lymphatics - mediastinal, bronchial, and paratracheal adrenal glands, liver, brain, bone
28
what are the tumors metastatic to the lung?
lung is most common site of tumor metastasis may receive metastases via blood or lymphatics most common growth pattern is MULTIPLE, SCATTERED NODULES common primary sites --> breast, colon, kidney, prostate, and urinary bladder
29
what are the elastic aa?
aorta, innominate, subclavian, common carotid, iliac arteries, and pulm arteries accommodate high pulsatile forces with capacity to recoil and transmit energy into forward blood flow
30
what are the muscular aa?
renal and coronary aa have concentric rings of medial SMCs which regulates vessel caliber and blood flow and bp
31
in most inflam rxns, vascular leakage occurs from...
postcap venules
32
veins are predisposed to what?
irregular dilatation, compression, and easy penetration by tumors and inflam processes
33
the lymphatics are important for...
disease dissemination the thin walls make them vulnerable to invasion
34
neointimal SMCs DO NOT...
contract but can continue to divide later can return to a nonproliferative state
35
what are the 3 types of arteriosclerosis?
arteriolosclerosis = hyaline and hyperplastic in arteries and arterioles Monckeberg medial sclerosis = calcific deposits in MUSCULAR arteries --> no clinical signifiance, may be seen INCIDENTALLY on x-ray or mammography ATHEROSCLEROSIS = most important
36
what are the non modifiable and modifiable risk factors for athersclerosis?
non modifiable = genetics (FH), age, gender (pre/postmenopausal women, role of estrogen therapy) modifiable - HYPERLIPIDEMIA and HYPERCHOLESTEROLEMIA (statins) - DM (PAD) - HTN - smoking - hyperhomocystinemia (increased levels = low folate and B12 or inborn error in metabolism) - metabolic syndrome (larger wiast, low HDL, increase TGs, insulin resistance, HTN) - lipoprotein a - alterations in hemostasis - inflammation
37
why is CRP important?
marker for inflammation it can be used to predict the risks of MI, stroke, PAD, and sudden cardiac death
38
...are the earliest lesions in athersclerosis
fatty streaks composed of foamy macrophages multiple minute flat yellow spots that eventually coalesce into elongated streaks not significant raised and DO NOT CAUSE FLOW DISTURBANCES
39
how does inflammation influence the atherosclerotic plaque?
decreases collagen synthesis and increase collagen degradation leading to destabilization of the fibrous cap integrity vulnerable plaques have thin fibrous caps, large lipid cores, and increased inflam, the opposite is true for a stable plaque
40
true vs false aneurysm
true = attenuated by intact arterial wall or thinned ventricular wall false = defect in vascular wall leading to extravascular hematoma that communicates with the intravascular space (PULSATING HEMATOMA)
41
what is the diagnostic marker for vasculitis?
cytoplasmic/anti-proteinase 3 = c-ANCA perinuclear/anti-myeloperoxidase = p-ANCA
42
what is raynaud phenomenon?
exaggerated vasoconstriction of DIGITAL AA and arterioles - PAROXYSMAL PALLOR or CYANOSIS of digits of hands or feet white, blue, and red --> vasoconstriction, cyanosis, and vasodilation
43
what vessels are most likely to be involved in varicose veins?
superficial veins of upper and lower leg
44
what are the risk factors for varicose veins?
female, FH, pregnancy, prolonged standing, obesity, and advanced age
45
what are the other sites for varicosities?
portal HTN due to cirrhosis - esophagus (at risk for rupture - upper GI hemorrhage) - hemorrhoids - periumbilical veins of ab wall (caput medusa) hemorroids --> varicose veins at anorectal junction due to prolonged pelvic vascular congestion due to pregnancy or straining to defecate
46
benign vs malig
benign = obvious vasc channels filled with blood cells or lymph, lined by monolayer of normal appearing endo cells malig = more cellular, cytologic atypia, proliferative (mitotic figures) - DO NOT FORM WELL ORGANIZED VESSELS - endo cell specific markers
47
what is the frank starling mechanism?
increased filling volume and moderate ventricular dilation enhances contractility
48
what are the layers of the cardiac valves?
fibrosa - structural integrity, dense collagenous core at OUTFLOW surface spongiosa - mobility, central core of loose CT elastin - pliability, on INFLOW surface
49
explain the conduction system
SA node --> AV node --> bundle of his --> left and right bundle branches --> purkinje network AV node has delaying transmission of signals as gate keeper by allowing the ventricles to fill before the next contraction
50
a blockage in the L main artery will lead to what?
no blood flow to the left ant descending and left circumflex
51
what are the most common causes of HF?
HTN and ischemic heart disease will have interstitial fibrosis and cardiomyocyte fibrosis because LVH --> ischemia --> interstitial fibrosis --> cardiac failure --> death
52
what are the mechanisms to maintain pressure and perfusion in the heart?
frank starling activation of neurohumoral systems - release of norepi by adrenergic cardiac nerves - activations of RAAS - release of ANP cardiac hypertrophy (increase weight and LV thickeness) - pressure overload causes concentric increase in ventricular wall thickness - volume overload leads to ventricular dilation
53
what does hypertrophic cardiomyopathy histo look like?
myocytes with enlarged nuclei (BOX CAR) due to DNA rep in absence of division lots of branching as well
54
what are the CHFs?
most common hospital admission of pxs >65 yrs LHF (MOST COMMON) RHF biventricular heart failure high-output heart failure (least common) --> AV fistula, anemia, sepsis (high venous return), liver and lung diseases decreases cardiac output and tissue perfusion pooling of blood in venous system LHF --> pulmonary edema RHF --> peripheral edema
55
what is the most common risk for IHD?
age M >/= 45, F >/= 55
56
what are the types of angina pectoris?
stable angina prinzmetal angina unstable angina
57
what is the epidemiology of MI?
increases with age more common common in men than women
58
what do each of the coronary a supply?
LAD = apex, anterior wall of LV, ant 2/3 of ventricular septum RCA = RV, posterobasal wall of LV, posterior 1/3 of ventricular septum LCX = lateral wall of LV
59
what are the patterns of infarct?
most are transmural causing STEMI --> chronic coronary atherosclerosis, acute plaque change, thrombosis subendo causes NON STEMI/ST DEPRESSION --> thrombus lysed before injury to full wall, also from prolonged, severe reduction in systemic bp multifocal microinfarct - involves smaller intramural vessels - microembolization, vasculitis, vasospam
60
what are the most common infarcts?
transmural 1. occlusion of LAD 2. occlusion of RCA 3. occlusion of LCX less common but these are the non transmural infarcts - transient/partial obstruction --> regional subendo infarct - global HTN --> circumferential subendo infarct - small intramural vessel occlusions = microinfarcts
61
what does nausea and vomiting indicate for MI?
posterior-inferior MI with vagal stimulation
62
in 24 hrs after an MI, you will see...
neutrophils also 1-3 days there will be dense acute inflam infiltrate in area of acute MI
63
in 3-7 days after an MI, you will see...
phagocytosis of necrotic myocytes by macrophages
64
in 7-14 days after an MI, you will see...
granulation tissue cap proliferation edema inflam cells
65
in >8 wks after an MI, you will see...
a well healed MI with replacement of necrotic fibers by dense collagenous scar
66
what does a ruptured MI look like histo?
coagulative necrosis, neutrophilic infiltration, lysis of myocardial CT have weakened infarcted myocardium
67
when will infarct reperfusion be most beneficial?
first 3-4 hrs
68
what is the most common cause of sudden cardiac death?
CAD lethal arrhythmia prognosis improved by pharm intervention, implantation of auto cardioverter defibrillators to counteract Vfib
69
what diseases do you have to differentiate from hypertrophic cardiomyopathy?
- deposition diseases of heart (amyloidosis) - hypertensive heart disease px comes in w/ chest pain EKG/ECG --> ventricular hypertrophy = diseases above young px with NO HISTORY = HYPERTROPHIC CARDIOMYOPATHY
70
what is the most common cause of myocarditis?
COXSACKIEVIRUS A and B and other enteroviruses most common less common = CMV, HIV< influenza, SARS Covid-19
71
what is important to note about drug hypersensitivity?
methyldopa and sulfonamides can give pxs eosinophilic myocarditis
72
what are the types cardiac tumors?
most are benign myxoma fibroma lipoma papillary fibroelastoma rhabdomyoma angiosarcoma (MOST COMMON PRIMARY MALIGNANCY)
73
explain the fetal circulation
- Umbilical vein brings high O2 blood from the placenta to fetus. This blood ultimately goes into the IVC and straight to the right atrium - This high O2 blood then goes from the RA to the LA via the foramen ovale, where it is then pumped out into the aorta. - In the right ventricle, blood is pumped into the pulmonary arteries. However, due to the high pressure/resistance in the lungs, this blood is not able to enter the lungs. Instead, the blood in the pulmonary arteries is routed to the aorta via the ductus arteriosus.
74
explain non cardiac tumors
most frequent metastatic tumors are carcinomas of lung and breast, melanomas, leukemias, and lymphomas
75
what is the most common type of pediatric heart disease?
congenital heart disease
76
what causes CHD?
from faulty embryogenesis during gestational week 3-8, when major cardiovasc structures form and begin to fxn most severe anomalies are INCOMPATIBLE with life, those compatible are focal incidence up to 5%, about 1% have significant CHD
77
what are the types of CHD?
L to R shunt R to L sunt and malformations causing an obstruction (coarctation of aorta, aortic valvular stenosis, and pulm valvular stenosis)
78
what are the L to R shunts?
VSD, ASD, and PDA
79
explain the ASD embryology
- The SEPTUM PRIMUM is a crescent-shaped membranous ingrowth that sits posteriorly between the right and left atria and partially separates them; the remaining anterior opening, called the OSTIUM PRIMUM, allows movement of blood from the R to LA during fetal development. - Before the growing septum primum completely obliterates the ostium primum, it develops a second posterior opening called the OSTIUM SECUNDUM. - The SEPTUM SECUNDUM is a subsequent membranous ingrowth located to the right and anterior of the septum primum. - As the septum secundum grows, it also leaves a small opening called the FORAMEN OVALE that is continuous with the ostium secundum—the foramen ovale/ostium secundum permits continued R to L SHUNTING OF BLOOD during intrauterine development. - The septum secundum continues to enlarge until it forms a FLAP OF TISSUE THAT COVERS the FORAMEN OVALE on its LEFT SIDE
80
what is a characteristic finding of myocarditis?
persistent tachycardia way out of proportion to fever 1 C = 10 bpm
81
what are the main causes of cor pulmonale?
diseases of pulm parenchyma (chronic obstructive pul disease and diffuse pul interstitial fibrosis diseases of pulm vessels disorders affecting chest movement disorders inducing pulm arterial constriction
81
acute vs chronic valve abnormalities
depend in valve, degree of impairment, how fast it develops sudden destruction of AV from infection may be rapidly fatal rheumatic MV stenosis develops slowly and is clinically well tolerated
82
mitral valve prolapse is common in...
younger pxs ex: young px diagnosed w/ no history, CHD all of a sudden diagnosed with mitral valve abnormality
82
stenosis vs insufficiency
stenosis = failure of valve to OPEN completely, impeding forward flow (pressure overload --> hypertrophy) insufficiency = failure of valve to CLOSE, allowing reversal flow (volume overload --> dilation) both can lead to HF
83
what are the conditions associated with turner syndrome?
lymphangioma coarctation of the aorta calcific aortic stenosis
84
what happens in a calcific aortic stenosis of a congenitally stenotic bicusp valve?
there is partial fusion at its center aka raphe
85
what is the cause of aortic regurg
aortic root dilation
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