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Anderson Cardio Flashcards

1
Q

most common neonatal malformation

A

interventricular septum defects (IVSD)

- holosystolic murmur (blood between r and l ventricle in systole)

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2
Q

what is IVS?

A

final event in separating aortic and pulmonary outflow from heart

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3
Q

25% of IVS defects occur in which portion?

A

membranous

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4
Q

tetrology of fallot

A

VSD (ventricular septal defect) dextraposed (aorta turned to right), pulmonary stenosis, RV hypertrophy

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5
Q

right atrium gets its blood supply from ____ and left atrium gets its blood from _____

A

IVC and SVC

pulmonary veins

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6
Q

which valves are on the right side?

which valves are on the left side?

A

right: tricuspid and pulmonic (draining venous into lungs)
left: mitral and aorta (draining lungs and pumping into body)

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7
Q

S1 is

S2 is

A

S1 (lub): closure of atrioventricular (tricuspid and mitral)

S2 (dub): closure of semilunar valves (aortic and pulmonic)

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8
Q

when is systole?

diastole?

A

between S1 and S2

between S2 and S1

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9
Q

regurgitation

stenosis

A

blood flowing backwards

hardening of valves = not enough blood flow

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10
Q

during systole which valves should be closed

during diastole?

A

tricuspid and mitral

aortic and pulmonic closed

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11
Q

closed valves are ____ and open valves are ______

A

regurg

stenotic

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12
Q

systolic murmurs

A

aortic and pulmonic stenosis

tricuspid and mitral regurg

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13
Q

diastolic murmurs

A

aortic and pulmonic regurg

tricuspid and mitral stenosis

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14
Q

CAD is usually on which side?

A

left

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15
Q

what part of the heart is supplied by the right coronary artery?
left?

A

right: right ventricle and post left ventricle
left: feeds anterior and lateral portions of left ventricle

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16
Q

cause of ischemia

complications of ischemia

A

angina pectoris
sudden cardiac death
coronary artery spasm
complications: LCHF, arrhythmias, MI

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17
Q

most common cause of LCHF

A

chronic ischemia

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18
Q

SA node is where

bundle branches are where

A

right atrium

one on right and two on left (follow coronary arteries and left branches)

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19
Q

actute vs subacute bacterial endocarditis

A

acute is more rare and attacks normal heart valves

subacute is more common and attacks abnormal heart and can have low virulent microbes that cause

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20
Q

rheumatic heart disease

A

post rheumatic sequelae (systemic reation to past beta hemolytic infection)

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21
Q

most common valve disease

A

mitral valve prolapse (heard between lub and dub)

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22
Q

what causes bacterial myocarditis

A

staph, strep, corynebacterium diptheria

dilation and flabby ventricular myocardium

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23
Q

what causes rickettsial myocarditis

A

typhus, rocky mt spotted fever

dilation and flabby chambers

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24
Q

most common myocardial disease

A

viral myocarditis

coxsacki-B, flu, CMV

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25
sequelae of myocardial disease
CHF
26
dilated cardiomyopathy
most common enlarged heart young people acute dyspnia is what is seen seen in alcoholics, hypothyroid, postpartum
27
restrictive cardiomyopathy
secondary disease (seen in Pompe's, Hurler's, sarcoidosis)
28
hypertrophic cardiomyopathy
idiopathic hypertrophic subacute stenosis
29
pericarditis
secondary to infection in lung or radiation understernum chest pain constrictive pericarditis
30
worst MI
transmural MI
31
right vagus nerve goes to left vagus goes to disruption leads to vagus innervation is
``` SA node (slows freqency) AV node (slows conduction) rhythm disfunction Parasympathetic ```
32
cardiac muscle at rest | During and AP there is
troponin (tp) and tropomysin (tm) block actin/myosin binding | Ca influx: Ca binds to Tp and Tm which leads to actin myosin binding, ATP to ADP and muscle contraction
33
which organelle takes ca out of muscle cell during relaxation phase
t-tubule
34
EPI does what in heart
cAMP and phosphorylation | it holds Ca channel open longer (important because you can alter cardiac strength this way)
35
cardiac AP has a
plateau because really long AP potential | -mediated by Ca channel
36
what are the areas of the sympathetic supply of the aorta?
``` celiac (esophagus to stomach) in mesenteric (duodenum to ascending colon and transverse colon to rectum) ```
37
vertebral arteries branch off what?
subclavian
38
what does subclavian change to?
subclavian, then axillary, then brachial
39
ext iliac artery becomes what?
femoral
40
benign tumors end in
oma
41
polyartaritis nodosa
necrotizing inflammation of small and med cranial vessels
42
temporal arteritis (giant cell arteritis)
inflammation in whole carotid tree | - notice by touching temples
43
Buerger's (thromboangitis obliterans)
men, heavy smokers, nodular phlebitis, gangrene
44
Raynaud's phenomenon
secondary in people who have SLE, Buerger's etc. | Raynaud's disease is primary idiopathic
45
aortic dissection
lumen of aorta dissects due to pressure and loss of patency. Looks like a double barrel. See severe back pain.
46
thrombi vs embolis
embolis: moving around. Broke of thrombus thrombus: clot that has formed in blood vessel
47
Kaposi's sarcoma
mostly seen in HIV purple black papules HHV infection can trigger dangerous
48
hemangioma | - can cause what disease
capillary: benign cavernous: larger, associated with Lindau van hipple (hemangioma in place of an organ)
49
where does the largest decrease in pressure occur?
the largest decrease in pressure occurs across the arterioles because they are the site of highest resistance
50
where is pressure highest and lowest in heart
highest: aorta lowest: venae cavae
51
HTN - difference between primary and secondary
> 140/90 mostly essential HTN and we don't know what causes it secondary HTN is due to some other disease
52
Cor Pulmonale
right ventricular hypertrophy secondary to pulmonary HTN
53
difference between serum and plasma
plasma: draw in tube that has anti-coagulant and all cloating factors stay in blood. serum: whole blood allowed to clot and clot removed
54
gamma globulin series
antibodies
55
lymphoid stem cells turn into what?
T-cells in thymus
56
difference between heme iron and non heme iron
heme iron: comes from meat and doesn't need transferring for uptake (easier to raise iron levels if you use heme iron) non heme iron: rust (body doesn't like this type because it oxidizes everything). Needs to be taken up by transferrin
57
ferrous iron | ferric iron
Fe 2+ | Fe 3+
58
lactoferrin
sequestering agent in blood used when infection active to keep Fe away from bacteria so replication is slower
59
porforin ring
place where you stick iron
60
ferrochelatase
puts Fe 2+ in middle of porforin ring and call it heme
61
where are reticuloendothelial cells
bone marrow, liver cells
62
where do you see ferritin in vascular world?
capillaries
63
porpherias
overproducing 1 or more porphorin's - intermediates to porforin ring are toxic - unexplained abdominal pain, neurologic symptoms
64
T hemoglobin
protected for that is folded up with no oxygens | it is a magnet for gases
65
myoglobin
muscle stored oxygen
66
is arterial or venous blood more acidic?
venous because it has higher levels of CO2
67
what stimulates dumping of O2?
acidity/CO2, increased temp, 2,3 BPG
68
what are three forms of CO2 that is brought to lungs?
dissolved carbaminohemoglobin HCO3 which is the major form (90%)
69
CO2 plus hemoglobin is called
carbaminohemoglobin
70
bohr affect
hide CO2 in bigger molecule and then release it when it gets to the lung (example HC03) *runs identically in two directions: CO2 to CO3 in peripheral tissue and then CO3 to CO2 in lungs
71
carbonic anhydrase
another example of bohr effect
72
How is anemia caused
decrease iron, poison mitochondria, put lead in system (don't form porforin), or decrease in vitamin B6
73
folic acid and B12/cobalamin always work together and are used in
methyl transfer reactions
74
most common reason for hemolytic anemia is
G6PD deficiency because no NADPH produced and don't recycle glutathione so RBCs blow up
75
what do you see in pernicious anemia? | what type of cells are affected?
atrophic gastritis with loss of parietal cells
76
heinz bodies
G6PD deficiency
77
teardrop cells, basophilic stippling, target cells
seen in both thalassemias
78
difference between alpha and beta thalassemia
born with defect in alpha or beta forming genes have thallasemia
79
see what type of anemia in thalassemia
hypochromic microcytic (small cells with higher Hgb)
80
polycythemia major
diagnosed as a young child
81
polycythemia minor
undiagnosed until they are an adult
82
crescent shaped cells
sickle cell anemia
83
anaplastic anemia
pancytopenia after exposure to drug, infection, etc.
84
polycthemia vera
myeloproliferative disease with high Hgb, viscous blood
85
multiple myeloma
lytic lesions plasma cells hypercalcemia
86
what type of proteins seen in urine of Multiple Myeloma patient
bence jones proteins
87
most common leukemia and cancer in children
acute lymphoblastic leukemia (ALL)
88
most common leukemia in adults
acute myeloblastic leukemia
89
which type of white cell dyscrasia has the philadelphia chromosome
Chronic myelogenous leukemia
90
most common overall leukemia and most common over 60
chronic lymphocytic leukemia
91
leukemia common in middle aged men with pancytopenia and B cells
Hairy Cell Leukemia
92
intrinsic pathway clotting cascade measured by drugs
blood trauma (turbulence and viscosity) or collagen and blood contact - measure by PTT - heparin
93
extrinsic pathway measured by drugs
damage outside of blood vessel (vitamin K dependent clotting factors 2,7,9,10) PT/INR
94
vitamin K dependent clotting factors in extrinsic pathway
2,7,9,10
95
Pouseuille's Equation
resistance to blood vessels | thicker blood = greater resistance
96
Hemophilia A
factor VIII def sex linked recessive males spontaneous bleeding of joints
97
Hemophilia B/Christmas Dz
factor IX def | male
98
Von Willebrand's
``` autosomal dominant VWF needed for platelet clumping spontaaneous bleeding from mucus membranes prolonged bleeding time and PTT normal platelets ```
99
what factors are vitamin K dependent? | what protein is def in vit k def?
needed for factors II,VII,IX,X | protein c
100
thrmobocytopenia
too few platelets | below 70,000
101
DIC
increased consumption of platelets
102
systemic response to hemorrhage
baroreceptors sense change in pressure and sends info to brain. Brain tells body to constrict arterioles and veins, decrease hydrostatic pressure, activate renin angiotensin system, activate aldosterone-sodium system to increase blood volume in response to hemorrhage
103
when does hypovolemic shock occur
when lose more than 20% of blood
104
oncotic pressure | hydrostatic pressure
keeps fluid in drives fluid out (starling forces)
105
anasarca
generalized edema (not seen often)
106
half of US deaths are caused by
cardiovascular disease resulting from myocardial or cerebral infarctions
107
B lymphocyte tumor maxilla or mandible EBV/malaria, Africa sequelae of non-hodgkins lymphoma
Burkitt's lymphoma
108
young adults or 60 yo curable intermittent spiking fever one node then spreads
Hodgkins lymphoma
109
most common lymphoma more deadly prognosis associated with Burkitt's lymphoma
non-hodgkins lymphoma
110
P wave coincides with ____
diastole/filling atrial depolarization
111
QRS segment coincides with ___
isovolumetric contraction (no valves open)
112
T wave coincides with
ejection/systole
113
Intrinsic ability of heart to adapt to changing blood volumes
Frank Starling law: the greater the heart is filled during diastole (preload), the greater the volume of blood that will be pumped into aorta
114
changes in arterial pressure (after load) have ___ effect on rate of pumping by heart
little
115
cardiac output =
cardiac output = heart rate x stroke volume CO = HR x SV * more ventricular pressure = more output
116
Right sided CHF
emphysema, mitral stenosis, left ventricular failure | pleural effusion, ascites
117
Left CHF
ischemic heart dz, systemic HTN | crackles, cough, cyanosis
118
cor pulmonale
right ventricular hypertrophy due to pulmonary HTN

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