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Flashcards in Anderson Cardio Deck (118)
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1
Q

most common neonatal malformation

A

interventricular septum defects (IVSD)

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

2
Q

what is IVS?

A

final event in separating aortic and pulmonary outflow from heart

3
Q

25% of IVS defects occur in which portion?

A

membranous

4
Q

tetrology of fallot

A

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

5
Q

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

A

IVC and SVC

pulmonary veins

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)

7
Q

S1 is

S2 is

A

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

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

8
Q

when is systole?

diastole?

A

between S1 and S2

between S2 and S1

9
Q

regurgitation

stenosis

A

blood flowing backwards

hardening of valves = not enough blood flow

10
Q

during systole which valves should be closed

during diastole?

A

tricuspid and mitral

aortic and pulmonic closed

11
Q

closed valves are ____ and open valves are ______

A

regurg

stenotic

12
Q

systolic murmurs

A

aortic and pulmonic stenosis

tricuspid and mitral regurg

13
Q

diastolic murmurs

A

aortic and pulmonic regurg

tricuspid and mitral stenosis

14
Q

CAD is usually on which side?

A

left

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

16
Q

cause of ischemia

complications of ischemia

A

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

17
Q

most common cause of LCHF

A

chronic ischemia

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)

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

20
Q

rheumatic heart disease

A

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

21
Q

most common valve disease

A

mitral valve prolapse (heard between lub and dub)

22
Q

what causes bacterial myocarditis

A

staph, strep, corynebacterium diptheria

dilation and flabby ventricular myocardium

23
Q

what causes rickettsial myocarditis

A

typhus, rocky mt spotted fever

dilation and flabby chambers

24
Q

most common myocardial disease

A

viral myocarditis

coxsacki-B, flu, CMV

25
Q

sequelae of myocardial disease

A

CHF

26
Q

dilated cardiomyopathy

A

most common
enlarged heart
young people acute dyspnia is what is seen
seen in alcoholics, hypothyroid, postpartum

27
Q

restrictive cardiomyopathy

A

secondary disease (seen in Pompe’s, Hurler’s, sarcoidosis)

28
Q

hypertrophic cardiomyopathy

A

idiopathic hypertrophic subacute stenosis

29
Q

pericarditis

A

secondary to infection in lung or radiation
understernum chest pain
constrictive pericarditis

30
Q

worst MI

A

transmural MI

31
Q

right vagus nerve goes to
left vagus goes to
disruption leads to
vagus innervation is

A
SA node (slows freqency)
AV node (slows conduction)
rhythm disfunction
Parasympathetic
32
Q

cardiac muscle at rest

During and AP there is

A

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
Q

which organelle takes ca out of muscle cell during relaxation phase

A

t-tubule

34
Q

EPI does what in heart

A

cAMP and phosphorylation

it holds Ca channel open longer (important because you can alter cardiac strength this way)

35
Q

cardiac AP has a

A

plateau because really long AP potential

-mediated by Ca channel

36
Q

what are the areas of the sympathetic supply of the aorta?

A
celiac (esophagus to stomach)
in mesenteric (duodenum to ascending colon and transverse colon to rectum)
37
Q

vertebral arteries branch off what?

A

subclavian

38
Q

what does subclavian change to?

A

subclavian, then axillary, then brachial

39
Q

ext iliac artery becomes what?

A

femoral

40
Q

benign tumors end in

A

oma

41
Q

polyartaritis nodosa

A

necrotizing inflammation of small and med cranial vessels

42
Q

temporal arteritis (giant cell arteritis)

A

inflammation in whole carotid tree

- notice by touching temples

43
Q

Buerger’s (thromboangitis obliterans)

A

men, heavy smokers, nodular phlebitis, gangrene

44
Q

Raynaud’s phenomenon

A

secondary in people who have SLE, Buerger’s etc.

Raynaud’s disease is primary idiopathic

45
Q

aortic dissection

A

lumen of aorta dissects due to pressure and loss of patency. Looks like a double barrel. See severe back pain.

46
Q

thrombi vs embolis

A

embolis: moving around. Broke of thrombus
thrombus: clot that has formed in blood vessel

47
Q

Kaposi’s sarcoma

A

mostly seen in HIV
purple black papules
HHV infection can trigger
dangerous

48
Q

hemangioma

- can cause what disease

A

capillary: benign
cavernous: larger, associated with Lindau van hipple (hemangioma in place of an organ)

49
Q

where does the largest decrease in pressure occur?

A

the largest decrease in pressure occurs across the arterioles because they are the site of highest resistance

50
Q

where is pressure highest and lowest in heart

A

highest: aorta
lowest: venae cavae

51
Q

HTN - difference between primary and secondary

A

> 140/90
mostly essential HTN and we don’t know what causes it
secondary HTN is due to some other disease

52
Q

Cor Pulmonale

A

right ventricular hypertrophy secondary to pulmonary HTN

53
Q

difference between serum and plasma

A

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
Q

gamma globulin series

A

antibodies

55
Q

lymphoid stem cells turn into what?

A

T-cells in thymus

56
Q

difference between heme iron and non heme iron

A

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
Q

ferrous iron

ferric iron

A

Fe 2+

Fe 3+

58
Q

lactoferrin

A

sequestering agent in blood used when infection active to keep Fe away from bacteria so replication is slower

59
Q

porforin ring

A

place where you stick iron

60
Q

ferrochelatase

A

puts Fe 2+ in middle of porforin ring and call it heme

61
Q

where are reticuloendothelial cells

A

bone marrow, liver cells

62
Q

where do you see ferritin in vascular world?

A

capillaries

63
Q

porpherias

A

overproducing 1 or more porphorin’s

  • intermediates to porforin ring are toxic
  • unexplained abdominal pain, neurologic symptoms
64
Q

T hemoglobin

A

protected for that is folded up with no oxygens

it is a magnet for gases

65
Q

myoglobin

A

muscle stored oxygen

66
Q

is arterial or venous blood more acidic?

A

venous because it has higher levels of CO2

67
Q

what stimulates dumping of O2?

A

acidity/CO2, increased temp, 2,3 BPG

68
Q

what are three forms of CO2 that is brought to lungs?

A

dissolved
carbaminohemoglobin
HCO3 which is the major form (90%)

69
Q

CO2 plus hemoglobin is called

A

carbaminohemoglobin

70
Q

bohr affect

A

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
Q

carbonic anhydrase

A

another example of bohr effect

72
Q

How is anemia caused

A

decrease iron, poison mitochondria, put lead in system (don’t form porforin), or decrease in vitamin B6

73
Q

folic acid and B12/cobalamin always work together and are used in

A

methyl transfer reactions

74
Q

most common reason for hemolytic anemia is

A

G6PD deficiency because no NADPH produced and don’t recycle glutathione so RBCs blow up

75
Q

what do you see in pernicious anemia?

what type of cells are affected?

A

atrophic gastritis with loss of parietal cells

76
Q

heinz bodies

A

G6PD deficiency

77
Q

teardrop cells, basophilic stippling, target cells

A

seen in both thalassemias

78
Q

difference between alpha and beta thalassemia

A

born with defect in alpha or beta forming genes have thallasemia

79
Q

see what type of anemia in thalassemia

A

hypochromic microcytic (small cells with higher Hgb)

80
Q

polycythemia major

A

diagnosed as a young child

81
Q

polycythemia minor

A

undiagnosed until they are an adult

82
Q

crescent shaped cells

A

sickle cell anemia

83
Q

anaplastic anemia

A

pancytopenia after exposure to drug, infection, etc.

84
Q

polycthemia vera

A

myeloproliferative disease with high Hgb, viscous blood

85
Q

multiple myeloma

A

lytic lesions
plasma cells
hypercalcemia

86
Q

what type of proteins seen in urine of Multiple Myeloma patient

A

bence jones proteins

87
Q

most common leukemia and cancer in children

A

acute lymphoblastic leukemia (ALL)

88
Q

most common leukemia in adults

A

acute myeloblastic leukemia

89
Q

which type of white cell dyscrasia has the philadelphia chromosome

A

Chronic myelogenous leukemia

90
Q

most common overall leukemia and most common over 60

A

chronic lymphocytic leukemia

91
Q

leukemia common in middle aged men with pancytopenia and B cells

A

Hairy Cell Leukemia

92
Q

intrinsic pathway clotting cascade
measured by
drugs

A

blood trauma (turbulence and viscosity) or collagen and blood contact

  • measure by PTT
  • heparin
93
Q

extrinsic pathway
measured by
drugs

A

damage outside of blood vessel (vitamin K dependent clotting factors 2,7,9,10)
PT/INR

94
Q

vitamin K dependent clotting factors in extrinsic pathway

A

2,7,9,10

95
Q

Pouseuille’s Equation

A

resistance to blood vessels

thicker blood = greater resistance

96
Q

Hemophilia A

A

factor VIII def
sex linked recessive
males
spontaneous bleeding of joints

97
Q

Hemophilia B/Christmas Dz

A

factor IX def

male

98
Q

Von Willebrand’s

A
autosomal dominant 
VWF needed for platelet clumping
spontaaneous bleeding from mucus membranes
prolonged bleeding time and PTT
normal platelets
99
Q

what factors are vitamin K dependent?

what protein is def in vit k def?

A

needed for factors II,VII,IX,X

protein c

100
Q

thrmobocytopenia

A

too few platelets

below 70,000

101
Q

DIC

A

increased consumption of platelets

102
Q

systemic response to hemorrhage

A

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
Q

when does hypovolemic shock occur

A

when lose more than 20% of blood

104
Q

oncotic pressure

hydrostatic pressure

A

keeps fluid in
drives fluid out
(starling forces)

105
Q

anasarca

A

generalized edema (not seen often)

106
Q

half of US deaths are caused by

A

cardiovascular disease resulting from myocardial or cerebral infarctions

107
Q

B lymphocyte tumor
maxilla or mandible
EBV/malaria, Africa
sequelae of non-hodgkins lymphoma

A

Burkitt’s lymphoma

108
Q

young adults or 60 yo
curable
intermittent spiking fever
one node then spreads

A

Hodgkins lymphoma

109
Q

most common lymphoma
more deadly prognosis
associated with Burkitt’s lymphoma

A

non-hodgkins lymphoma

110
Q

P wave coincides with ____

A

diastole/filling atrial depolarization

111
Q

QRS segment coincides with ___

A

isovolumetric contraction (no valves open)

112
Q

T wave coincides with

A

ejection/systole

113
Q

Intrinsic ability of heart to adapt to changing blood volumes

A

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
Q

changes in arterial pressure (after load) have ___ effect on rate of pumping by heart

A

little

115
Q

cardiac output =

A

cardiac output = heart rate x stroke volume
CO = HR x SV
* more ventricular pressure = more output

116
Q

Right sided CHF

A

emphysema, mitral stenosis, left ventricular failure

pleural effusion, ascites

117
Q

Left CHF

A

ischemic heart dz, systemic HTN

crackles, cough, cyanosis

118
Q

cor pulmonale

A

right ventricular hypertrophy due to pulmonary HTN