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NPLEX I > Anderson Cardio > Flashcards

Anderson Cardio Flashcards

1
Q

What is the most common cardiac congenital defect?

A

Interventricular Septal Defect

SSX: asymptomatic holosystolic murmur or CHF, increase risk of endocarditis

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2
Q

What four abnormalities form the Tetralogy of Fallot?

A

VSD, dextraposed aorta overriding the VSD, pulmonic stenosis, RV hypertrophy

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3
Q

What condition may a bicuspid aortic valve lead to later in life?

A

Aortic stenosis

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4
Q 
What's happening? 
S1
S2
Between S1 and S2
Between S2 and S1
A

Closure of mitral/tricuspid valves
Closures of aortic/pulmonic valves
Systole
Diastole

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5
Q

Right and left coronary arteries fill during _________. (diastole or systole)

A

Diastole - blood falls down into the vasculature.

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6
Q

Which is larger right or left coronary artery? What part of the heart do they feed?

A

Right is larger and supplies right and posterior left ventricle.

Left carries less blood , but divides and fess the anterior and lateral portions of the left ventricle.

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7
Q

Describe the conduction of the heart starting with the SA node and the location.

A

SA node - right atrium
AV node - right atrium
Right bundle of his - right ventricle (unifascicular)
Left bundle of his - left ventricle (bifascicular)

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8
Q 
Acute or Subacute Bacterial Endocarditis: 
More rare
Abnormal heart
Normal Heart 
Virulent organisms
Low virulence organism
A 
Acute
Subacute
Acute 
Acute
Subacute
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9
Q

What infection precedes rheumatic heart dz?

A

Grp A beta-hemolytic strep

AI, endocarditis esp of left valves, mitral stenosis, migratory polyarthritis

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10
Q

What histological finding is pathognomonic for rheumatic heart dz?

A

Aschoff bodies.

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11
Q

What is the MC valve disease?

A

Mitral Valve Prolapse

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12
Q

What condition is often the result of arteriosclerosis and a congenitally bicuspid aortic valve?

A

Aortic stenosis

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13
Q

What is the MC cause of myocarditis?

A

Viral infection (e.g. coxsackie B, flu, CMV, ECHO)

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14
Q 
List common organisms that cause myocarditis: 
Bacterial 
Rickettsial
Viral
Parasitic
Immune
A 
Staph, strep, cornebacterium diptheria
Typhus, Rocky Mt. Spotted Fever
Cocksackie B, Flu, CMV, ECHO
Toxoplasmosis, Trypansosoma cruzi, Trichinosis 
SLE, Scleroderma

Effects: Flabby ventricular myocardium, four chamber dilation, endocardium and valves unaffected, may be asymptomatic or get CHF.

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15
Q

What is the MC form of cardiomyopathies?

A

Dilated - young adults. Bilateral heart failure.

SSX: acute onset exertional intolerance (DOE)

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16
Q

What are the three forms of cardiomyopathy?

A

Dilated, restrictive, hypertrophic

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17
Q

Idiopathic Hypertrophic Subacute Stenosis (IHSS) pathology.

A

Interventricular septum is hypertrophies/anterior leaflet of mitral valve misplaced. Outflow is restricted. Wall of left ventricle hypertrophied.

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18
Q

What is restrictive cardiomyopathy usually secondary to?

A

Lysosomal storage disease or connective tissue/deposition disease. E.g. Hurler’s, Pompe’s, sarcoidosis, hemochromatosis.

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19
Q

Term for blood in the pericardial sac. Often occurs with MI where there is traumatic perforation.

A

Hemopericardium - causes cardiac tamponade

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20
Q

Where does METS to the heart mostly come from?

A

Lungs

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21
Q

Name the node:
Right vagus nerve
Left vagus nerve

A

SA

AV

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22
Q

Describe the process of muscle contraction.

A

Action potential - Ca influx - Ca binds Tp/Tm - actin/myosin binding - ATP to ADP - muscle contraction - relaxation - Ca returns to sarcoplasm via T-tubules

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23
Q

What two enzymes are responsible for phosphorylating actin/myosin?

A

Calmodium and light chain kinase

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24
Q

How do you modulate cardiac muscle strength?

A

Manipulating Ca channels - cAMP mechanism

Cardiac muscle does not recruit individual muscle units, syncytium - the whole thing contracts.

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25
Q

Name the muscle type: (cardiac/smooth/skeletal)
Recruitment of motor units/AP frequency regulates strength

AP duration regulates strength

Membrane potential/biochemical modulation of Ca sens regulates strength

A

Skeletal
Cardiac
Smooth

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26
Q

What is the longest vein in the body? Where does it come off of?

A

The great saphenous vein.

Come off femoral vein.

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27
Q

Arteriosclerosis vs. Atherosclerosis

A

Arteriosclerosis - thickening and loss of elasticity of arterial wall. Literal hardening of arteries

Atherosclerosis - intimal thickening and lipid deposition

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28
Q

Name the pathology: vasculitis of small/medium cranial vessels especially the temporal artery. Genetic predisposition, HA, pain tenderness, facial pain.

What is the most serious complication?

A

Temporal Arteritis

Blindness

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29
Q

Name the pathology: MC in young men, heave smokers, nodular phlebitis, instep claudication, gangrene, inflammation of arteries of extremeties

A

Thromboangiitis Obliterans/Buerger’s

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30
Q

Idiopathic vascular spasm causing extremities to turn white/blue/black.

A

Raynaud’s dz

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31
Q

Emboli vs. Thrombi

A 
Thrombi = clotted blood
Emboli = anything in the blood that shouldn't be there
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32
Q

Name the pathology: HIV infected patient, purple/black papules that may scale, metastatic, and deadly

A

Kaposi’s Sarcoma

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33
Q

Name the pathology: Children born with large hemangioma in place of an organ (eye/brain)

A

Lindau von Hipple

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34
Q

Where does the largest decrease in pressure occur in the vascular system?

A

Arterioles

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35
Q

T/F: Hypertension is most commonly symptomatic.

A

F

36
Q 
Essential or Secondary HTN: 
95% of cases
Lifestyle causes
Renal disease
ETOH abuse
A

Essential
Essential
Secondary
Secondary

37
Q

Right ventricular hypertrophy secondary to pulmonary HTN?

A

Cor pulmonale

38
Q

What is the difference between serum and plasma?

A

Serum = plasma - clotting factors

39
Q 
Heme or Non-Heme iron: 
Requires transferrin 
Comes from meat 
AKA Rust 
Oxidizes without transferrin 
Unregulated uptake
A 
Non-heme
Heme
Non-heme
Non-heme
Heme
40
Q

Ferrous vs. Ferric

A

Ferrous 2+

Ferric 3+

41
Q

Free iron absorption is blocked by…

A

High plasma Fe, phytates, tannins, oxylates, phosphates.

42
Q

Iron chelator that is released when infection is active to sequester Fe from bacteria.

A

Lactoferrin

43
Q

What enzymatic process of forming the heme?

A

B6 + Succinate (succinyl-CoA) , Glycine (ALA synthase)
ALA (ALA Dehydrogenase)
Porphyrin (ferrochelatase - requires Ferrous 2+)
Ferric is converted to Ferrous via CYP 450
HEME

44
Q

What enzyme puts Ferrous 2+ in the porphyrin molecule creating heme?

A

Ferrochelatase

45
Q

What is methemoglobin?

A

Fe 3+ iron instead of Fe 2+ - binds much more strongly to O2

46
Q

Once the iron and globulins are broken down, what is left over?

A

Biliverdin

47
Q

Bilirubin is conjugated to “direct” bilirubin in what organ?

A

Liver

48
Q

What inhibits the conjugation pathway?

A

Acetaminophen, hepatitis, toxic ingestion (mushrooms)

49
Q

Where is biliverdin converted to “Indirect” or unconjugated bilirubin? What cofactor is required?

A

Reticulo-endothelial cells

NADPH

50
Q

Name the pathology: overproducing a certain porphyrins and they are excreted in urine.

A

Porphyria

51
Q

R vs. T Hemoglobin
4 open O2 sites
No open O2 sites

A

R

T

52
Q

What are the globulin subunits of adult hemoglobin?

A

2 alpha, 2 beta

53
Q

Normal pH of the blood?

A

pH 7.37-7.4

Slightly more acidic in venous supply due to CO2

54
Q

O2 saturation of arterial vs. venous blood.

A

Arterial 97%

Venous 70%

55
Q

What stimulates oxygen release from hemoglobin?

A

Increased acidity, CO2, temp, 2,3 BPG

Increase salt-bridge formation.

56
Q

What are the three forms of CO2 carried to lungs?

A

1) dissolved CO2
2) Carbaminohemoglobin
3) HCO3- hydrated CO2 90%!!!

57
Q

What enzyme takes CO2 and H2O to become H2CO3, but can also reverse the reaction?

A

Carbonic anhydrase

58
Q

Describe the Bohr Effect.

A

Makes CO2 into bicarb - in periphery
Makes bicarb into CO@ - in lungs

Equal and opposite.

59
Q

What two enzymes does lead interfere with causing microcytic anemia?

A

ALA dehydrogenase, ferrochelatase.

60
Q

Most common cause of hemolytic anemia?

A

G6P deficiency

61
Q

Name the anemia:
bite cell anemia/heinz bodies
teardrop cells/basophilic stippling/target cells
pancytopenia, failure of myeloid stem cells
splenomegaly
leg ulcers, strokes, claudication

A 
G6P deficiency
Thalassemia 
Anaplastic anema 
G6P deficiency 
Sickle cell
62
Q

Name the pathology; myeloproliferative dz, high Hgb, viscous blood, tx is phlebotomy

A

Polycythemia vera

63
Q

Thalassemia major vs. minor

A

Major inherit genes from both parents (alpha or beta)
Inherit gene from one parent (alpha or beta)

Alpha has 4 genes, Beta has 2 genes

64
Q

What cancer of plasma cells causes Bence-Jones proteins in urine?

A

Multiple myeloma

65
Q

Which leukemia is MC in children?

A

Acute Lymphoblastic Leukemia

66
Q

Which leukemia is MC in adults? What is the histological finding?

A

Acute Myeloblastic Leukemia

Auer rods

67
Q

What form of leukemia is associated with the Philadelphia chromosome? Which cell line is involved?

A

Chronic Myelogenous Leukemia

Can be any cell type

68
Q

What is the MC overall Leukemia and MC after 60yo? Which cell line is involved?

A

Chronic Lymphocytic Leukemia

Well-differentiated B-Cell

69
Q

What leukemia has B-cells with hair-like projections?

A

Hairy Cell Leukemia

70
Q

Vitamin K dependent clotting factors?

A

2, 7, 9, and 10

71
Q

Which pathway is measured by PTT? Which is measured by PT/INR?

A

Intrinsic

Extrinsic

72
Q

What are the active substance causing positive feedback in the clotting cascade?

A

Thrombin

73
Q

What doe Poiseuille’s Equation give us?

A

Resistance

74
Q 
Name that clotting disorder:
Facto VIII def, 
Factor IX def, male only 
Facto VIII activating protein deficiency, milder
Vitamin deficiency for factors 2,7,9, 10
A

Hemophilia A
Hemophilia B
Von Willebrand’s
Vit K def

75
Q

What are three general causes of thrombocytopenia?

A

Increased destruction - e.g. AI
Decreased production - e.g. congenital or acquired (i.e. drug)
Increased consumption - e.g. DIC seen in sepsis or with embolism during childbirth

76
Q

How does the body respond to hemorrhage (decrease arterial pressure)?

A

1) Baroreceptor reflex - Increase HR, contractility, vasoconstriction
2) Increase Renin - Increase Angiotensin II leading to increased aldosterone, Na+ reabsorption, increase blood volume
3) Hydrostatic pressure drops, increases fluid absorption, increase blood volume

77
Q

T/F: Edema occurs when hydrostatic pressure exceeds oncotic pressure.

A

T

78
Q

Transudate vs. Exudate

A

Trans - protein poor, found in edema secondary to the alteration of Starling’s forces

Ex - protein rich, found in acute inflammatory states

79
Q

T/F: Interstitial edema = pitting edema

A

T

80
Q

What is anasarca?

A

Generalized edema

81
Q

What are the three stages of shock?

A

1) Nonprogressive stage - like hemorrhage
2) Progressive stage - hypoperfusion and metabolic acidosis
3) Irreversible shock - end organ damage and death

82
Q

T/F: Lymphatics absorb the difference between hydrostatic and oncotic pressure in the arteries.

A

F, in the capillaries.

83
Q

Name the lymphoma:
B-cell lymphoma, associated with EBV/malaria infxn
Young adults or 60yo, Reed-Sternberg cell
Most common lymphoma, more deadl

A

Burkitt’s - maxilla or mandible
Hodgkin’s - curable, familial
Non-hodgkin’s - assoc with Burkitt’s and Immunoblastic lymphomas

84
Q

What is the main point of the Frank Starling Law?

A

It established the physiologic limits of the heart in terms of blood volume. Changes in arterial pressure have little effect on the rate of pumping by the heart (WNL).

Patient with heart failure have a narrowed limit.

85
Q

T/F: Cardiac Output = Heart Rate x Stroke Volume

A

T

86
Q

Causes of right sided CHF

A

Emphysema, mitral stenosis, left ventricular failure

87
Q

Causes of left sided CHF

A

Ischemic heart dz, systemic hypertension, aortic or mitracl valve dz

NPLEX I (12 decks)

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