Cardiovascular System Flashcards
Tetralogy of fallout
Congenital heart disease.
Most common cyanotic congenital heart defect is 50-70%.
Cause unclear.
Associated chromosome 22 deletion.
4 heart abnormalities:
- Stenosis of the right ventricular outflow tract
- Right ventricular hypertrophy (boot-shaped heart on x-ray)
- Ventricular septal defect (shunting of blood between the ventricles going from the right ventricle to the left ventricle and then through the aorta)
dextroposed aorta overriding pulmonic stenosis, RV hypertrophy
Babies:
Cyanosis
Clubbing in fingers and toes
Feeding difficulty
Failure to gain weight
What are the phases of the heart?
Atrial Systole
Ventricular Systole
Atrial and Ventricular Diastole
LUB-DUB
Atrioventricular valves closing
Mitral valve and tricuspid valve
Semilunar valves closing
Bacterial endocarditis
Streptococcus gallolyticus Staph aureus Heart valve dysfunction in 85% of patients. This may lead to congestive heart failure in 30-40% of patients Symptoms: - chest pain when you breath - fatigue - fever - chills - night sweats - fast heart rate - SOB
Rheumatic heart disease
secondary myocarditis
children following group A hemolytic strep infection
autoimmune, Aschoff bodies, endocarditis esp left valves
mitral stenosis, migratory polyarthritis
Mitral valve prolapse
Most common valve disease
Valve leaflets prolapse into atria during systole.
Calcific aortic stenosis
Aortic semilunar valve becomes calcified creating decreased aortic flow and increased left ventricular pressure
Most commonly due to calcification of a congenital bicuspid (instead of tricuspid) aortic valve
Ischemic heart disease
Reduced coronary flow due to atherosclerotic narrowing of coronary vessels and or thrombosis
Also maybe due to coronary artery spasm
Cause: angina pectoris, sudden cardiac death
COmplications: LCHF, arrhythmias, MI
Infectious Myocarditis
Inflammation of the muscle of the heart
Myo = muscle
cardiac = heart
itis = inflammation
Can lead to heart failure as the contractility of the heart decreases due to inflammation
Viral infections:
- due to coxsackie B is the main cause of myocarditis
- due to trypanosomacruzi - chagas disease
- trichinella - roundworm that moves from intestines to parts of the body. It causes myocarditis
- Lyme disease
Non-infectious myocarditis
SLE (lupus) Polymyositis Drug associated giant-cell Symptoms: - chest pain depending on the position - Arrythimias - Fatigue - Fever - SOB In severe cases, heart failure can occur
What is the main cause of B1 deficiency?
Alcoholism
Just know
The internal carotid arteries do not “feed” any tissue until they get to the brain
The external carotid feds the face
Organs that get direct branching from the aorta
Lungs through the bronchioarteries
Adrenals from the super renal arteries
Gonads from the gonadal arteries
Just know
Most abdominal drainage of venous blood is going to go through the liver (portal vein) with the exception of gonadal veins and the renal veins.
Thromboangitis Obliterans/Buerger’s disease
thrombo = clot -angitis = inflammation of arteries obliterans = blockage Men > women Heavy smokers Inflammation of arteries of extremities. Gangrene = death of tissue due to lack of blood supply. Nodular phlebitis Instep claudication
Claudication
Claudication is a pain in the legs or arms that comes on with walking or using the arms.
Gangrene
Gangrene is a serious condition where a loss of blood supply causes body tissue to die. It can affect any part of the body but typically starts in the toes, feet, fingers, and hands.
Nodular phlebitis
Serious complication.
It is an inflammatory condition.
There is always a clot or thrombus in the superficial vein.
6-40% will have a DVT
Up to 1/3 will have a pulmonary embolism (clot on the lungs) as the emboli might travel to the lungs.
Nearly always occurs in the legs.
Painful, tender, movement makes it worse, there is usually a lump.
Usually occurs in the great saphenous vein.
Diagnosed with ultrasound.
Raynauds Phenomenon
Vasoconstriction of arteries near the skin.
Color changes in fingers and toes
Sometimes affects nose, ears, and lips
Numbness, tingling, pain
The fingers turn white then blue then red due to cold weather.
Reynaud’s disease
primary Raynaud phenomenon Affects fingers and toes symmetrically Severity stays constant Arteries remain undamaged Common triggers: Stress, cold temperatures, nicotine, caffeine, medications that affect the sympathetic nervous system
Reynaud’s syndrome
secondary Raynaud phenomenon
Affects fingers and toes asymmetrically
Hypothalamus
Body’s thermostat
Aneurysms
Abnormal bulge in vessel due to weakening of the walls of blood vessels.
Usually affects arteries instead of veins due to higher pressure.
1.5x bigger than usual
Usually occur in the area of the aorta (abdominal 60% and thoracic 40%) where BP is higher.
Secondary to atherosclerosis, vasculitis, smoking, congenital.
Lower back pain
Men > women
>60
Marfan syndrome
A congenital disease that affects connective tissue
Symptoms:
- Back pain
- Blurred vision
- Bulging or sunken chest
- Fatigue, scoliosis small pupils, stretch marks
Aortic dissection
Lumen of aorta dissects due to pressure and loss of patency.
It creates a false lumen
Takes on a double-barrel shape
Part of the tunica intima is torn.
Causes:
- Hypertension, increase in volume.
Secondary to Marfan’s syndrome, Ehlers-Danlos syndrome, aneurysm
Emergency - can lead to hypotension
Arteriosclerosis
thickening and loss of elasticity
Arterio = artery
Sclerosis = hardening
Irritants (chemicals) or high BP causes damage to endothelial cells.
Certain proteins come inside and deposit themselves inside the tunica media.
Monocytes follow them and eat them but they die from too much eating.
They release cytokines bringing other cells in which in turn will also die and stay deposited in there…
Atherosclerosis
Formation of an atheromatous plaque
… this causes a lesion called fatty streak which is thrombogenic.
Platelets release platelet-derived growth factors encouraging smooth muscle growth.
Arteriolosclerosis
hardening of arterioles
olo = arterioles
Vasculitides
a group of disorders that cause vasculitis, which is inflammation in the walls of the blood vessels.
Since blood vessels pass through organs - vasculitis damages those organs and mimics a variety of diseases.
There are usually systemic symptoms like fever, fatigue, joint pain, and weight loss; as well as organ-specific symptoms that may literally involve any organ.
Erythrocyte sedimentation rate (ESR or sed rate)
a test that indirectly measures the degree of inflammation present in the body. The test actually measures the rate of fall (sedimentation) of erythrocytes (red blood cells) in a sample of blood that has been placed into a tall, thin, vertical tube.
Giant cell arteritis - most common vasculitis in individuals over the age of 50
Polyarteritis nodosa
individuals with hepatitis B/C. Multi-system disease Can occur anywhere in the body. in the skin, it can cause livedo reticularis and palpable purpura. Numbness, pain, burning, muscle weakness
Giant cell arteritis
or
Temporal Arteritis
inflammatory artery disease
Vessel giant cell inflammation of blood vessels going to the temporal artery (portion of external carotid artery).
50% of patients have vision loss
Thrombus vs emboli
Thrombus - Any coagulum inside the vessel. Clotted blood
Emboli - Anything in the blood that shouldn’t be there
Kaposi’s sarcoma
caused by Human Herpesvirus 8 Mostly seen in patients with HIV. 1 of 7 oncoviruses Risk factors: - Immunocompromised - Organ transplant - Immunosuppressive meds
Latent phase vs lytic phase
In the latent stage of the virus life cycle, a limited number of viral gene products are expressed. In contrast, a large number of proteins are expressed during lytic cycle replication.
Hemangioma
Capillary and cavernous types
Capillary type is benign.
Cavernous type is typically found on the skin of the head and neck, and are larger/ If associated with Lindau von Hipple disease = large hemangiomas of brain/eye and internal organs.
Where does the largest decrease in pressure occur?
Across the arterioles, because they are the site of highest resistance.
Hypertension
BP over 140/90 in anyone over 18 years of age.
120/80-139/89 considered pre-hypertension.
Most are asymptomatic
Need three readings to diagnose
Divided into essential and secondary
Essential hypertention
95% of cases
Mainly lifestyle causes
Leads to increased stroke and CHF, renal fibrosis, and coronary artery disease.
Secondary hypertension
5% of the cases
Secondary to renal/adrenal/thyroid/toxemia/aortic/CNS disease, also cocaine, descongestant, and ETOH abuse/use
Blood proteins
Plasma is the fluid portion of the blood. If the whole blood is allowed to clot and the clot is removed, the remaining fluid is called serum. Plasma proteins can be separated by size by electrophoresis.
Prealbumin
thyroxine, vitamin A
Albumin
Oncotic pressure
Binds hormones, drugs
Where are the LDLs, IDLs, and VLDLs formed?
From the free cholesterol pool in the liver and they are transported out of the liver.
What are the binding sites?
Chylomicrons - ApoE
LDL - ApoB 100
ApoA1 - HDL
Myeloid stem
Make megakaryocyte cells (then PLT), proerythroblast cells (retic’s then RBC’s), and monoblast (then myeloblast and then WBC’s)
Remember
We do not want free iron running around that is going to cause oxidation.
Where is iron stored?
Ferritin in the liver
Heme iron
Through diet from meat - unregulated uptake - put into plasma - used for erythropoiesis
Non-heme iron
From plants - regulated uptake - bound to transferrin - exported to the plasma - goes to cells or into the liver to bind with ferritin.
What does heme do?
Holds on to oxygen
What is the life span of hemoglobulin?
120 days
Where in the body do I find reticuloendothelial cells?
Liver, spleen, and bone marrow.
What are reticuloendothelial cells coupled with?
Leakest capillaries
Bilirubin has two states
pre-state or unconjugated or indirect and conjugated bilirubin or direct
Heme synthesis
?????
Hemoglobin
Heme - iron
globin - protein
Hb is a tetramer with 4 O2 binding sites
Myoglobin
Oxygen storage site in muscle. It is similar to Hb, but binds the O2 more tightly, and will only let it go under low O2 situations.
What is more acidic: arterial or venous blood?
Venous due to CO2
What happens when you have vitamin B12 deficiency?
Megaloblastic anemia
Role of glutathione
It reduces peroxide to water so my RBC’s are stable
What operates the NADH system?
Glucose-6-phosphate dehydrogenase. It converts NADP to NADPH to form oxidized glutathione so it can reduce peroxide into water.
If there is a deficiency of glutathione, I will end up having too much peroxide in RBC damaging it
Anemia
Anemia is a condition in which you lack enough healthy red blood cells to carry adequate oxygen to your body’s tissues
Sickle cell anemia
Autosomal recessive
A genetic disease where RBC takes shape of a sickle.
They are easily destroyed causing anemia.
Defective hemoglobin cause.
Life span of RBCs is 20 days
Chronic hemolytic anemia, vasoocclusive complications > leg ulcers, strokes, bone infarcts, pain, 1/2 survive to age 40.
Hemolytic anemia
Increase RBC hemolysis due to own antibodies target RBCs for destruction.
Idiopathic.
Medication side effect
Extrinsic because our immune system cells believe our RBCs are foreign.
Hemolytic anemia
Increase RBC hemolysis due to own antibodies target RBCs for destruction.
Idiopathic.
Medication side effect
Extrinsic because our immune system cells believe our RBCs are foreign.
Intravascular or extravascular (spleen), increased total body iron, jaundice, splenomegaly
G6PD: MOST common. Bite cell anemia, Heinz bodies
Pernicious anemia
atrophiic gastritis with loss of parietal cells and IF, B12 def.
Megaloblastic anemia = macrocytic
Pernicious anemia
atrophic gastritis with loss of parietal cells and IF, B12 def.
Megaloblastic anemia = macrocytic
Alpha thalassemia
4 genes for alpha chain, 1 hurt = silent killer, 2 hurt = AT minor/trait, 3 hurt hemolytic throughout life, 4 genes hurt = fetal death
Beta thalassemia
2 genes for beta chain heterozygotes = minor/trait, minimal or no anemia, homozygotes = severe anemia
Both thalassemias: teardrop cells, basophilic stippling, target cells.
Hypochromic, microcytic; small cells with bigger Hgb than in iron def.
Aplastic anemia
pancytopenia, failure/suppression of myeloid stem cells after exposure to drug, infection, idiopathic
Polycythemia Vera
Myeloproliferative disease, high HgB, middle age, viscous blood, tx phlebotomy, survive 10 years
Multiple myeloma
Cancer that arises from the bone marrow, from malignant transformation of plasma cells.
Myeloma = cancerous plasma cells
Myeloma cells produce unwanted substances such as paraprotein that can damage other organs.
Bone eating type of lesion
Bone pain
Plasma cells overproduce Ig’s.
Hairy Cell Leukemia
B cells with hair-like projections Virus related, pancytopenia Middle-aged men most common Most survive > 10 Rare
Leukemia
Leukemia is a cancer of white blood cells. White blood cells (also called leukocytes or WBCs) fight infections and other diseases. In leukemia, the bone marrow (spongy material inside the bones) makes many white blood cells that aren’t normal. These abnormal WBCs crowd the bone marrow and get into the bloodstream.
ALL or Acute Lymphocytic Anemia
Most common type of cancer in children.
Associated with virus, down’s, radiation exposure.
Remission or cure with tx. Fever/ bone pain
ALL or Acute Lymphocytic Anemia
Most common type of cancer in children.
Associated with virus, down’s, radiation exposure.
Remission or cure with tx. Fever/ bone pain
Survivable
Acute Myoblastic Leukemia
Most common type of leukemia in adults.
This type of cancer gets worse if not treated fast.
Risk factors: chemotherapy, smokers
Symptoms: fever, SOB, easy bruising or bleeding, fatigue, weight loss or loss of appetite.
Not survivable
Chronic Myelogenous Leukemia
well-differentiated granulocytic, Philadelphia chromosome
25-60 slow for 3 years, then blast crisis when 85% die (accelerated phase)
May include any cell line. Hepatosplenomegaly, generalized
Chronic lymphocytic leukemia
Leukemia of retirement
Most common overall Leukemia and most common after 60
Well-differentiated B-cell lymphocytic
More males/ Never Asian.
Acute state RARE unlike CML
Extrinsic
I cut myself and I need to clot on the outside of my body
Creates thromboembolic phenomenon and creates strokes, MI
Factors 2 7 9 10 - vitamin K dependent
Intrinsic
Not cut myself, I will clot inside my blood vessels
Factor 10 like in intrinsic
What does the prothrombin activator going to do?
Activate prothrombin to thrombin (with calcium and vitamin K).
Then thrombin is going to activate fibrinogen to fibrin
clotting
positive feedback
factor 10 comes down and activates prothrombin to thrombin
Factor 10 activates factor 8
It activates these two so more thrombin can be produced so there could be more clotting
Poiselle’s
Thickness and resistance of blood
the only one that has pie
Hemophilia A
Factor VIII deficiency, sex-linked recessive, males (female carrier), spontaneous bleeding into joints with associated pain and swelling.
Blood in urine or stool.
Bruising
Nosebleeds
Hemophilia B/Christmas disease
factor IX deficiency, male-only (female carrier)
Same symptoms as A, but less severe
Von Willebrand’s
Autosomal dominant
Deficiency of factor activator
Not enough working von Willebrand factor to help with platelet adhesion to bind and carry factor VIII to stop bleeding.
Hydrostatic pressure
Equal to blood pressure
Edema
Fluid exchange = balance of [Hydrostatic Pressure (drives out) and Oncotic Pressure (keeps in)] (Starling’s laws).
Arterial hydrostatic pressure drives fluid out, Oncotic (Albumen) pressure tries to attract it in. Leftover fluid collected by lymphatics.
Anasarca
generalized edema
End stage heart failure
Lymph
Vascular system
One-way flap valves
Burkitt Lymphoma
lymph = Lymphocytes Oma = tumor
B lymphocyte tumor
Rapid proliferation of B lymphocytes.
Lump on jaw
Dyspnea and pain
Predominantly affects children and teenagers
EBC (Epstein Barr virus) associates with this disease
EBV
Human Herpesvirus 4
Spreads through saliva
It can cause mononucleosis
It is associated with Nasopharyngeal carcinoma
Hodgkin’s lymphoma
Common in people at the age of 20s and after 60.
Painless enlargement of lymph nodes.
Curable, familial, prognosis depends on the stage.
Fever, fatigue, itchy skin, weight loss.
Reed-Sternberg cell
Frank-starling
The intrinsic ability of the heart to adapt to changing blood volumes.
Basic idea: The greater the Heart is filled during diastole (PRELOAD) the greater the volume of blood that will be pumped into the aoorta.
Within normal limits, changes in arterial pressure (afterload) have little effect on the rate of pumping by the heart.
Rules about heart
The cause of the failure is generally the place I am pumping to. The symptoms and signs are the places I am draining inside of that heart.
Right-side heart failure is almost caused by pulmonary heart failure or a failed left heart that backs up into the pulmonary circuit.
Pulmonary pressure increase for any reason will cause the right side to fail
Right-side heart failure
Usually has to do with the pulmonary system or the left heart. Symptoms are: - poor drainage of the venous circuit. - Jugular venous distention - Portal hypertension - Ascites
Right-side heart failure
Usually has to do with the pulmonary system or the left heart.
- emphysema, mitral stenosis, left ventricular failure
- poor drainage of the venous circuit.
- Jugular venous distention
- Portal hypertension
- Ascites
Left-side hypertension
coronary artery disease systemic circulation Symptoms: - Lung symptoms such as pulmonary edema Ischemic heart disease, systemic hypertension Aortic or mitral valve disease; exertional dyspnea PND, tachycardia, cardiac asthma Crackles, cough, cyanosis
Cor Pulmonale
Right ventricular hypertrophy secondary to pulmonary hypertension
