Pathophysiology1 -Test3

Front 1

1. What are the components of the hematologic system?

Back 1

Composition of blood:
90% water and 10% solutes
6 quarts (5.5 L)
Plasma:55% to 60% of the blood volume
Cellular components:
Erythrocytes
Leukocytes-fighting white spikey surface cells so they attach to target
Thrombocytes- (platelets
Lymphoid organs:Spleen,Lymph nodes
Mononuclear phagocyte system (MPS):
Formerly called reticuloendothelial system (RES)
Consists of a line of cells that originate in the bone marrow (monoblasts, promonocytes, and monocytes), then are transported into the bloodstream (monocytes), and finally settle in the tissues as macrophages(they come from monocytes)
Cells of the MPS (mostly in the liver and spleen) ingest and destroy microorganisms and foreign material

Front 2

2. Where are the macrophages derived from in the mononuclear phagocyte system?

Back 2

macrophages(they come from monocytes)

Front 3

3. What percent of the erythrocytes are stored in the peripheral blood?

Back 3

0%

Front 4

4. Where is iron located in a hemoglobin molecule? What is its function?

Back 4

at the ends of the x-polypeptide chain. its function is to transport oxygen

Front 5

5. What organs may store iron?

Back 5

Liver and Spleen

Front 6

6. What organs are involved in bilirubin metabolism and excretion?

Back 6

liver and kidney

Front 7

7. What are the etiologic events of anemia?

Back 7

Impaired RBC production
Acute or chronic blood
Increased RBC destruction

Front 8

8. List 6 examples of anemia according to the classification by mechanism.

Back 8

-Iron deficiency anemia (B)
-Pernicious anemia (vitamin B12 deficiency) (C)
-Folate deficiency anemia (D)
-Hemolytic anemia (G)
-Sickle cell anemia (L)
-Aplastic anemia

Front 9

9. What are the pathophysiologic changes in the body due to anemia?

Back 9

Oxygen is low -hypoxemia
Claudication- not enough strength in muscles
Cardiovascular -the one that will compensate when anemic- (heart angina pain)
Kidney will produce erthropoietin to compensate
DPG is diphosphoglycerate
RBC does not have mitochondria (aerobic metabolism) which produces ADP
Pathological changes of anemia and involves all the organs

Front 10

10. What is polycythemia? How is the relative type different from the absolute type

Back 10

Overproduction of red blood cells.
Relative is due to dehydration or stress -Fluid loss results in relative increases of red cell counts and Hgb and Hct (RBC percentage or the hemanocrit values)
and Absolute is due to Primary absolute:Abnormality of stem cells in the bone marrow, such as polycythemia rubra vera (rubra vera means “a true red”)
Secondary absolute:
Increase in erythropoietin as a normal response to chronic hypoxia or an inappropriate response to erythropoietin-secreting tumors

Front 11

11. What are the definitions of leukocytosis and leukopenia?

Back 11

Leukocytosis
An increase in the number of leukocytes
A normal protective physiologic response to physiologic stressors
Leukopenia
A decrease in the number of leukocytes
Not normal or beneficial
A low white count predisposes a patient to infections

Front 12

12. What are the characteristics of infectious mononucleosis?

Back 12

Acute, self-limiting infection of B lymphocytes transmitted by saliva through personal contact
Commonly caused by the Epstein-Barr virus-EBV85%
B cells have an EBV receptor site
Others viral agents resembling IM
Cytomegalovirus (CMV), hepatitis, influenza, and HIV
Symptoms: fever, sore throat, swollen cervical lymph nodes, increased lymphocyte count, and atypical (activated) lymphocytes
Serious complications are infrequent (< 5%)
Splenic rupture is the most common cause of death
> 50% lymphocytes and at least 10% atypical lymphocytes

Front 13

13. Differentiate among leukemia, myeloma, and lymphoma.
--just read

Back 13

Leukemias:Malignant disorder of the blood-forming organs
Bone marrow cancer
Excessive accumulation of leukemic cells
Immature white blood cells
Acute leukemia
Presence of undifferentiated or immature cells, usually blast cells
Chronic leukemia – too old cells
Predominant cell is mature but does not function normally
Signs and symptoms of leukemias
Anemia, bleeding purpura, petechiae(small patches), ecchymosis(bruises all over body) thrombosis, hemorrhage, DIC(diseminated intravascular,Coagulation-wide spread clotting) infection, weight loss, bone pain, elevated uric acid, and liver, spleen, and lymph node enlargement
Myeloma Definition: Proliferation of plasma cells
The tumor may be solitary or multifocal (multiple myeloma)
The malignant plasma cells produce abnormally large amounts of one class of immunoglobulin or incomplete immunoglobulin (Bence Jones proteins), which can pass through the glomerulus and damage the renal tubular cells(damage the kidney structure)
Multiple myeloma causes increased osteoclastic bone destruction
Clinical manifestations
Cortical and medullary bone loss
Skeletal pain
Recurring infections due to loss of the humoral immune response
lymphoma definition:

Front 14

14. What is the difference between splenomegaly and hypersplenism?

Back 14

Splenomegaly-structure enlarged
Congestive splenomegaly- too much blood, heart can not circulate blood so it gets stuck
Infiltrative splenomegaly- due to virus causing enlargement
Hypersplenism- and function enlarged
Overacticity of spleen
Can happen to both

Front 15

15. What is Virchow’s triad for the thromboembolic disease?

Back 15

Three factors that predispose a person to the thromboembolic disease
Endothelial injury
Alterations in blood flow-
Hypercoagulability-blood in high coagulated state like dehydration

Front 16

16. What is the feature of hemolytic disease of the newborn?

Back 16

Hemolytic disease of the newborn (HDN): Also known as erythroblastosis fetalis,Maternal antibody directed against fetal antigens,ABO incompatibility occurs in 20% to 25% of cases, while Rh incompatibility occurs in less than 10%,Clinical manifestations: Anemia,
Hyperbilirubinemia, Icterus neonatorum, Kernicterus

Front 17

17. What is the mechanism of sickle cell disease?

Back 17

Disorders characterized by the presence of an abnormal hemoglobin and Deoxygenation and dehydration cause the red cells to solidify and stretch into an elongated sickle sha

Front 18

18. What does each of the waves or wave complexes on the ECG represent?

Back 18

P- atrial depoloarization
QRS - ventricular depolarization and atrial repolarization
T- ventricular repolarization

Front 19

19. How does the autonomic nervous system affect the cardiovascular system?

Back 19

because it affects the fight or flight’ reaction from the heart muscle, can make you vomit or sweat prfusely in reaction from your ANS.

Front 20

20. Explain why an increased heart rate may not increase the cardiac output?

Back 20

because it does not increase the stroke volume

Front 21

21. Where is the integration center of baroreceptor and chemoreceptor reflexes located?

Back 21

baroreceptors are located in both the carotid sinus and aortic arch...
medula oblongotta

Front 22

22. How is the blood pressure regulated through cardiac output and peripheral resistance?

Back 22

The more blood pumped from the heart per minute (that is, the larger the cardiac output), the higher the blood pressure, kidneys can regulate with the amount of urine

Front 23

23. How is atherosclerosis developed in the arterial wall?

Back 23

Atherosclerosis
A form of arteriosclerosis
Thickening and hardening are caused by accumulation of lipid-laden macrophages in the arterial wall
Plaque development

Front 24

24. What is the difference between primary and secondary hypertension?

Back 24

Primary hypertension
Essential or idiopathic hypertension
Genetic and environmental factors
Affects 90% to 95% of individuals with hypertension
Secondary hypertension
Caused by a systemic disease process that raises peripheral vascular resistance or cardiac output, e.g. renal and endocrine diseases

Front 25

25. What are the etiologic factors for primary hypertension?

Back 25

decreased dietary potassium magnesium and calcium,increased sodium, insulin resistance, obesity, renal glomerular and tumbular inflamation, dysfunction of natriuetic hormones, endothelial dysfunction, RAA up, SNS up, genetics

Front 26

26. What is the difference between thrombosis and embolism?

Back 26

Thrombus formation
Blood clot that remains attached to the vessel wall (thromboembolus), which may lead to thrombophlebitis---clot induced
Embolus formation
Bolus of matter that is circulating in the bloodstream
Dislodged FAT BAT (fat aggregate, air bubble, thrombus, bacteria, amniotic fluid, tumor cells)

Front 27

27. What is the difference Raynaud phenomenon and Raynaud disease?

Back 27

the phenomenon is Episodic vasospasm in arteries and arterioles of the fingers, less commonly the toes. Raynaud phenomenon is secondary to other systemic diseases or conditions
Collagen vascular disease (scleroderma), smoking, pulmonary hypertension, myxedema, and environmental factors (cold and prolonged exposure to vibrating machinery)
Raynaud disease is a primary vasospastic disorder of unknown origin

Front 28

28. What is the difference between varicose vein and deep vein thrombosis?

Back 28

Varicose veins:A vein in which blood has pooled, Distended, tortuous, and palpable veins caused by trauma or gradual venous distention
Deep venous thrombosis: Obstruction of venous flow leading to increased venous pressure, Predisposing factors include venous stasis, venous endothelial damage, and hypercoagulable states

Front 29

29. What are the risk factors for coronary artery disease?

Back 29

Risk factors:
Dyslipidemia
Hypertension
Cigarette smoking
Diabetes mellitus
Obesity/sedentary lifestyle

Front 30

30. What are the ECG changes in myocardial ischemia and infarction?

Back 30

ST segment depression, T wave inversion (goes down), ST segment elevation(S wave remains high rather than going completely down

Front 31

31. Differentiate among dilated, hypertrophic, and restrictive cardiomyopathy.

Back 31

Dilated cardiomyopathy
Congestive
Means it is weak
Hypertrophic cardiomyopathy
Asymmetrical septal hypertrophy(Muscle is thicker)
Hypertensive (valvular hypertrophic) –heart working harder with weaker contraction
Restrictive cardiomyopathy
Amyloid deposits- do not know where these are from just abnormal chemicals in the muscle (maybe too much starch in diet)

Front 32

32. How is the left-sided heart failure different from the right-sided heart failure?

Back 32

Systolic heart failure
Inability of the heart to generate adequate cardiac output to perfuse tissues – left sided heart failure
Diastolic heart failure – not related to contraction problem, right sided heart failure which can result in edema and can occur all over the body

Front 33

33. List 6 examples of dysarrhythmias. What is the most life-threatening one?

Back 33

Tachycardia, flutter, fibrillation, bradycardia, premature ventricular contractions (PVCs), premature atrial contractions (PACs), and asystole.

The most life threatening is Ventricular tachycardia (V-tach or VT) -tachycardia, or fast heart rhythm, that originates in one of the ventricles of the heart. This is a potentially life-threatening arrhythmia because it may lead to ventricular fibrillation and sudden death.

Front 34

34. List 3 examples of left-to-right shunt and 1 example of right-to-left shunt congenital heart defects

Back 34

Patent ductus arteriosus (PDA)Failure of the ductus arteriosus to close
PDA allows blood to shunt from the aorta to the pulmonary trunk, hence increased blood flow to the lungs...
Atrial septal defect (ASD) Abnormal communication between the two atria, and Ventricular septal defect (VSD)...
Abnormal communication between the two ventricles
Most common type of congenital heart defects...Tetralogy of Fallot (TOF)Syndrome represented by four defects: Ventricular septal defect (VSD),
Overriding aorta straddles the VSD,
Pulmonary valve stenosis, and
Right ventricle hypertrophy

Front 35

35. What are the structures of upper and lower respiratory tracts, respectively?

Back 35

Upper respiratory tract (URT)
---Nasal cavity
---Pharynx: naso-, oro-, and laryngopharynx
---Larynx: connects upper and lower airways
Lower respiratory tract (LRT):
---Trachea
---Bronchi
---Terminal bronchiole

Front 36

36. How are the respiratory volumes and capacities measured?

Back 36

Spirometer

Front 37

37. Define dyspnea, orthopnea, hyperpnea, tachypnea, and apnea.

Back 37

;Dyspnea:Subjective sensation of uncomfortable breathing
Orthopnea:Dyspnea when a person is lying down...
Abnormal breathing patterns:
Kussmaul respirations (hyperpnea)...
Cheyne-Stokes respirations (oscillation of ventilation between apnea and hyperpnea)...
Tachypnea (rapid,shallow breathing)

Front 38

38. What are the common symptoms and signs of the pulmonary disease?

Back 38

Hypoventilation and hyperventilation
Cough
Hemoptysis
Cyanosis
Chest pain
Clubbing
Abnormal sputum

Front 39

39. What is the difference between atelectasis and bronchiectasis?

Back 39

Atelectasis is Incomplete expansion of the lung and Bronchiectasis is
Persistent abnormal dilation of the bronchi

Front 40

40. What is the difference between pneumothorax and flail chest?

Back 40

Chest wall restriction:Flail chest
Instability of a portion of the chest wall, resulting from fracture of several consecutive ribs in more than one place, or fracture of sternum plus several consecutive ribs.

Front 41

41. What is the spectrum of COPD?

Back 41

Chronic obstructive pulmonary disease is (COPD):Airway obstruction that is worse with expiration. Common signs and symptoms are Dyspnea and wheezing.....
Spectrum of COPD is Emphysema, Chronic bronchitis, Bronchial asthma

Front 42

42. What is the mechanism of cor pulmonale?

Back 42

Cor pulmonale (pulmonary heart disease)
Right ventricular enlargement due to pulmonary hypertension

Front 43

43. What is the leading cause of death in premature newborns?

Back 43

Respiratory Distress Syndrome (RDS)

Front 44

44. What are the clinical manifestations of cystic fibrosis?

Back 44

Exocrine or mucus-producing glands secrete abnormally thick mucus due to defective epithelial ion transport
In the lungs, thick secretions obstruct the bronchioles and predispose the lungs to chronic infections
Chronic inflammation leads to hyperplasia of goblet cells, bronchiectasis, pneumonia, hypoxia, fibrosis, etc.

Front 45

45. What are the potential risk factors for sudden infant death syndrome?

Back 45

Potential risk factors:Infant sleeping in a prone position,
Prematurity and low birth weight,
Infant not firstborn or product of a multiple gestation mother,
SIDS in a prior sibling,
Young/unmarried mother,
Low socioeconomic status,
Short intergestational interval,
Maternal smoking or drug abuse