Weakness, angina, fainting, tachycardia, sweating and pallor, pain in his bones and sternum
Signs of Anemia
What causes Iron deficiency Anemia?
- Hypochromic and microcytic erythrocytes
- Poikilocytosis (Irregular Shape)
-Anisocytosis (Irregular Size)
Type 1 cells
Form up to 97% of the alveolar cells; are flat and allow for exchange to the adjacent capillaries
Type 2 cells
Form up to 3% of the alveolar cells; are large and round; secrete surfactant; proliferate after lung damage; are source of precursors for new alveolar cells (type 1 & 2)
Panacinar (panlobar) emphysema
Characterized by dilation of the ENTIRE acinus (including the respiratory bronchioles, alveolar ducts, and alveolar sacs), distributed uniformly throughout the lung. Associated with AL- ANTITRYSPIN DEFICIENCY
Characterized by dilation of the PROXIMAL part of the acinus (the respiratory bronchioles). The pattern of involvement is more irregular, and is often localized to the upper parts of the lungs. Associated with SMOKING
Destruction of alveolar walls lead to the loss of elastic recoil within the lung and dilation of the terminal air spaces
Mediated by a TYPE 1 HYPERSENSITIVITY reaction involving IGE, MAST CELLS, often BEGINS IN CHILDHOOD, in patients with a FAMILY HISTORY OF ALLERGY
Includes asthma associated with CHRONIC BRONCHITIS as well as exercise or cold induced asthma
Acute respiratory distress sysndrome (ARDS)
A syndrome that results from DIFFUSE ALVEOLAR DAMAGE and LEAKAGE OF FLUID OUT OF THE PULMONARY CAPILLARIES into the intterstitium and alveolar spaces.
Bronchogenic carcinoma, is the leading cause of cancer related death in both men and women and is closely linked with cigarette smoking
Infection of lung parenchyma is a major cause of morbidity and mortality, accounting for nearly 10% of all hospital admissions and for approximately 80,000 deaths in the U.S. each year.
What can cause Pneumonia?
Viral URI, alcohol abuse, cigarette smoking, and COPD (Chronic Obstructive Pulmonary Disease)
1/3 of the world's population has been affected by this disease, and there 2-3 million deaths due to this disease.
Fast-response action potentials
Occurs in the atrial and ventricular myocytes and Purkinje fibers. Fast inward Na+ current. Causes depolarization. Occurs in phase 0
Slow-response action potentials
Occurs in the SA (Sinoatril) and AV (Atrioventricular) nodes. Slow inward Ca2+ current. Causes re-polarization (Potassium leaves cell)
The load seen by cardiac myocytes while the heart is in its relaxed state. It represents the stretch on the filled ventricle during diastole, before contraction takes place.
Load against which the myocytes must contract to generate cardia output. It represents the force that must be generated to push blood from LV into the aorta.
The volume of blood pumped per minute from either ventricle, which should be equal in the absence of pathology
RAAS (Renin-angiotensin 1 -aldosterone system)
Activated by decreased blood pressure
Renin is secreted and increases conversion of angiotensiogen to angiotensin,
Abnormalities of electrical rhythm that result from alterations of impulse conduction, impulse formation, or both
Hypertension risk factors
African American race, obesity, diabetes, advanced age, oral contraceptives, family history, excessive alcohol consumption, and cigarette smoking
BP more than 140/90 mmHg, confirmed on THREE separate occasions, or single reading of more than 170/110 mmHg.
Hypertension treatment "THERAPEUTIC LIFESTYLE MODIFICATIONS"
Weight loss, decreased alcohol intake, increased exercise, reduced NA intake, and smoking cessation
Rapid increase in BP, usually higher than 240/120 mmHg, associated with organ damage ("Flea -bitten kidneys")
Acute infective endocarditis
Affects normal heart valves and is often caused by Staphylococcus aureus to colonize normal valves
Subacute infective endocarditis
Colonizes a previously damaged valve (after oral surgery or poor dentition). It is most often caused by Streptococcus viridans
Fever, chills, weight loss, systemic emboli, petechiae, Janeway's lesions, Osler's nodes, splinter hemorrhages, and valvular involvement
Congestive Heart Failure (T/F)
Defined as the inability of the heart to generate a sufficient cardiac output to meet the metabolic demands of the body.
Congestive Heart Failure Presentation (T/F)
Dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, pulmonary edema, reduced renal perfusion, and an S3 heart sound. Most of these are due to failure of LV output and increased pulmonary venous pressure. Generally caused by left heart failure.
Is caused by group A beta-hemolytic streptococci. Usually affects children 5-10 years
Tachycardia, oliguria, hypotension, weak pulses, mental status changes, and cool extremities
Also called Variant angina, it presents as intermittent chest pain at rest that is not related to activity, stress, or BP. Occurs at night and at rest due to coronary artery vasospasm
Myocardial Infarction (MI) (T/F)
Due to myocardial necrosis (died) secondary to inadequate cardiac tissue perfusion. Q wave and ST will be seen on ECG
Myocardial Infarction (MI) Presentation
Patients will describe prolonged (more than 30-45 minutes) crushing chest pain similar to angina, but not relieved by nitroglycerin, nausea, vomiting, sweating, shortness of breath and weakness
Starts to elevate 4-6 hours after the pain starts and last 7-10 days. It is more specific than CK-MB. It is the best to measure MI.