Pathophysiology

Leucopenia = Decrease in absolute number of leukocytes (WBC) in blood. Neutropenia is a subategory of Leucopenia (Thus for more detailed expl. see there)

Etiology: Inherited, Cancer, Blood cell or bone marrow conditions, Autoimune and infectious diseases (HIV)
Patophysiology: reduction of WBC
Clinical Manifestations: fever, chills, tiredness, repeated infections

Leukocytosis = WBC above normal levels

etiology: Inflammatory response or result of infection, bone tumors or leukemia, immune system disorder
Patophysiology: WBC above normal level
Clinical Manifesations: fever, fatigue, sweating,.., if cancerous -> see leukemia (bruises, bleeding (low plateletes))

Polycythemia = Abnormally high RBC

Etiology: Malfunction in bone marrow or reaction to chronical low O2 levels (Hypoxia including smoing and heart diseases), or water deprivation/losses
Patophysiology: Higher count of RBC (absolute) or loss of plasma volume (relative). Usually higher platelet count -> increased viscosity
Clinical manifestation: Hypertension -> headache, hemmorages and thromboembolism

self limiing lymphoproliferative disorder

Etiology: caused by Epstein-Barr virus(EBV) or other viruses, mostly in young adults (Kissing virus), remains in B-Lymphocytes forever
Patophysiology: ?? (not really able to find much)
Clinical Manifestations: Incubation 4-6 weeks, feeling ill, anorexia and chills, feer, enlarged lymph nodes, extrem fatigue. Hepatitis can occur as complication

Hemostasis is the stopping fo blood flow. It is normal wen it seals blood vessels to stop blood loss and hemorrage. Abnormal when it causes blood clothing or insufficient when it fails to stop blood flow

1. Vascular constriction
2. Formation of platelet plug
3. Blood coagulation

Vascular constriction: Smooth muscles contract wall to reduce blood flow (hormonal and nervous local factors secreted from plateletes contribute)

Platelet plugs seal small ruptures. Thrombopoietin (protein from liver, kidney, BM) controlls platelet production (megakaryocytes). Plateletes adhere to collagen fibers and attract additional plateletes

Blood coagulation converts fibrinogen into insuluble fibrin- Created mesh cements plateletes together to a cloth. Many substances control this process (prothrombin-> thrombin-> fibrinogen-> fibrin)

Thrombocytopenia: Reduction in platelet number

Thrombocytosis: elevation in platelet count

Etiology: loss of BM function, Leukemia, Radiation therapy and drugs. Infection with immunodeficiency virus (HIV) supress production of megakaryocytes. Platelets poling in spleen
Patophysiology: decreased production, increased destruction or decreased longelivity. 
Clinical Manifestations: Risk of bleeding

Etiology: Disease that stimulates Thrombopoietin (hormone that regulates megakaryocyte), tissue damage due to surgery, infection, cancer and chronic inflammation conditions. 
Pathophysiology: Increased megakaryocyte production thaus plateleta production
Clinical manifestations: thrombosis and hemorrage (bleeding from blood vessel). Thrombosis leads to embolism, occlusion of arterioles by platelet aggregation

Disseminated Intravascular Coagulation

Widspread coagulation and bleeding in vascular compartment. Occurs as a complication of a variety of conditions

Etiology: Trauma, bacterial sepsis or cancer (extrinsic pathways). Endothelial damage by virus, infection immune mechanism or temp. extremes (intrinsic pathways)
Patophysiology: Begins with massiv coagulation sequence (unregulated thrombin generation) Anticoagulants are reduced. Causes vessel occlusion and ischemia (not recieving enough O2), Multiple organ failure.
Clinical manifestations: Bleeding problems, tissue hypoxia and thus damage to organ structures. 

Heart failure is a condition in which the heart with normal pressure (otherwise it would be shock) is unable to maintain adequate output to meet the bodys needs.

Most common causes: Coronary artery disease (CAD, plaque build up in arteries that supply heart), hypertension, Dilated Cardiomyopathy (DCM, ventricles thin and grow larger), valvular disease and ventricular dysfunction

Systolic and diastolic, based on the ejection fraction (blood pumped out the ventricle with each contraction)

Systolic: commonly result from conditions that impair the contractile performance of th heart (decreased ejection fraction)

Diastolic: result from commonly from abnormal relaxation of the heart (ejection fraction stays the same but decreased ventricular filling -> decreased preload)

In Left ventricle. Decreased ejection fraction which leads to increase in preload and a rise in ventricular end diastolic pressure.
Accumulation of blood in atria (and venous system) (could cause edema)

Abnormal relaxation thus filling of ventricles is abnormal which compromises Cardiac output (CO). Influenced by heart rate (HR) which determines time available for ventricular filling. Preload is decreased.

Elevated pressure in ventricles because and left atrium due to build up of fluid

(NEED TO REVISE AGAIN NOT SURE ANSWER IS CORRECT)

Conditions that obstruct bloodflow into lungs or compromise pumping of right ventricle (e.g. left sided heart failure due to not enough blood from right atrium).
Pulmonary hypertension due to increased workload of Right ventricle

Right ventricle fails -> reduction in deoxygenated blood moving in pulmonary circulation -> decreased Cardiac output due to less bloo in left ventricle. 
Congestion of Right Atrium  or venous system -> increased venous and right atrial pressure -> peripheral edema (blood "falls" back (gravity) and liver becomes enlarged and cells could die

Periperal edema, Anorexia or weight loss because of GI-tract congestion, "liver"-pain

Hypertension (increased resistance for left ventricular to pump), acute myocardial infarction, Stenosis (narrowing) or leaking of vales 

Decreased Cardiac Output -> blood accumulates in left ventricle and atrium -> accumulation in pulmonary circutit thus higher venous pulmonary pressure -> pulmonary edema
Pulmonary congestion also impaires gas exchange
 

Decreased Cardiac output und therefore decreased tissue perfustion. Leads to Hypoxia.
hortness of breath and dyspnea

Cardiac reserve is maintained by those compensatory responses

Frank-starling Mechanism: Increased stretch of ventricle leads to increased force in contraction
Symphathetic nervous system activation: increases heart rate (tachycardia), vasoconstriction
Renin-Angiotensin-Aldosterone: Low CO = low glomerulal filtration rate -> renin secretion to vasoconstrict

 

Increased diastolic filling, increases stretching and thus the force of the next contraction and the CO.
In heart failure contractility is decreased thus stroke volume will also decrease (no matter the preload).

Water retention (due to decreased CO) will increase vascular volume and preload back to normal (within limits only)

Lowered Cardiac outpur results in decreased renal blood flow and filtration rate -> increased renin secretion from kidneys -> Angiotensin II (due to renin) leads to vasoconstriction and norepinephrin release -> Angiotensin II stimulates Aldosterone production -> Aldosteron increases tubular absorption (water and sodium retention) 

Compensatory mechanism for increased workload of the heart. Hypertrophy (increased muscle cell growth) and Remodeling of heart muscles. Can often lead to further dysfunctions

Ischemic heart disease (or Acute coronary syndrome, ACS) is a heart disease by insufficient blood flow to the heart tissues.
It includes different types like unstable angina UA, ST-segment elevation myocarial infarction STEMI and others.

1. Development of unstable plaque that can rupture
2. Obstruction such as spasm, constriction and dysfunction
3. Narrowing of coronary lumen (Thrombus?)
4. Inflammation
5. Physiologic state causing ischemia due to decreased O2 supply

Acute ST-segment Elevation myocardial Infarction is when the blood flow to the heart is blocked -> heart attack

Blood flow to heart is blocked or impaired, thus not enough O2 in heart. Depending on where the endo-, myo-, or epicardium is included. Loss of conractile function and changes in cell structure. Irreversible within 40 minutes.
Wal thining, healing (if reversible), hypertrophy and dilation of infarcted areas. Neighbouring areas undergo hypertrophy to take over work of infarcted area

severe and crushing pain, oten radiates to left arm, jaw, neck or chest area.
GI complaints are common, fatigue, weakness. Pain can give rise to tachycardia, anxiety and restlessness. Pale skin, cool and moist.

blood flow does not meet metabolic demands of heart, resulting from atherosclerosis, vasospasm. 
For example Chronic stable angina (Angina=constriction), silent myocardial ischemia,...

Chest pain is most common clinical manifestation

Hardening of the arteries characterized by formation of fibrofatty lesions

major risk factor is Hypercholesterolemia and hig levels of LDL (low density lipids). Can be modified by dietary and lifestyle changes.
Age and family history, as well as beeing male are also risk factors. Smoking, obesity and visceral fat ( fat stored in abdominal cavities), hypertension and diabetes. 
Damage of endothelial tissue (e.g. by smoking)