Hemodynamic Disorders

Explanation -
Arterial thrombi :
are frequently occlusive; the most common sites in decreasing order of frequency are the coronary, cerebral, and femoral arteries. They typically consist of a friable meshwork of platelets, fibrin, red cells, and degenerating leukocytes. Although these are usually superimposed on a ruptured atherosclerotic plaque, other vascular injuries (vasculitis, trauma) may be the underlying cause.

Venous thrombosis (phlebothrombosis)- is almost invariably occlusive, with the thrombus forming a long luminal cast. Because these thrombi form in the sluggish venous circulation, they tend to contain more enmeshed red cells (and relatively few platelets) and are therefore known as red thrombi or stasis thrombi. Venous thrombi are firm, are focally attached to the vessel wall. 

Accumulation of excess fluid in tissue is called edema

Explanation -
Hyperemia is an active process in which arteriolar dilation (e.g., at sites of inflammation or in skeletal muscle during exercise) leads to increased blood flow. Affected tissues turn red (erythema) because of increased delivery of oxygenated blood. 
Sympathetic activation play a role.

Explanation: Atherosclerosis is the most common cause of coronary artery disease

Line of zahn are marked in thrombi formed within aorta

Explanation :
Causes of distributive shock -
Septic shock
Anaphylaxis 
Spinal cord injury

Explanation: pleural fluid accumulates as a result of either increased hydrostatic pressure or decreased osmotic pressure (‘transudative’ effusion, as seen in cardiac, liver or renal failure), or from increased microvascular pressure due to disease of the pleura or injury in the adjacent lung(exudative)

Heart failure occurs following MI due to reduced ventricular contractility

Explanation -
Localized edema is generally due to cellulitis, chronic venous insufficiency, deep vein thrombosis, lymphedema, or May-Thurner syndrome. 

Explanation :
The dominant cause of IHD syndrome is insufficient coronary perfusion relative to myocardial demand, due to chronic, progressive atherosclerotic narrowing of the epicardial coronary arteries

Explanation: Peptic ulcer disease is the most common Cause of acute upper gastrointestinal haemorrhage

Anesthetic accident produces neurogenic shock

Explanation -
Most pulmonary emboli (60% to 80%) are clinically silent because they are small. With time they become organized and are incorporated into the vascular wall; in some cases organization of the thromboembolus leaves behind a delicate, bridging fibrous web.

• Sudden death, acute right heart failure (cor pulmonale), or cardiovascular collapse occurs when emboli obstruct 60% or more of the pulmonary circulation( Large emboli). 

• Embolic obstruction of medium-sized arteries with subsequent vascular rupture can result in pulmonary hemorrhage but usually does not cause pulmonary infarction.
• Embolic obstruction of small end-arteriolar pulmonary branches often does produce hemorrhage or infarction.
• Multiple emboli over time may cause pulmonary hypertension and right ventricular failure.

Most common cause of thrombosis is endothelial injury

Explanation: LPS &teichoic acid are septic shock inducer.

Explanation -
Causes of transudative oedema :
Protein energy malnutrition 
Liver cirrhosis
Malnutrition 
Protein losing gastroenteropathy

Causes of exudative ascities :
Heart failure
Cirrhosis
Portal vein thrombosis
Tuberculosis
Peritoneal tumor.

Smoking remains most important modifiable risk factor in CAD

Explanation -
Causes of stroke in old age -
HTN,DM,OHD,Atherosclerosis 
Causes of stroke in young age -
Vulvular heart disease, 
Rupture barry aneurism 
Arterio venous malformation 
Vasculitis

Explanation -
In the early nonprogressive phase of shock, various neurohumoral mechanisms help maintain cardiac output and blood pressure. These mechanisms include baroreceptor reflexes, release of catecholamines and antidiuretic hormone, activation of the renin-angiotensin-aldosterone axis, and generalized sympathetic stimulation. The net effect is tachycardia, peripheral vasoconstriction, and renal fluid conservation; cutaneous vasoconstriction causes the characteristic “shocky” skin coolness and pallor (notably, septic shock can initially cause cutaneous vasodilation, so the patient may present with warm, flushed skin). Coronary and cerebral vessels are less sensitive to sympathetic signals and maintain relatively normal caliber, blood flow, and oxygen delivery. Thus, blood is shunted away from the skin to the vital organs such as the heart and the brain.

Fat embolism is common in fracture

Explanation -
Amniotic fluid embolism is the fifth most common cause of maternal mortality worldwide; it accounts for roughly 10% of maternal deaths in the United States and results in permanent neurologic deficit in as many as 85% of survivors.
Amniotic fluid embolism is an ominous complication of labor and the immediate postpartum period.Mortality rate is up to 80%.
The onset is characterized by sudden severe dyspnea, cyanosis, and shock, followed by neurologic impairment ranging from headache to seizures and coma, and by DIC. 

Phlebothrombosis is thrombosis of vein with no inflammation. It mainly occurs in calf vein. Usually produces few sign & symptoms.

Explanation :
Target organ damage by hypertension -
Blood vessels
Central nervous system 
Retina
Heart
Kidneys

White infarct occurs in spleen

In case of Distributive shock there is peripheral vasodilation & pooling of blood in periphery.

Explanation :
Cardinal signs of right heart failure  -
Raised JVP
Ascities
Pitting oedema
Hepatomegaly

Cardinal signs of left heart failure :
Bilateral basal crepitation
Gallop rhythm
Pulsus alternans
Orthopnea

Reference: Davidson 23rd , Page : 505

Explanation :
In progressive phase of shock -
Persistent oxygen deficit leads to intracellular aerobic respiration is replaced by anaerobic glycolysis with excessive production of lactic acid. The resultant metabolic lactic acidosis lowers the tissue pH, which blunts the vasomotor response; arterioles dilate, and blood begins to pool in the microcirculation.
Peripheral pooling not only worsens the cardiac output but also puts endothelial cells at risk for the development of anoxic injury with subsequent DIC.
With widespread tissue hypoxia, vital organs are affected and begin to fail.

[Robbins 9th 123]

Von Willebrand factor is synthesised by endothelial cells