What is the most common cause of hypovolemic shock? What are other related causes?
Acute hemorrhage is most common cause; others include: dehydration from vomiting or diarrhea, burns, pancreatitis
Elderly and babies are most at risk.
What is disruptive shock caused by? Is there a loss of fluid from the body?
Inadequate circulation due to increased vasocilation. No actual loss of fluid.
What is another term for Disruptive Shock? What effect does disruptive shock have on the venous system?
Anaphylaxis. Due to vasodilation and increased perm, the venous system loses sympathetic tone so the blood pools in the venous system and is not circulated back to the heart. The body sees this as a loss of volume, even though it has not been lost from the body.
What does disruptive/anaphylaxis cause?
profound hypotension due to the lack of circulating blood
What is the overall cause of cardiogenic shock? What is the most common cause of cardiogenic shock?
Overall cause: pump failure
Most common: MI
What is a common result of cardiogenic shock? Explain.
Pulmonary edema because the heart cannot pump blood froward and it gets backed up in the pulmonary vein, then it seeps out into the alveoli.
What are common causes of cardiogenic shock? What is the most common cause?
Most common cause = MI
Other causes include vavlualar heart disease, ventricular rupture, congenital heart defects, papillary muscle rupture and cardiomyopathy
Describe Obstructive Shock and provide an example.
Obstructive shock occurs when something prevents the heart from pumping out, such as right ventricle failure due to a pulmonary embolism. The heart cannot fill up with blood.
Describe the overall consequence of shock.
Decreased cardiac output leading to ischemia leading to hypoxia leading to cell injury and death
What are the three stages of shock and which one is not reversable?
Compensatory, Progressive, and Refractory. Refractory is not reversable, it will end in death.
What are the two main goals of the compensatory stage of shock?
Maintenance of cardiovascular function and restoration of vascular volume
What happens to heart rate, cardiac contractility, and blood flow during the compensatory stage?
Heart rate and cardiac contractility increase to compensate for the loss of volume. Blood flow is shunted from the periphery to the organs.
What happens to ADH, the hypothalmus, and aldosterone in the compensatory stage of shock? What are the effects on the GI tract?
ADH is released to signal reabsorption of water
Hypothalamus tells the patient he is thirsty
Aldosterone signals sodium retention
The GI tract will slow = oliguria
During the Progressive stage of shock, do the vessles constric or dilate? What happens to the blood flow to the organs and what is the end result?
During the progressive stage of shock, there is vasodilation and a reduction of blood flow to the organs and tissue → infarction →cell death/necrosis.
Increased capillary permeability and sluggish blood flow during progressive shock cause an increase in anaerobic metabolism. What is the end product of this?
Lactic acidosis in blood
If perfusion is restored, is the refractory stage of shock reversable?
No, yo ass gunna die.
What is the definition of atherosclerosis?
Progressive narrowing and hardening of arteries.
Describe some soft risk factors for atherosclerosis. What are soft risk factors?
Soft risk factors are what we are almost sure contribute to risk. They inlude increased age, obesity and lack of exercise. Remember: "Old fat people who don't exercise are soft.)
What are hard positive risk factors for atherosclerosis? Describe some.
We are sure hard positive risk factors contribute to atherosclerosis. Examples include: Males are more affected until 65 then it evens out. Females are more affected after menopause than before, smoking, hyperlipidemia, diabetes, and hypertension.
Describe the values for hyperlipidemia.
Total Cholesterol = 200
LDL = 100
HDL = 50
Total triglycerides = 150
Increased plasma lipoprotein levels
List some novel factors for atherosclerosis.
High serum homocysteine levels, elevated C-reactive proteins (serium marker for systemic inflammation and a predisposition to thrombus formation), and infectious agents like herpes that may increase inflammation response.
Describe the pathogenesis of the development of a fatty streak.
Injury to endothelial lining of vessel wall from something like hypertension or smoking → monosites enter intima through injury and change to macrophages → LDLs enter intima and get oxidized →Lymphocytes call smooth muscle cells from media layer into intima and the smooth muscle cells and macrophages eat the oxidized LDLs and become the foam cells that form the fatty streak.
Decribe the pathogenesis of the development of the fibrous plaque in atherosclerosis.
Foam cells and smooth muscles cells call fibroblast that secrete collagen. Smooth muscle cells and collagen for a fibrofatty plaque roof over the fatty streak.
Describe various complications of atherosclerosis.
Narrowing/Calcification of vessels: this causes blockage, downstream gets fucked, plus calcium can cause the fibrous roof over fatty streak to break.
Thrombus formation: if the roof breaks platelets will aggregate and form clot.
Peripheral Emboli: the clot will dislodge, get stuck somewhere and fuck up downstream
Weakening of Vessel Wall: the backup can weaken the wall and cause an emboli
What are the JNC 7 Guidlines values for hypertension?
Normal = 120/80
Prehypertension = 120-139 / 80-89
Stage 1 hypertension = 140-159 / 90-99
Stage 2 hypertension = 160+/100+
What is the hallmark of chronic hypertension?
Total Peripheral Resistance (TPR)
Provide an example of a secondary etiology for hypertension.
Diseases can cause hypertension, the most common is renal disease.
Describe Malignant Hypertension. What is another term for it?
It is characterized by signs/symptoms of Target Organ Disease. If you see signs/symptoms the it is a MEDICAL EMERGENCY. Two people can have the same BP, if one has signs then that is they malignant hypertension. The person who does not show signs does not have malignant hypertension.
What are some clinical manifestations of hypertension?
Can be asymptomatic or symptomatic. Suboccipital pulsing headache that is worse in the AM, dizziness, blurred vision, dyspnea, chest pain, epistaxis (nose bleed) dependent edema
do pear shape or apple shape have more risk for hypertension?
Apple shape, because more visceral fat. Pear shape better, the lower you carry your fat the lower your risk.
What is the definition of a MI?
Death of myocardium due to complete occlutsion from thrombus. The complete occlusion is what separates it from angina.
What are collaterals?
Collaterals are vessels that form on the heart around an occlusiont that keep the heart supplied with some blood.
In relation to an MI, what is "transmural damage"?
The necrosis goes through the entire heart wall.
What does an elevated ST segment tell us?
The elevated ST segment, sometimes seen as a tombstone, suggest actue cell injury or ischemia. It suggest ischemic injury is ongoing and efforts to increase perfusion or decrease O2 demand may help.
What does an inverted T wave or deep/wide Q wave indicated?
Necrotic tissue that is no longer electrically active.
What side is the mitral (bicuspid) valve on?
What is ANP and what is its function?
Atrial Naturetic Peptide; secreted as the heart stretches and normally promotes the excretion of sodium. Should cause vasodilation because the sodium excretion leadsd to decreased volume.