Dr. Zachow - 12/14 Flashcards
WHat are some possible area of damage due to RAAS?
LVH - leads to increased wall stress and O2 demand. Will have reduced ejection fraction.
Carotid Stenosis
Kidney Damage
What drugs can you use to manage HTN?
Beta Blockers Alpha2 agonists Alpha1 antagonists HCTZ (diuretic) ACE inhibitors Calcium channel blockers ARB Aldosterone antagonists
Match the drug name with the type of drug it is:
Losartan, HCTZ, amlodipine, verapamil, atenolol, enalapril
Losartan - ARB (angiotensin receptor blocker)
HCTZ - diuretic (thiazides)
Amlodipine - calcium channel antagonist
Verapamil - Ca2+ antagonists
Atenolol - beta blocker
Enalapril - ACE inhibitor (impede production of angiotensin II)
Secondary Hypertension
USually involved with some sort of pathological disorder that can usually be identified and potentially fixed. Often brought on due to renal disease, endocrine disease, drugs, meds, alcohol. Even after taking 3 meds the HTN will not subside. Abrupt onset.
TPR =
TPR = (Pa-Pv)/Qt
Qt is total flow
At what point is there the greatest drop in pressure?
Across the arterioles. This is because they are full of smooth muscle so they can expand.
What part of flow is considered capacitance? Exchange? Resistance?
Resistance: aorta –> artery –> arteriole –>
Exchange: Capillary
Capacitance: Venules –> Veins –> Vena cava
WHat two things can happen to Ensure that flow through the capillaries is constant and with a norma Pressure?
deltaP = Q x R
It change change pressure in the arteriole or resistance in the arteriole by changing sphincteric diameter.
Pcap
Pif
PiCap
PiIf
Pcap - pressure of the blood pushing out onto the walls of the capillaries.
Pif = small amount of pressure pushing onto the wall of the capillary trying to come inside.
PiCap = oncotic pressure of the plasma in the capillary that is attracted to the albumin in the capillary, causing it to stay in the capillary.
PiIf = oncotic pressure in the interstitium that wants to bring water out of the capillary
How is edema caused?
1) increased arterial pressure
2) increased capillary permeability
3) Decreased venous return
4) compromised lymphatic function
Mechanisms of action regulating vasodilation in VSM
1) epinephrine (low concentration)
2) vasodilatory factors - CO2, H+, lactic acid, histamine, thrombin, and prostaglandins.
- Basically the target is cGMP an PKG. All of the previous things hit their respective receptors, which activate eNOS (epithelial nitric oxide synthase), and eventually makes PKG and cGMP. PKG inactivated type L calcium channels, which will impede inward calcium movement So that there is relaxation. PKG also activates SERCA, which sequesters calcium and causes relaxation.
Mechanisms promoting vasoconstriction in VSM
PKC is the key here. Epinephrine in high concentrations, will eventually, downstream, activate PKC. Once PKC is activated it will activate type L calcium channels and cause increased calcium flow and therefore vasoconstriction. It will also inactivate SERCA through aracodonic acid and PGF2alpha so that there will be no sequestration of calcium and therefore there will be vasoconstriction.
Explain what occurs in a sick left heart (systolic heart failure)
In a sick left heart the left ventricle will be unable to pump out proper amounts of blood. Because of this, the ejection fraction will increase and there will be more blood left in the left ventricle. This will cause an increase in pressure, which will cause an increase in pressure in the left atrium. This will then cause an increase in pressure in the pulmonary system and then the right ventricle will be unable to empty proper and eventually pressure will build up all the way back at the right atrium.
Explain what occurs in right Sick heart
Increased right ventricular pressure will have all. Of the normal. Pathologies that we would expect in addition to hepatic portal hypertension, pulmonary HTN, and jugular vein distention. This is because this is where the IVC, SVC, and pulmonary trun.
When is there greater blood flow to the coronary arteries, diastole or systole?
Diastole, there is also maximal O2 uptake here.