Cases and Team Learning Flashcards
what determines a patients blood pressure?
amount of blood moving into the vessels as well as the resistance to that blood
Stage 1 and Stage 2 BP
Stage 1 hypertension. Stage 1 hypertension is a systolic pressure ranging from 130 to 139 mm Hg or a diastolic pressure ranging from 80 to 89 mm Hg.
Stage 2 hypertension. More severe hypertension, stage 2 hypertension is a systolic pressure of 140 mm Hg or higher or a diastolic pressure of 90 mm Hg or higher.
long term effect on left ventricle due to high blood pressure
increased thickness of muscle, eventual limit of oxygen being able to perfuse that thickened muscle
2 commonly used drugs to treat HBP
Lisinopril and HCTZ
Lisinopril
ACE inhibitor
Side Effects:
1- Cough
• ACE also breaks down of bradykinin and substance P potent
stimulants of cough
• By blocking this enzyme bradykinin and Substance P build up in the
upper respiratory tract causing cough.
HCTZ - hydrochlorothiazide
diuretic, increases reabsorption of sodium in renal tubules
Side Effects:
- dehydration
- hypercalcemia
- increased uric acid reabsorption —> gout
- increase potassium excretion –>hypokalemia (diuretics do this)
immediate homeostatic response to profound hypotension in a trauma patient with active bleeding
The very first response to hypovolemic shock has to be rapid and it is –it is the release of Norepinephrine (NEpi.) and Epinephrine (Epi)
from the adrenal glands and nerves. NEpi. contraction of the
small arterioles especially in the skin and GI tract shunting blood to
the heart and brain this occurs through Alpha 1 receptor stimulation
increase SVR narrow pulse pressure (main effect of
Norepinephrine) Diastolic pressure reflects SVR –Systolic Pressure
SV
• Alpha 1 receptors on the arteriole wall stimulated by
Norepinephrine an alpha 1 agonist causes constriction of the
arteriolar lumen.
Through release of Epinephrine (adrenal medulla) there is also B1
stimulation of the cardiac cells which increase cardiac contractility
The problem is the Volume in the Left Ventricle of the Heart is so
low due to blood loss that Cardiac output does not change as much
as SVR initially until fluid is given
Alpha 1 receptor
• Alpha 1 receptors on the arteriole wall stimulated by
Norepinephrine an alpha 1 agonist causes constriction of the
arteriolar lumen.
Beta 1 receptor
Beta 1 increases cardiac contractility and increases Heart Rate (HR)
modifiable and non modifiable risks for hypertension
modifiable: lifestyle
non modifiable: age, gender, family history
MAP
mean arterial pressure
MAP = CO (HR*SV) * TPR
MAP = 1/3 SBP + 2/3 DBP
MAP = SBP + 2DBP/3
Compare and contrast the basic pathophysiology of Type 1 versus Type 2 Diabetes
Mellitus (DM).
Classically taught Type 1 Diabetes Mellitus (DM) is the result of an autoimmune destruction of
the beta cells of the pancreas. These cells produce Insulin and their complete destruction
results in complete absence of Insulin. It is usually seen at a younger age group and the
treatment is Insulin. These patients are said to be sensitive to Insulin. Give these patients a
normal amount of Insulin and they will be well controlled. In the Emergency Room, when they
present with very high Glucose levels (500-600mg dL), often they need a small amount of
Insulin to get their serum levels of Glucose back to normal.
Type 2 DM is an acquired disease in which Insulin is produced by the beta cells but there is
Insulin Insensitivity. Typically, in these patients, Insulin levels are very high but the muscle,
adipose cells, and liver do not respond to the normal metabolic control exerted by Insulin. It is
frequently accompanied by obesity.
(Although a number of investigations are showing that Type 1 DM may have similar properties
to Type 2 it is much better for teaching purposes to learn the accepted concepts and then
exceptions can be learned )
Compare and contrast the difference in treatment between Type 1 and Type 2 DM
Treatment Type 2 DM
1- Life Style changes are key, whether or not medical treatment is needed. Exercise
weight loss healthy diet if possible make treatment much easier.
Metformin is the most common medication used to treat Type 2 DM. It is taken as a pill twice a
day and is concentrated in the liver (mitochondria) where Gluconeogenesis is decreased and
Glycogen Production increased. Both of these affects lower Glucose level in the serum.
In addition, Metformin increases uptake of glucose by the muscle and adipose cells.
Mechanism of action- inhibits respiratory chain of the mitochondria of the liver and this reduces
energy available for Gluconeogenesis
Metformin does have an effect on Lipid Metabolism however not to the same affect it has on
glucose metabolism and frequently a second medication is needed to control the
Hypertriglyceridemia, high VLDL low HDL and LDL that is smaller and denser and more
atheromatous than normal LDL.
Metformin increases uptake of VLDL into certain adipose tissue
Minor complication GI upset diarrhea cramping
Major complication Lactic Acidosis seen in patients with renal failure and also liver disease
Inhibits Gluconeogenesis in the liver so lactate pyruvate glucose
Lactate in the muscle is transported to the liver where gluconeogenesis converts the lactate to
glucose -this is inhibited by Metformin and lactate builds up especially in Renal Failure where it
is a contraindication to use Metformin.
Treatment of Type 1 DM
Classically Insulin has been used to treat Type 1 DM and it is also not infrequently used in
patients with Type 2 DM where oral medication is not controlling the glucose level adequately.
There are long acting Insulins which give a nice level for 24 hours and also rapid acting Insulin
which has a rapid onset and short half-life and everything in between. The key is to keep a
constant level of glucose avoiding peaks and troughs.
Insulin Pumps and Pancreatic Islet transplant has also found success in treating Type 1 DM
Briefly explain the relationship between Insulin Resistance and Triglyceride (TG) and
VLDL elevation in the serum.
Insensitivity to Insulin results in increased production of VLDL (rich in Triglycerides) by the liver
secreted into the blood. The abnormal fat metabolism seen in patients with Type 2 DM is due
to in large part to elevated levels of Triglycerides. VLDL (very low-density lipoprotein) is
produced by the liver in increased amounts in the absence of Insulin or in Type 2 DM where
Insulin Insensitivity is present. VLDL is very rich in Triglycerides. Insensitivity to Insulin results in increased production of VLDL (rich in Triglycerides) by the liver
secreted into the blood. The abnormal fat metabolism seen in patients with Type 2 DM is due
to in large part to elevated levels of Triglycerides. VLDL (very low-density lipoprotein) is
produced by the liver in increased amounts in the absence of Insulin or in Type 2 DM where
Insulin Insensitivity is present. VLDL is very rich in Triglycerides.
Briefly explain the relationship between Insulin Resistance and HDL and LDL
metabolism
The high level of VLDL
stimulates transfer of Triglycerides to HDL (the good cholesterol). This change decreases the
half-life of HDL and increases its metabolism thus decreasing the concentration of HDL.
HDL acts to transport cholesterol deposited in the sub-intimal layer of arteries to the liver where
it is secreted in the bile thus having a protecting effect against atherosclerosisLDL the bad cholesterol is made worst due to the high levels of Triglycerides. Like with HDL –
the LDL accepts Triglycerides and give up cholesterol esters however this exchange like in the
case of HDL is bad. The new LDL is a smaller, denser LDL. It is very atherogenic (it
produces atherosclerosis). Know this for your exams and step1 really important for
clinical medicine. The typical lipid pattern for Type 2 DM is Elevated Triglycerides,
Elevated VLDL (Triglyceride rich), Decrease HDL and this is key the LDL concentration is
often normal but this LDL is smaller and more denser and is very atherogenic - it is a marker
for Insulin Resistance and for increased risk of atherosclerosis.
LDL the bad cholesterol is made worst due to the high levels of Triglycerides. Like with HDL –
the LDL accepts Triglycerides and give up cholesterol esters however this exchange like in the
case of HDL is bad. The new LDL is a smaller, denser LDL. It is very atherogenic (it
produces atherosclerosis). Know this for your exams and step1 really important for
clinical medicine. The typical lipid pattern for Type 2 DM is Elevated Triglycerides,
Elevated VLDL (Triglyceride rich), Decrease HDL and this is key the LDL concentration is
often normal but this LDL is smaller and more denser and is very atherogenic - it is a marker
for Insulin Resistance and for increased risk of atherosclerosis.
