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70 Cards in this Set

  • Front
  • Back
what is the target organ of damage for HTN?
the kidney i the target organ for hypertension.
what disease of the kidneys is associated with HTN?
benign nephrosclerosis is due to hyaline arteriosclerosis of cortical vessels
what type of lab findings must a patient have to be diagnosed with DM?
Glucose > 126 mg/dL on two occasions or random reading of > 200 with symptoms of DM
how do you calculate an LDL?
Cholesterol - HDL - Trig/5
what is significant about African Americans white blood cell count?
normal blood cell count usually has a low WBC because African Americans have a greater marginating pool than circulating pool
T/F
Systolic blood pressure reflects the stroke volume, while the diastolic pressure correlates with the tone of peripheral resistance arterioles and the amount of blood remaining in the arteries while the heart is filled up in diastole
True
T/F
increased vasoconstriction of the peripheral resistance arterioles will increase the diastolic pressure while dilation will decrease the diastolic pressure
True
T/F
the diagnosis of essential HTN requires three or more readings taken during one visit to the doctors office
False
three or more readings must be taken on two additional visits to a doctors office, or follow JNC-7 recommendations
T/F
Sphygomomanometer cuffs that are too short or too narrow will give a falsely high reading
True
T/F
Blood pressure = CO x TPR
true
Describe what is seen in Benign nephrosclerosis.
BNS is the kidney disease associated with essential HTN
there is symmetrical atrophy of both kidneys and a cobblestone appearing cortex, much like the surface of a football.
what is BNS due to?
BNS is due to the small vessel disease of HTN, mainly hyaline arteriolosclerosis. Increased pressure in the lumen of the small vessels insudates plasma proteins into the wall of the vessels giving them hyalinized appearance.
Glomerular and tubular atrophy eventually occur, primarily in the cortex giving rise to the cobbelstone appearance of the kidneys. The GFR is normal or slightly decreased
Mild proteinuria is usually present
IF HTN is left uncontrolled what can BNS progress to?
Chronic Renal Failure
T/F
control of blood pressure has its greatest effect on decreasing risk of developing an acute MI.
False
It has its greatest reduction in reducing risk of stroke mortality
how many of the different types of strokes are directly related to HTN?
three
intracerebral hemorrhage
berry aneurysms
lacunar strokes
T/F
the left ventricular hypertrophy in this patient (case 1) is directly attributed to an increase in preload in the Left ventricle.
False
LVH is of the concentric type and is due to contraction of the ventricle against an increased afterload in the peripheral resistance arterioles
if your patient had problems controlling her blood pressure, advanced HTN retinophathy, an epigastric bruit, and evidence of atherosclerotic disease involving her abdominal aorta and peripheral arteries, you would suspect non-compliance as the reason for uncontrolled HTN.
False
all of these symptoms related to renovascular HTN due to reduced blood flow to the renal artery
The most effective lifestyle modification for reducing this patients blood pressure is a low sodium diet.
False
weight reduction is the most effective way of lowering blood pressure
T/F
A laterally displaced PMI indicates pulmonary HTN
False
it is due to LVH which may be related to essential HTN
Target organs that can be affected in a patient with HTN include the heart, kidneys, retina, and peripheral vascular system
True
T/F
if your patient had two serum glucose readings of > 120 mg/dL and a family history of diabetes, the diagnosis of type 2 DM has been confirmed in this patient.
False
Fasting glucose must be > 126 mg/dL or a 2 hour post prandial > 200 mg/dL with symptoms of polyuria, polydipsia, weight loss, or a Hgb A1C > 6.5%
T/F
IN an African American patient does a decrease leukocyte count render they susceptible to infection
False
African Americans have an increased marginating pool in the peripheral blood owing to increased adhesions. This does not affect their response to infection
T/F
obesity, HTN, type 2 DM, and hyperlipidemia are characteristic features of metabolic syndrome
True
hyperinsulinism due to insulin resistance is a key feature to this disease
T/F
By lowering the cutoff for the fasting glucose from 140 mg/dL to 126 mg/dL to diagnose DM, this increases the predictive value of a positive test
False
lowering the value increases the sensitivity and the predictive value of a negative test result.
Specificity and the predictive value of a positive test decrease
T/F
IN white coat syndrome the patient has normal readings at home and increased readings when visiting the doctor's office as long as the diastolic is not > 105 mm Hg
True
T/F
Tension headaches are described as tight pressing band often encircling the head
they are often associated with moderate tenderness and pain with compression of the scalp and may be aggravated by light or sound. they are not usually accompanied by nausea.
True
T/F
Grade I hypertensive retinopathy is associated with arteriolar narrowing
True
Mild AV nicking is also observed
An S4 heart sound can be due to blood entering a volume overloaded ventricle or a concentrically hypertrophied ventricle
True
it is caused by problems with ventricular filling following a vigorous atrial contraction.
This occurs with concentric hypertrophy of the ventricle or with volume overloaded ventricles
T/F
when the sum of the millimeter negative deflection of the S in v1 plus the millimeters positive defelction of R in V5 is more than 35 > LVH is present
TRUE
the increased LV thickness is reflected in large QRS duration
The QRS complexes are exaggerated in both height and depth
NOrmally the S wave in lead V1 is deep, however in LVH, the S wave is even deeper in Lead V1 (negative defleciton) since the depolarization is going away from lead V1 and towards the more lateral leads V5 which represents LV.
The R wave in lead V5 shows a more pronounced positive deflection
T/F
sings of benign nephrosclerosis is mild proteinuria, hyaline cast, and a slight increase in BUN and creatinine
False
Benign nephrosclerosis is due to hyaline arteriosclerosis of the afferent and efferent arterioles resulting in tubular atrophy and glomerular scleriosis. this may eventuate in chronic renal failure
T/F
You place a patient on an ACE-inhibitor and a thiazide diuretic for treatment of HTN. If the patient develops a chronic cough on this combined medication, she should be switched to an angiotensin receptor inhibitor
True
ACE in addition to converting ATI into ATII degrades bradykinin. ACE inhibitors therefore cause an increase in bradykinin, which is responsible for the chronic cough.
Giving ATII receptor blocker circumvents this problem
T/F
elevated glucose in a patient that has had an MI is due to the release of catecholamines after the AMI and the breakdown of glycogen in the liver
True
what increases gluconeogenesis after an acute MI?
release of catecholamines
breakdown of glycogen in the liver
release of cortisol
insulin release is transiently reduced due to reduced pancreatic blood flow.
a patient had a random serum glucose level drawn that was <200 mg/dL. Does this define DM?
NO
what is an elevated CK-MB after an AMI due to?
myocardial necrosis and release of enzymes into the blood
what is the absolute neutrophilic leukocytosis due to after an acute MI?
increased leukocyte count and increase in segmented and band neutrophils is due to catecholamine release from pain with a subsequent release in activation of neutrophil adhesion molecules causing displacement of the marginating poll into the circulating pool
what type of inflammation is an AMI an example of?
acute inflammation
what is a left-sided shifted smear?
an increase in band neutrophils > 10% in the peripheral blood
what is BNP used to measure?
BNP is a useful test in the evaluation of patients with dyspnea, useful in ruling out HF in symptomatic patients.
where does BNP come from?
BNP is released from the ventricles and elevation related to patients symptomatic LV dysfunction.
Any value > 400 mg/dL is a dyspneic patient is consistent with congestive heart failure.
why is CK-MB index abnormal in a patient with an AMI?
CK-MB is abnormal because it peaks in 24 hours and disappears by 3 days in patients that have had an acute MI due to necrosis of cardiac myocytes
what is a Troponin?
Troponin-I: due to myocardial necrosis
normally are involved in calcium dependent muscle contraction
Gold standard for diagnosing an AMI because they last longer than CK-MB
downside to Troponin is that they cannot be used for diagnosing reinfarction since they remain in the blood for us to 10 days
what is the reappearance of CK-MB after 3 days post AMI represent?
reinfarction
T/F
Necrosis of skeletal muscle does not falsely elevated the concentration of troponin-I
True
When do you not draw blood gases?
ABG's from a noncompressible vascular structure are contraindicated
T/F
Q waves are the initial manifestation on an ECG of a Q wave type of AMI.
False
the order is:
1. peaked T waves: area of ischemia
2. ST segment elevation: area of injury, loss of normal myocardial cell membrane ion pumps
3. Symmetric T wave inversion : area of ischemia
4. Q wave: area of infarction with cell death
T/F
you would expect venoconstrition and arteriolar vasodilation to decrease cardiac output
False
venconstriction increases the venous pressure with concomitant increases in venous return to the right heart > increases cardiac output
Arteriolar vasodilation decreases the peripheral resistance which increases the return of blood to the right heart thus increasing cardiac output and potential for high output failure
T/F
you would expect venodilation and loop diuretics to reduce preload in the left ventricle
True
Venodilation decreases venous return to the heart > decreasing preload
Loop diuretics cause diuresis of water and salt with a reduction in the ECF volume > decreasing preload
They also have direct venodilating effects
T/F
the heart is dependent on an interaction between the parasympathetic and sympathetic nervous system
True
Vagus nerve: parasympathetic system reduces the heart rate by increasing the release of acetylcholine in the SA node
Thyroxine increases the synthesis of b-receptors in the heart so that the sympathetic system can interact with these receptors and increase the heart rate
what is norepinephrines effect on the heart?
NE is directly released from the sympathetic nerves in the cardiac muscle while EP is released from the adrenal medulla and is delivered to the heart muscle by circulation
How does fever control heart rate?
Fever controls heart rate via direct action on the SA node cells
T/F
increasing the heart rate decrease the duration of diastole allowing less time for filling of the ventricles in coronary arteries
True
when heart rate approximately 180 bpm diastole is too short for adequate filling of the ventricles > decreases preload > decreasing stroke volume and cardiac output
Since the coronary arteries fill during diastole they are under filled
T/F
The change in cardiac output that occurs with a heart rate > 180 bpm is MOST closely related to decrease in stroke volume
True
the cardiac output is equal to the stroke volume times the heart rate
as HR increases the CO increases until HR is above 180 bpm
this most closely relates to a decrease in SV due to shortening time for diastole, or the time for the ventricles to fill
The less the LVEDV the less the SV
Will a patient that has orthopnea and GERD have to sit up in bed at night to get the symtoms to subside?
YES
patient with orthopnea is due to L-sided heart failure. Sitting up reduces venous return to the right heart
Raising the head of the bed is a good non-pharmacological treatment for GERD, because of the effect of gravity, reduces GERD
T/F
Dyspnea is a sign
Tachypnea is a symptom
False
Dyspnea is a symptom: what the patient complains about
Tachypnea: is a sign since the clinician must count the number of respiratoins
T/F
long history of nocturnal cough in a patient that has acute MI and GERD, the nocturnal cough is due to L-sided heart failure from ischemic heart disease.
False
GERD with reflux of acid into esophagus, trachea, and mouth when lying flat at night most likely cause these symptoms
History of water brash, hoarse throat can be due to acid reflux at night.
what is GERD a consequence of?
GERD is due to a relaxed lower esophageal sphincter related to fatty foods, coffee, alcohol, and smoking, etc.
what is a fever due to when a patient has pulmonary edema associated with AMI.
The fever is due to necrosis associated with myocardial infarction and the release of pyrogens from neutrophils
T/F
a waist to hip ratio of > 1.0 is a risk factor for coronary artery disease
True
an even greater indicator is increased visceral fat best ascertained with an MRI
T/F
Diaphoresis refers to the severe chest discomfort a patient feels
False
Diaphoresis refers to sweating that the patient experiences
T/F
The absence of neck vein distention, heptomegaly, dependent pitting edema in a patient indicates that right sided heart failure is NOT present
TRUE
T/F
a pericardial friction rub in the first week of an acute MI is called Dressler's syndrome and is due to an autoimmune reaction against pericardial tissue
FALSE
Dressler's syndrome occurs after 6 weeks. Since it requires time to develop the autoantibodies against the pericardial tissue
A pericarditis in the first week is due to a transmural infarction with increased vessel permeability causing a fibrinous pericarditis
T/F
Mitral insufficiency is secondary damage to the valve incurred by an acute MI.
False
it was due to stretching of the MV ring by the excess volume of blood in the LV.
Valves are avascular
T/F
Kerley B lines are linear lines representing fluid in the interlobar septa that are perpendicular to the pleura in the lower lobes
True
T/F
Hyperglycemia in any patient indicates DM
False
Must do proper lab work-up to diagnose DM
in patients with AMI > due to glycogenolytic effect of catecholamines and the glucogenic effect of cortisol hence it is self-limited
T/F
The mild increased anion gap metabolic acidosis in an AMI patient is due to lactic acidosis from an increase in anaerobic glycolysis plus tissue hypoxia related to poor gas exchange in the lungs from pulmonary edema
True
T/F
the increased serum BUN/Cr ration > 15 indicates the progression of disease into acute renal failure due to low cardiac output
False
It is prerenal azotemia due to decreased cardiac output
describe renal azotemia
BUN: Cr ratio is < 15:1
it should be underscored that most common cause of renal azotemia is prerenal azotemia because of blood flow is decreased in portions of the nephron most susceptible to hypoxia are at risk for undergoing coagulation necrosis
the key finding in ischemic acute tubular necrosis
T/F
Troponin I differs from CK-MB isoenzymes in that it remains elevated beyond 3 days in an AMI and can identify reinfarction
False
troponin does remain elevated after 3 days
Troponin cannot diagnose a reinfarction
Reinfarction is defined as reappearance of CK-MB after 3 days
A specific gravity of 1.035 of urine indicates that a patient is concentrating their urine and ADH is present
True
ADH is present for two reasons:
1. the cardiac output is decreased
2. Pain is a stimulus for ADH release
3. Presence of ADH is responsible for final concentration of urine