Cps: Cardiovascular Exam

Front 1

what is the target organ of damage for HTN?

Back 1

the kidney i the target organ for hypertension.

Front 2

what disease of the kidneys is associated with HTN?

Back 2

benign nephrosclerosis is due to hyaline arteriosclerosis of cortical vessels

Front 3

what type of lab findings must a patient have to be diagnosed with DM?

Back 3

Glucose > 126 mg/dL on two occasions or random reading of > 200 with symptoms of DM

Front 4

how do you calculate an LDL?

Back 4

Cholesterol - HDL - Trig/5

Front 5

what is significant about African Americans white blood cell count?

Back 5

normal blood cell count usually has a low WBC because African Americans have a greater marginating pool than circulating pool

Front 6

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

Back 6

True

Front 7

T/F
increased vasoconstriction of the peripheral resistance arterioles will increase the diastolic pressure while dilation will decrease the diastolic pressure

Back 7

True

Front 8

T/F
the diagnosis of essential HTN requires three or more readings taken during one visit to the doctors office

Back 8

False
three or more readings must be taken on two additional visits to a doctors office, or follow JNC-7 recommendations

Front 9

T/F
Sphygomomanometer cuffs that are too short or too narrow will give a falsely high reading

Back 9

True

Front 10

T/F
Blood pressure = CO x TPR

Back 10

true

Front 11

Describe what is seen in Benign nephrosclerosis.

Back 11

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.

Front 12

what is BNS due to?

Back 12

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

Front 13

IF HTN is left uncontrolled what can BNS progress to?

Back 13

Chronic Renal Failure

Front 14

T/F
control of blood pressure has its greatest effect on decreasing risk of developing an acute MI.

Back 14

False
It has its greatest reduction in reducing risk of stroke mortality

Front 15

how many of the different types of strokes are directly related to HTN?

Back 15

three
intracerebral hemorrhage
berry aneurysms
lacunar strokes

Front 16

T/F
the left ventricular hypertrophy in this patient (case 1) is directly attributed to an increase in preload in the Left ventricle.

Back 16

False
LVH is of the concentric type and is due to contraction of the ventricle against an increased afterload in the peripheral resistance arterioles

Front 17

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.

Back 17

False
all of these symptoms related to renovascular HTN due to reduced blood flow to the renal artery

Front 18

The most effective lifestyle modification for reducing this patients blood pressure is a low sodium diet.

Back 18

False
weight reduction is the most effective way of lowering blood pressure

Front 19

T/F
A laterally displaced PMI indicates pulmonary HTN

Back 19

False
it is due to LVH which may be related to essential HTN

Front 20

Target organs that can be affected in a patient with HTN include the heart, kidneys, retina, and peripheral vascular system

Back 20

True

Front 21

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.

Back 21

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%

Front 22

T/F
IN an African American patient does a decrease leukocyte count render they susceptible to infection

Back 22

False
African Americans have an increased marginating pool in the peripheral blood owing to increased adhesions. This does not affect their response to infection

Front 23

T/F
obesity, HTN, type 2 DM, and hyperlipidemia are characteristic features of metabolic syndrome

Back 23

True
hyperinsulinism due to insulin resistance is a key feature to this disease

Front 24

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

Back 24

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

Front 25

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

Back 25

True

Front 26

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.

Back 26

True

Front 27

T/F
Grade I hypertensive retinopathy is associated with arteriolar narrowing

Back 27

True
Mild AV nicking is also observed

Front 28

An S4 heart sound can be due to blood entering a volume overloaded ventricle or a concentrically hypertrophied ventricle

Back 28

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

Front 29

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

Back 29

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

Front 30

T/F
sings of benign nephrosclerosis is mild proteinuria, hyaline cast, and a slight increase in BUN and creatinine

Back 30

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

Front 31

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

Back 31

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

Front 32

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

Back 32

True

Front 33

what increases gluconeogenesis after an acute MI?

Back 33

release of catecholamines
breakdown of glycogen in the liver
release of cortisol
insulin release is transiently reduced due to reduced pancreatic blood flow.

Front 34

a patient had a random serum glucose level drawn that was <200 mg/dL. Does this define DM?

Back 34

NO

Front 35

what is an elevated CK-MB after an AMI due to?

Back 35

myocardial necrosis and release of enzymes into the blood

Front 36

what is the absolute neutrophilic leukocytosis due to after an acute MI?

Back 36

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

Front 37

what type of inflammation is an AMI an example of?

Back 37

acute inflammation

Front 38

what is a left-sided shifted smear?

Back 38

an increase in band neutrophils > 10% in the peripheral blood

Front 39

what is BNP used to measure?

Back 39

BNP is a useful test in the evaluation of patients with dyspnea, useful in ruling out HF in symptomatic patients.

Front 40

where does BNP come from?

Back 40

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.

Front 41

why is CK-MB index abnormal in a patient with an AMI?

Back 41

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

Front 42

what is a Troponin?

Back 42

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

Front 43

what is the reappearance of CK-MB after 3 days post AMI represent?

Back 43

reinfarction

Front 44

T/F
Necrosis of skeletal muscle does not falsely elevated the concentration of troponin-I

Back 44

True

Front 45

When do you not draw blood gases?

Back 45

ABG's from a noncompressible vascular structure are contraindicated

Front 46

T/F
Q waves are the initial manifestation on an ECG of a Q wave type of AMI.

Back 46

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

Front 47

T/F
you would expect venoconstrition and arteriolar vasodilation to decrease cardiac output

Back 47

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

Front 48

T/F
you would expect venodilation and loop diuretics to reduce preload in the left ventricle

Back 48

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

Front 49

T/F
the heart is dependent on an interaction between the parasympathetic and sympathetic nervous system

Back 49

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

Front 50

what is norepinephrines effect on the heart?

Back 50

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

Front 51

How does fever control heart rate?

Back 51

Fever controls heart rate via direct action on the SA node cells

Front 52

T/F
increasing the heart rate decrease the duration of diastole allowing less time for filling of the ventricles in coronary arteries

Back 52

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

Front 53

T/F
The change in cardiac output that occurs with a heart rate > 180 bpm is MOST closely related to decrease in stroke volume

Back 53

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

Front 54

Will a patient that has orthopnea and GERD have to sit up in bed at night to get the symtoms to subside?

Back 54

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

Front 55

T/F
Dyspnea is a sign
Tachypnea is a symptom

Back 55

False
Dyspnea is a symptom: what the patient complains about
Tachypnea: is a sign since the clinician must count the number of respiratoins

Front 56

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.

Back 56

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.

Front 57

what is GERD a consequence of?

Back 57

GERD is due to a relaxed lower esophageal sphincter related to fatty foods, coffee, alcohol, and smoking, etc.

Front 58

what is a fever due to when a patient has pulmonary edema associated with AMI.

Back 58

The fever is due to necrosis associated with myocardial infarction and the release of pyrogens from neutrophils

Front 59

T/F
a waist to hip ratio of > 1.0 is a risk factor for coronary artery disease

Back 59

True
an even greater indicator is increased visceral fat best ascertained with an MRI

Front 60

T/F
Diaphoresis refers to the severe chest discomfort a patient feels

Back 60

False
Diaphoresis refers to sweating that the patient experiences

Front 61

T/F
The absence of neck vein distention, heptomegaly, dependent pitting edema in a patient indicates that right sided heart failure is NOT present

Back 61

TRUE

Front 62

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

Back 62

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

Front 63

T/F
Mitral insufficiency is secondary damage to the valve incurred by an acute MI.

Back 63

False
it was due to stretching of the MV ring by the excess volume of blood in the LV.
Valves are avascular

Front 64

T/F
Kerley B lines are linear lines representing fluid in the interlobar septa that are perpendicular to the pleura in the lower lobes

Back 64

True

Front 65

T/F
Hyperglycemia in any patient indicates DM

Back 65

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

Front 66

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

Back 66

True

Front 67

T/F
the increased serum BUN/Cr ration > 15 indicates the progression of disease into acute renal failure due to low cardiac output

Back 67

False
It is prerenal azotemia due to decreased cardiac output

Front 68

describe renal azotemia

Back 68

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

Front 69

T/F
Troponin I differs from CK-MB isoenzymes in that it remains elevated beyond 3 days in an AMI and can identify reinfarction

Back 69

False
troponin does remain elevated after 3 days
Troponin cannot diagnose a reinfarction
Reinfarction is defined as reappearance of CK-MB after 3 days

Front 70

A specific gravity of 1.035 of urine indicates that a patient is concentrating their urine and ADH is present

Back 70

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