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Internal Medicine > Midterm 1 > Flashcards

Midterm 1 Flashcards

1
Q

History of Chief Complaint

A
  1. Onset
  2. Progression
  3. Quality
  4. Radiation
  5. Severity
  6. Temporal Characteristics
    * Social/Diet/Smoking/Family History*
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2
Q

5 Most Prevalent Conditions in North America

A 
Cancer
Myocardial Infarct
Hypertension
Stroke
Diabetes
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3
Q

Inspection

A
  • Appearance (shen), eyes, body habitus (constitution), deformity, posture (antalgic)
  • Facial expressions
  • Ambulation (movement of patient), Gait
  • Weight
  • Respiration, Voice
  • Tongue
  • Edema/swelling, wounds/bruises
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4
Q

What does HIPPIRONNA stand for?

A
  • History
  • Inspection
  • Palpation
  • Percussion
  • Instrumentation
  • Range of motion
  • Orthopedic testing
  • Neurologic testing
  • Non-organic findings
  • Ancillary studies
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5
Q

Diagnosis should be a fluid procedure incorporating:

A
  1. Information from the patient (interrogation)
  2. Physical examination of the patient (observation/palpation)
  3. Information from medical tests performed on the patient
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6
Q

What does Prognosis mean?

A

Prediction of how a patient’s disease will progress, and whether there is a chance of recovery

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7
Q

What does Natural History of a Diagnosis mean?

A

Refers to the history of the diagnosis, the natural progression of the disease, and how different treatments (or no treatments) effect the outcome of the disease.

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8
Q

What are the 2 definitions of a Diagnosis?

A
  1. “the recognition of a disease or condition by its outward signs and symptoms”
  2. “the analysis of the underlying physiological/biochemical cause(s) of a disease or condition”
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9
Q

Diagnosis Info

A
  • To properly diagnose a patient in western medicine, physicians use clinical reasoning and problem solving skills.
  • Diagnosis is the key element of investigation, as all diagnoses have studied and pre-determined treatment protocols.
  • Patient management is “at arms length”, based on the etiology and prognosis of disease.
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10
Q

How does TCM manage patients concerns?

A

By eliminating any and all elements of an individual’s life that may negatively impact his/her health.

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11
Q

How does Western medicine differ from TCM patient care?

A

Western medicine seems rather cold in comparison, as it treats a patient without regard or compassion for individuality.

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12
Q

How to ask patient history

A
  1. The use of open ended questions allow patient to express the nature of their problem.
  2. Direct questions are used to elaborate on specific symptoms/signs and complaints.
  3. Important/relevant facts are isolated to aid in forming an initial concept of the problem.
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13
Q

What and how to palpate?

A
  • Evaluate the patient for swelling/edema, nodules, sensory deficits, skin temperature, pulses, etc.
  • Abdominal pulse assessment for lateral expansion (aortic aneurysm)
  • Painless nodules in axilla and tail end of breast (carcinoma of breast tissue)
  • Palpation beyond region of complaint to determine pain referral patterns.
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14
Q

Why use Percussion?

A
  • Used to assess thoracic cage, abdomen or other peripheral structures for pathology.
  • Percussion can assess for the presence of fracture or swollen mesenchyme as in delineating or outlining the size of the organs.

•Mesenchyme: mesodermal tissues that differentiate into connective tissue, bone, cartilage, smooth muscle, and circulatory and lymphatic systems.

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15
Q

Types of Instrumentation used

A

•Objective recordings used to quantify tissue deficits.

  • Sphygmomanometer (BP)
  • Stethoscope
  • ECG/EKG
  • EEG
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16
Q

What does ROM mean and what does it stand for?

A

Range of Motion

Relative term describing the motion in an affected body region.
•May be active (AROM) or passive (PROM)
•Numerical data can be ascertained using an inlcinometer (angle), goniometer, or by eye.

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17
Q

Whats Active Range of Motion

A

objective measure of patients ability/willingness to move a body part

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18
Q

What is Passive Range of Motion?

A

amount/type of movement available at a joint complex

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19
Q

What does a Goniometer do?

A

used to measure ROM of bone joints.

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20
Q

What is a Wrist Inclinometer?

A

used to measure forearm pronation and supination.

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21
Q

What are Orthopaedic Tests used for?

A
  • Orthopedic tests are inquiry-strategy tools for obtaining information to resolve your hypothesis.
  • Maneuvers are designed to elicit signs of patient’s problems by duplicating Sx.
  • The tests are not a substitute for thinking, and cannot be used in isolation to determine a diagnosis.
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22
Q

What does Sensitivity mean?

A

•Sensitivity: % of patients with condition who test +ve. Evaluates true +ves.

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23
Q

What is Specificity?

A

Specificity: % of patients without the condition who test -ve. Evaluates true -ves.

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24
Q

What does Relevance mean?

A

Appropriateness of test to formulate a diagnostic impression of hypothesis

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25
Q

How are Clinical Reasoning tests applied?

A

Their based on: 1. Sensitivity

                       2. Specificity
                       3. Relevance
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26
Q

Why is it important deciding which tests to perform?

A

Will help support your hypotheses and will eliminate differential hypotheses

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27
Q

What does a neurological evaluation assess?

A

changes in CNS and PNS.

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28
Q

What is the earliest signs and symptoms of a CNS/PNS pathology?

A

Changes in sensation

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29
Q

Dissociation of sensory modalities often relates to?

A

Segmental spinal cord lesions

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30
Q

General Sensory/Motor deficits in an extremity without pain typically implicates what?

A

Spinal Cord Tract Lesion

  • Can also be caused from ~ example passing out with arm over a chair and waking up from a nerve being pinch, not always a spinal cord lesion!*
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31
Q

What does Anesthesia mean?

A

Loss of Feeling

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32
Q

What does Hypesthesia mean?

A

Diminished Sensation

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33
Q

What does Hyperpathia mean?

A

Increased pain sensation

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34
Q

What does Allodynia mean?

A

Pain from innocuous stimulation

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35
Q

What can a Subjective Paresthesia also be affected by?

A

A patients emotional state ie. Stress

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36
Q

What are Neurology Objective Sensory Signs?

A

Anesthesia
Hypesthesia
Hyperpathnia
Allodynia

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37
Q

What does Objective mean?

A

Symptoms that can be measured

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38
Q

Non Organic Findings

A
  • A series of orthopedic tests have been designed to detect malingering (faking injury) by patients.
  • Psychological factors markedly affect the way people express and experience pain.
  • Keep observations as facts. Do not tag a patient as “a depressed patient” or a “malingerer”.
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39
Q

What is an Ancillary Study?

A
  • Other evaluations, aside from those aforementioned, that a physician may use to formulate an initial impression.
  • These other studies could also be used to solidify a list of differential diagnoses.
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40
Q

Diagnostic Decisions

A
  • To properly care for a patient, you have to know what is wrong.
  • In many cases, all available data may be insufficient to make an affective diagnosis.
  • You must often proceed with your “best guess” of what you are treating.
  • Regenerate your hypothesis and re-formulate exam findings with your chief complaint history and physical examination data.
  • Formulate a list of differential diagnoses (DDx) that could probably account for your patient’s Sx complex. Prioritize list based on prevalence and incidence of Sx causing conditions in your society.
  • From your DDx list, select a working diagnosis (WDx) and select a treatment plan that will allow you to re-assess your decision making in assessing the patient progress.
  • Using the acronym VINDICATES, determine which mode(s) of pathology is underlying your patient’s Sx complex.
  • Assess your WDx for coherency, adequacy and its parsimonious nature. (least complex explanation for condition)
  • The only purely logical verification of your Dx is the patient’s response.
  • In Western Medicine, the alleviating of Sx is proof of accurate Dx.
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41
Q

What does VINDICATES stand for?

A
  • Vascular
  • Inflammatory
  • Neoplasm
  • Degenerative
  • Intoxication
  • Congenital
  • Auto-immune
  • Trauma
  • Endocrinopathy
  • Somatic dysfunction
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42
Q

Charting Intensity Grading

A
  1. Minimal
  2. Slight
  3. Moderate
  4. Marked
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43
Q

What does Minimal Intensity Grading mean?

A

Sn/Sx constitute an annoyance but cause no impairment in the performance of a particular activity.

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44
Q

What does Slight Intensity Grading mean?

A

Sn/Sx can be tolerated but would cause some impairment in performance of an activity that precipitates the Sn/Sx.

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45
Q

What does Moderate Intensity Grading mean?

A

Sn/Sx would cause marked impairment in the performance of an activity that precipitates the Sn/Sx.

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46
Q

What does Marked Intensity Grading mean?

A

Sn/Sx preclude any activity that precipitates the Sn/Sx.

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47
Q

4 Types of Frequency Grading

A
  1. Intermittent
  2. Occasional
  3. Frequent
  4. Constant
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48
Q

Definition of 4 types of Frequency Grading

A
  1. Intermittent - Sn/Sx occur less than 25% of the time while awake
  2. Occasional - Sn/Sx occur between 25%-50% of the time while awake
  3. Frequent - Sn/Sx occur between 50%-75% of the time while awake
  4. Constant - Sn/Sx occur between 75%-100% of the time while awake
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49
Q

Where do the standardized medical term meanings of medical charting come from?

A

American Medical Association Guidelines 1989

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50
Q

What is high blood pressure?

A

•Primary (Essential) Hypertension is /= 90mm Hg diastolic Or are taking anti-hypertensive medication.

Greater occurrence in African American adults (32%) than in White (23%) or Mexican American (23%) adults.

Morbidity and mortality are greater in African Americans.

BP increases with age until 55 or 60.

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51
Q

Is there a cause for Primary High Blood Pressure and how is it regulated in the arterioles?

A

No identifiable cause. It is a multi-factorial risk factor with many sources of origin. Considered a risk factor and not a disease.

The primary regulation of BP is the Arterioles.

a) Mean arterial pressure is 96mm Hg for an average BP of 120/80mm Hg.
b) Arterioles provide bulk of resistance that drops Pulse Pressure (systolic-diastolic) from 40mm Hg to zero.
c) Mean arterial pressure from 96mm Hg to 30mm Hg which maintains forward blood flow in capillaries

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52
Q

Primary High Blood Pressure Facts

A
  1. Accounts for approximately 95% of HTN
  2. HTN usually appears between the ages of 25 & 55. Left unaltered it progresses in severity.
  3. HTN before the age of 20 is almost always secondary in nature.
  4. Hereditary factors influencing HTN are of weak penetrance. Lifestyle and diet exert a greater influence on its origins and age of onset.
  5. BP is elevated by Sympathetic NS hyperactivity.
    a) Stimulants like caffeine, ephedrine, etc.
    b) Increased catecholamines or insensitivity of baroreceptors
  6. HTN can be exacerbated by Obesity, Lack of Exercise, Smoking, and alcohol use
    a) Consuming 2-3 drinks (20-30g) per day leads to a 1.4:1 relative risk of developing HTN.
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53
Q

How to diagnose people with Primary BP?

A
  1. A minimum of 2 BP readings on each of three days before patient is Dx with HTN.
  2. BP must not be taken until the patient has been sitting or lying down for more than 5 minutes.
  3. More BP determinations recommended for people in the low HTN range and for patients with markedly labile BP.
  4. Normal BP is much lower in infants and children.
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54
Q

Facts about Secondary High Blood Pressure

A
  1. HTN where underlying cause is clearly identified.
  2. Tends to occur at younger ages with much higher pressures.
  3. Renal Vascular HTN is the most common cause resulting from fibrous dysplasia of the renal arteries
    a) This may occur in older patients with atherosclerosis of the renal arteries
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55
Q

What is Estrogen Induced Hypertension?

A

Estrogen-Induced HTN can be caused by chronic-low doses of estrogen in OCA’s. This is most significant in Obese women over 35, taking estrogen for over 5 years.

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56
Q

What is the name for pregnancy induced High Bp?

A

pre-eclampsia and eclampsia

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57
Q

What is Malignant Hypertension?

A
  1. HTN that results in symptomatic damage to the “end organ(s)” such as the Brain, heart and/or kidneys.
  2. Usually defined at specific pressure values, but rarely occurs at pressures less than 160/110mm Hg.
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58
Q

What is Hypotension?

A
  1. Low BP with a systolic pressure less than 100mm Hg or a diastolic pressure less than 60mm Hg.
  2. Greatest risk is that of stagnant blood resulting in tissue edema and hypoxia or the formation of arterial blood clots damaging capillary beds
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59
Q

What is Orthostatic Hypotension?

A

Results with change of posture. “Spells” of lightheadedness with paroxysmal headaches, perspiration, palpitations or panic/anxiety.

Most often caused by anti-HTN medication OD.

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60
Q

Effects of Chronic Hypertension?

A

1.Abrupt increases in BP along with elevated levels of circulating vasoactive substances (angiotensin II, norepinephrin, and vasopressin) may induce chronic vasoconstriction.

  1. An intact endothelium favors vasodilation.
    a) Prostacyclin (PGI2 - prostaglandin vasodilator) and EDRF (endothelium derived relaxing factor). are normally tonically released to counterbalance vasoconstrictors derived from platelets. Thereby inhibiting platelet aggregation and vaso-reactivity.
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61
Q

What happens to the injured epithelium?

A
  1. An injured epithelium favors vasoconstriction (vasospasm).
    a) Excessive platelet aggregation occurs in the absence of PGI2 and EDRF Platelets then release vasoconstrictors (serotonin, thromboxane A2, ADP)
    b) As the epithelium becomes hypoxic, the basement membrane will thicken and endothelial cells will mass-produce large numbers of mitochondria in an attempt to recover from hypoxia.
    c) In turn, the endothelium will release vasoconstrictors in an attempt to limit cellular damage.
    d) This cycle represents the development of atherosclerosis
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62
Q

What Atherosclerotic agents should we avoid?

A

a) Cigarette smoking
b) Exposure to cold
c) Emotional stress and hyperventilation
d) Vasoconstrictive drugs such as ephedrine, caffeine, amphetamine analogues, etc.

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63
Q

CNS Complication Signs and Symptoms of Hypertension

A

a) Severe headache (HA)
b) Visual changes (cortical, not in the eyes)
c) Generalized or focal weakness and parasthesias (tingling, pricking, numbness)
d) Disorientation, seizures, focal neurologic deficits

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64
Q

Retinal Signs and Symptoms of Hypertension

A

a) Blurred or double vision (diplopia)

b) Retinal hemorrhage, exudates, floaters, papilledema (optic disc swelling d/t increased intracranial pressure)

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65
Q

Renal Signs and Symptoms of Hypertension?

A

a) Nocturia - nighttime urination
b) Oliguria - decreased urine production
c) Hematuria - blood in the urine
d) Flank Pain and tenderness
e) Peripheral edema, fatigue and weakness

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66
Q

Cardiovascular Signs and Symptoms of Hypertension

A

a) Chest, intrascapular and/or abdominal pain
b) Palpitations, nausea, vomiting
c) DOE (dyspnea on exertion) and SOB
d) Murmurs = S3 “galllop” (3rd heart sound)
e) Abdominal bruits = “venous hum” caused by blood rushing past an obstruction

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67
Q

What is Hematuria?

A

Blood in the Urine

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68
Q

What is Oliguria?

A

Decreased Urine Production

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69
Q

What is Nocturia?

A

Nighttime Urination

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70
Q

What 2 conditions can athletes drop dead from?

A
  1. Hypertrophic occlusive cardiomyopathy

2. Eccentric ventricular hypertrophy->”re-entry”

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71
Q

Whats another name for Hypertensive Myocardial Hypertrophy?

A

Left Vetricular hypertrophy (LVH)

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72
Q

What is LVH?

A

Left Ventricle Hypertrophy is found in 20-30% of chronic hypertensives

The severity depends on:

a) The level/severity of HTN
b) The duration of the HTN

Info:

  1. LVH is a significant risk for mortality and morbidity.
  2. LVH has a negative synergistic effect in combination with alcoholism or coronary artery disease.
  3. LVH in response to HTN begins as concentric development of the left ventricle and intra-ventricular septum.
    a) Leads to reduced end ventricular volume within the left ventricle
    b) Reduced ventricular compliance (stretch)
    c) Increased heart rate = tachycardia (by Starling’s Law)
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73
Q

Whats the best way to test LVH?

A

Echocardiograms are more sensitive than electrocardiograms (ECG) at determining LVH [ECG’s can only detect the mean ventricular axis]

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74
Q

What is Hypertensive Encephalopathy?

A
  1. Cerebral edema can result from large, abrupt increases in BP.
  2. Diastolic BP exceeding 130mm Hg destroys the integrity of the blood-brain barrier.
  3. Excessive intracranial pressure forces the brain stem down through the foramen magnum generating significant neurological deficit.
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75
Q

How do you diagnose Hypertensive Encephalopathy?

A
  1. Retinal examination reveals papilledema and flame hemorrhages.
  2. Stroke is a normal consequence of these manifestations.
  3. Dx: Head CT scan
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76
Q

Hypertension in Pregnancy

A
  1. Patients should be aware of their BP before trying to get pregnant.
  2. Pre-eclampsia - elevated BP with proteinuria and/or marked edema usually during the last half (20 weeks) of pregnancy and throughout parturition and even up to 2 weeks post-partum
  3. Eclampsia - Exacerbation of pre-eclampsia to the point of convulsions or coma.
  4. Classic Triad - HTN, edema, and proteinuria.Patients should be aware of their BP before trying to get pregnant.
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77
Q

Dissecting Thoracic Aneurysm cause and signs and symptoms

A
  1. HTN is the major cause for dissecting aneurysms.
  2. Acute chest or intrascapular pain marks the onset of the intima (inner layer of blood vessel) tearing.
  3. Patient may appear in shock: diaphoresis, pallor, anxiety, tachypnea and tachycardia.
  4. Patient may exhibit distension of the jugular veins and Sx’s of acute abdomen due to extension of the aorta.
78
Q

What are the lab tests to diagnose Dissecting Thoracic Aneurysm?

A
  1. X-ray - (not as reliable)
  2. Ultrasonography (good)
  3. Computer tomography with radiopaque dye (better, but radiation exposure)
  4. MRI (Good)
79
Q

What is Renovascular Hypertension?

A

•Acute or chronic elevation of systemic BP caused by partial or complete occlusion of one or more renal arteries or their branches
Causes HTN by inciting the release of Renin from the juxtaglomerular cells of the affected kidney. The lumen must be decreased by >/= 70% before stenosis is hemodynamically significant

80
Q

Causes of Renovascular Hypertension?

A
  • Atherosclerosis in men >50 years old.
  • Younger patients = fibrous dysplasias (usually women)
  • Accounts for
81
Q

SSX of Renovascular Hypertension?

A
  • Diastolic HTN develops in 55 year old patients
  • When previously stable HTN accelerates
  • Trauma to back or flank with or without hematuria
  • Systolic-diastolic bruit in epigastrium, usually transmitted to one or both upper quadrants and sometimes through the back
82
Q

How do you diagnose Renovascular Hypertension?

A
  • Ultrasonography (stenosis >60%), but stenosis of >60% is not 100% indication that it is the cause of HTN
  • Magnetic resonance angiography
  • Digital Subtraction angiography
  • Seldinger arteriography*
  • Radionucleotide imaging
83
Q

How to treat Renovascular Hypertension?

A
  • Revascularization
  • Angioplasty, sometimes with stent placement [PercutaneousTransluminal Angioplasty (PTA) w/stent] Rarely, bypass graft
  • Removal of ischemic kidney
  • Antihypertensive drugs

• NB: Recurrence of stenosis 2yrs after angioplasty in 50% of the cases due to atherosclerosis

84
Q

How to manage Hypertension

A
  1. TCM treatment.
  2. Avoid pressure inducing substances.
  3. Weight reduction, diaphragmatic breathing, relaxation techniques.
  4. Regular aerobic exercise.
  5. Limit alcohol intake.
  6. Dietary changes, supplementation.
  7. Are these goals achievable?
  8. Drug therapy.
85
Q

What is Arteriosclerosis?

A

1.Arteriosclerosis is the thickening and stiffening of arterial walls which reduces arterial compliance.

It is caused by a variety of pathological states as well as the daily inflammation caused by somatomedins released in conjunction with insulin.

86
Q

What is the most common form of arteriosclerosis?

A

Atherosclerosis

87
Q

What is Atherosclerosis?

A

a) Results from an inflammatory reaction between the intima and media layers of arteries.
b) Monocytes accumulate within the wall of the blood vessel and begin storing fats and cholesterol that reduce arterial compliance. These fatty deposits are known as plaques.

88
Q

What occurs in the larger arteries and is associated with 90% of heart attacks?

A

Atherosclerosis

89
Q

Where’s the most common sites of aneurysm?

A

At bifurcations of the larger blood vessels in regions of augmentation

90
Q

What are the Risks for patients with Peripheral Arterial Disease?

A
  1. Family History
  2. Age
  3. Hypertension
  4. Smoking
  5. Diabetes
  6. High Cholesterol
  7. Waist Girth
91
Q

What disease is PAD (Peripheral Arterial Disease) more common in?

A

Diabetics –> 4X more common than in people without diabetes

~These patients suffer foot ulceration, neuropathy and the more severe morbidity factors associated with diabetes.

92
Q

How does PAD affect Diabetic Patients?

A

Plaques within artery wall results in loss of arteriolar compliance.

a) Therefore the pulse pressure is not absorbed by distention of the arterioles and the blood enters the capillaries under a pulse pressure of almost 40mm Hg.
b) This can result in edema, anasarca or capillary rupture - in the case of cerebral arteries = CVA.

93
Q

What is Anasarca?

A

extreme generalized edema

94
Q

What is the most common cause of PAD and how does it occur?

A

Atherosclerosis

As the vessels diameter decreases, the tissue it supplies becomes hypoxic.

95
Q

Atherosclerosis is clinically silent until?

A

severe arterial stenosis
aneurism
thrombosis
embolism

96
Q

Where are the most common sites of PAD?

A

In order of occurrence:

  1. Femoral-popliteal occlusion - leg/calf pain
  2. Popliteal-tibial occlusion - foot/ankle pain
  3. Aorto-iliac occlusion - hip/buttock pain
  4. Illiofemoral occlusion - thigh pain
  5. Brachio-ulnar occlusion - hand/forearm pain
97
Q

What are the “5 P’s of Wiles”:

A
  1. Paresthesia
  2. Pain
  3. Pallor
  4. Pulselessness
  5. Paralysis
98
Q

What is Paresthesia?

A

a)Morbid and abnormal sensations
b)Burning, tingling, prickling, formication.
c)Pain
d)Ischemic muscles cramp during exercise.
e)Ischemic pain is normally “tingling and burning”.
f)Pain notably diminishes within a few minutes of rest.
~In late stages: the pain is more severe and occurs at rest.

99
Q

What can Paresthesia resemble?

A

Neurogenic Intermittent Claudication

100
Q

What is a major cause of restless leg syndrome?

A

Ischemia

101
Q

Changes of Pallor Stages and the signs and symptoms

A

~Pallor and trophic changes primarily occur when PAD affects a distal extremity.

Early Stage: Pallor may only appear when exercise induced
I.Altered nail bed blanching.
II.Skin is cool to the touch.

Chronic Stage ischemia induces trophic changes:
I.Hair loss in area of involvement
II.Skin may appear pale and “waxy”
III.Later, skin appears “dry and chalky”
IIII.Nails become thick, opaque, irregular and brittle
lllll. Ulcerations form in the webs of the fingers and toes, or on tips.

End-stages = gangrene.

102
Q

Pulselessness

A

~Usually only noted when exercise induced and the pulse is detectable but faint.

~ Pulse may be lost on the elevation of the affected limb.

103
Q

Paralysis

A

~Truly a late-stage event and related directly to the degree of arterial occlusion.

~Muscle atrophy is seen with true loss of motor function.

104
Q

What is Acute Ischemia?

A

It is caused by arterial occlusion by embolization from the heart, proximal arteriosclerotic plaque or aneurysm.

105
Q

What are the signs and symptoms of Acute Ischemia?

A
  1. Sudden onset of severe pain, coldness, numbness and/or pallor.
  2. Pulses are absent distal to occlusion.
106
Q

Risk factors for PAD?

A
  1. Atherosclerosis is the most common form of occlusive PAD
  2. It most often involves the lower extremity
  3. It is most often seen in the elderly
  4. It is more common in males
  5. It is often associated with diabetes mellitus
  6. Classic Presentation: occlusion of the femoral-popliteal segment causing calf pain on exercise
107
Q

What is the name of the test to check PAD?

A

Buerger’s Test

108
Q

How to apply the Buerger’s Test and what to observe?

A

Part 1: Elevate involved extremity for 1-3 min.

I.Pallor on elevation occurs with poor circulation
II.This is a positive result

Part 2: After elevation for 1-3 min., quickly place limb in a gravity dependent position

I.Observe color change
II.Normal reactive hyperemia should occur within 10 sec.
III.ABNORMAL: Delayed reactive hyperemia
IIII.ABNORMAL: Dependent rubor = a ‘ruddy’ or plum colored redness may occur more than 30 sec. After the limb is placed in a gravity dependent position. Called “rubor of cyanosis”

109
Q

Whats the Allen’s Test?

A

Used to assess PAD in the upper extremity, particularly the median versus ulnar arteries. - not reliable.

110
Q

What’s the Dewiest Test?

A

Have patient exercise to the point of pulselessness. Exercise testing can be contraindicated in patients with PAD due to the concommitant risk of coronary artery disease (CAD).

111
Q

What are the Western Diagnostic Techniques for Atherosclerosis?

A
  • Arteriography

* Doppler Ultrasonography

112
Q

What is Arterial Intermittent Claudication?

A

Is a form of exercise induced PAD. Worse going upstairs

~It is characterized by a fixed threshold distance, a short tolerance distance and a brief refractory period.

113
Q

When is Arterial Intermittent Claudication more Noticeable?

A

When the patient is walking uphill or up a flight of steps.

114
Q

Progressive signs and symptoms of PAD?

A

paresthesia and pain with exercise
pain at rest
ischemic ulcerations
digital gangrene

115
Q

When does Neurogenic Intermittent Claudication mimic PAD>

A

When the patient exercises

116
Q

Neurogenic Intermittent Claudication origin and characteristics

A

~Its origin is due to a stenotic spinal canal

~It is characterized by a variable threshold distance, a tolerance distance that is twice the threshold distance and a variable refractory period

117
Q

When is Neurogenic Intermittent Claudication more noticeable and what is it exacerbated by?

A

~ Neurogenic intermittent claudication would be more noticeable when the patient is walking downhill or down a flight of stairs.

~ Neurogenic intermittent claudication would be exacerbated by lumbosacral extension and somewhat relieved by knee and/or lumbosacral flexion.

118
Q

What is an Aneurysm?

A

localized dilations of blood vessels resulting from weakened arterial walls

I.Most common
II.Secondary to effects of arteriosclerosis
III.Plaquing of arteries at sites of augmentation

119
Q

Whats a Dissecting Aneurysm?

A

I.Tear in the intima allows blood to flow between the media and the externa
II.Usually occur in the aortic notch
III.Commonly seen with eclampsia or Marfan’s syndrome

120
Q

Whats a Berry Aneurysm?

A

I.Spherical dilations due to congenital weakness of the vessel wall
II.Found at the circle of Willis or at the carotid bifurcation
III.Due to discontinuous muscularis mucosa at focal sites

121
Q

Whats a Traumatic Aneurysm?

A

I.Approximately 2% of aneurysms

II.Can be caused by helmet straps

122
Q

What’s a Syphilitic Aneurysm?

A

Historically common in infants born with congenital syphilis

123
Q

Most Aneurysms are asymptomatic until?

A

They dissect

OR

Occlude blood flow through the aorta

124
Q

What is a Dissecting Thoracic Aneurysm?

A
  1. Aortic aneurysm is actually a hematoma of the aorta
  2. Begins as an intimal tear often just centimeters above the aortic valve or just distal to the left subclavian artery
  3. Blood entering the tear forms a hematoma and “dissects” the aorta
  4. This dissection can run the entire length of the aorta
  5. The symptoms and clinical manifestations differ based on the different origins and dissections. (FYI DeBakey Classifications)
125
Q

Risk Factors of a Dissecting Thoracic Anyrusm

A

a) Incidence: 5.9 cases per 100 000 people/yr
b) Most occur between the ages of 40-70yrs
c) Men are more afflicted than women by a 2:1 ratio
d) Most patients have a history of HTN
e) For unknown reasons, pregnancy is a risk factor for dissection
f) Cardiopulminary surgical interventions can cause dissections
g) Atherosclerosis is not an independent risk factor for dissection

126
Q

A patient with Dissecting Thoracic Aneurysm usually presents..

A

a) Acute, severe anterior chest pain (if ascending off the aortic arch)
b) Acute, severe intra-scapular pain (if descending down the aorta)
c) Pain is of an abrupt “unbearable” pain that is “stabbing” or “ripping”
d) HTN: (80% of patients)

127
Q

Thoracic Aortic Aneurisms

A
  1. Most are associated with atherosclerosis
  2. Other causes include congenital syphilis, trauma, vasculitis, congenital malformations and tearing caused by rapid cervicothoracic acceleration-deceleration trauma
  3. Most aneurysms are asymptomatic until they progress and/or rupture
128
Q

SSX of Thoracic Aortic Aneurisms

A

a) Pressure on the trachea causing dyspnea, stridor (high pitched sound) or cough
b) Pressure on the esophagus causing dysphagia
c) Pressure on the left recurrent pharyngeal nerve causing hoarseness
d) Pressure on the superior vena cava leading to edema in the upper extremities

129
Q

Abdominal Aortic Aneurysm

A
  1. Most common form of aneurysm encountered by field practitioners
  2. On palpation (bimanual in the supra-umbilical region):

~Normal abdominal aorta is 2.5 - 4.0cm at the level of the umbilicus
~Normal pulsation is brief

a) 95% are located between the renal arteries and the umbilicus (iliac crests)
b) 80% are readily palpable as an expansile, pulsatile mass
c) 50% are asymptomatic and found incidentally, until impending rupture

130
Q

AAA SSX

A

a) Lumbosacral pain that mimics a herniated disc or ureteral colic
b) Abdominal pain mimicking renal or biliary colic, appendicitis, or pancreatitis
c) These symptoms may indicate “impending” rupture”. Meaning it may rupture within minutes, hours, days, or weeks

131
Q

3 Complications of an Anyrusm

A

a) Lower extremity vascular intermittent claudication
b) Embolization of the lower extremity
c) Rupture resulting in shock

132
Q

What size does an aneurysm have to be to only produce an emboli that will lodge in distal arteries?

A

Less than 5 cm

133
Q

Complications of an aneurysm greater than 6 cm?

A

I.50% risk of death in one year
II.75% risk of death within two years
III.Aneurysms that are approximately 7 cm or greater in diameter carry the peak incidence of rupture

134
Q

2 Types of treatment for aneurisms?

A

Surgery

Endovascular stent grafting

135
Q

What is Deep Vein Thrombosis?

A
  1. Thrombosis is the formation of a thrombus (clot) along the endothelium and expanding into the lumen of a blood vessel
  2. Slower moving venous blood allows for static blood to pool and form thrombi
136
Q

Risk factors for a thrombi formation?

A

a) Atherosclerosis
b) Diabetes
c) Smoking
d) Sedentary lifestyle
e) More than 6 consecutive years of OCA use
f) Increased risk in late pregnancy

137
Q

2 veins that thrombi will form?

A

Ileofemoral

Popliteal

138
Q

Illeofemoral DVT

A

a) Patient complains of pain or soreness with standing or walking that is relieved by rest or elevation of affected leg
b) At rest, people may report “congestion” or “numbness” of affected leg
c) Regional tenderness with a hard palpable cord representing the occluded vein within the femoral traingle
d) Dilation of superficial veins in the femoral triangle and lower abdomen
e) Edema and increased tissue ‘turgor’ of the thigh and leg
f) Skin discoloration along the thigh or leg

139
Q

Popliteal DVT

A

a)Same as Illeofemoral:
Patient complains of pain or soreness with standing or walking that
is relieved by rest or elevation of affected leg
At rest, people may have congestion/numbness of affected leg
b)Regional tenderness with a hard palpable cord within popliteal space
c)Edema and increased tissue ‘turgor’ of leg and ankle
d)Skin discoloration along leg
e)Ankle dorsiflexion with knee extended causes “muscle like” leg pain (AKA Homan’s Sign)

140
Q

What is Homan’s Sign?

A

Ankle dorsiflexion with knee extended that causes “muscle like” pain

141
Q

What are the 2 Etiologies of DVT?

A

Sedentary postures
I.“Couch potatoes”
II.Attendants who stand all day at work

b)Superficial or deep leg trauma
I.Commonly seen in female smokers taking OCA’s
II.Of greatest concern with hip and proximal tibial fractures

142
Q

Where does a normal abdominal aortic artery sit?

A

2.5 - 4.0cm at the level of the umbilicus

143
Q

What is a normal pulse for an Abdominal Aorta?

A

brief and succinct

144
Q

What is the most serious complication of DVT?

A

pulmonary embolism that is often fatal

I.Patients who report leg pain with quiick onset of SOB = always consider pulmonary embolism pathology
II.Long drives and airline flights pose increased risks for patients with pre-existing phlebitis and preexisting thrombophlebitis

145
Q

What is distal venous congestion?

A

Emboli may lodge in larger, partially occluded, veins that reduce venous return from larger areas of the body

146
Q

What is Chronic Venous Insufficiency?

A

A long term consequence of DVT

~Chronic leg Sx exacerbated by walking and relieved by rest and leg elevation

~Venous insufficiency results in edema, stasis pigmentation, stasis dermatitis and stasis ulceration

147
Q

What is Reynaud’s Phenomenon

A

•Reactive vasospasm of the superficial arteries of the fingers or nose on exposure to cold or emotional stress. It results in bluish pink - white discoloration of the skin and normally follows a peripheral nerve distribution. Pain results from tissue ischemia

148
Q

What is Phlebitis?

A

•Inflammation condition of regional veins or a vein. It predisposes patients to thrombophlebitis or the formation of thrombi as part of the inflammatory cascade

149
Q

What is Varicosities?

A

•Defective venous valves fail to maintain directional venous flow resulting in longitudinal distension of the veins or the venous plexus. This is most commonly seen as varicose veins of the greater saphenous vein. It also occurs within the:

  • hemorrhoidal plexus - rectum (hemorrhoids)
  • esophageal plexus - neck
  • pampiniform plexus - varicocele of the testes
  • Long term consequences are similar to those seen with venous insufficiency.
150
Q

Where is the esophageal plexus?

A

Neck

151
Q

Where is the pampiniform plexus?

A

varicocele of the testes

152
Q

Diagnosis Differentiation for sudden onset leg pain?

A
  1. PAD
  2. OA at hip or knee
  3. Peripheral neuritis
  4. Nerve Root (intervertebral disc) compression
153
Q

3 other types of Venous Conditions?

A

Phlebitis
Reynaud’s
Varicosities

154
Q

Top 6 risk factors of Coronary Heart Disease?

A
  1. Age
  2. Family Hx of cardiovascular disease
  3. HTN
  4. Smoking
  5. Diabetes
  6. Lowered serum high density lipoproteins (HDLs)
  7. Waist Girth

•This information is based on males with heart disease

155
Q

Several forms of heart disease are female specific and influenced by?

A

a) OCA HTN
b) Pre-eclampsia
c) Toxemia: Toxic Shock Syndrome
d) Peri-partum cardiomyopathy

156
Q

Age risks for Coronary Heart Disease?

A

Starting at 45 for men, and 55 for women

157
Q

Family History of Coronary Heart Disease

A
  1. Positive male Hx: Myocardial Infarct (MI) or sudden death before the age of 55 for a father or brother
  2. Positive female Hx: MI or sudden death before age of 65 for a mother or a sister
158
Q

Hypertension is a more common risk factor for who, men or women?

A

HTN is a more common risk factor for women

159
Q

How does cholesterol levels affect men and women to diagnose Coronary Heart Disease?

A
  1. In women, low HDL level is a better predictor of CHD risk than high LDL levels
  2. In men, LDL is a better predictor of CHD risk than low HDL level

•Aside: HDL is the “good” cholesterol” that scavenges excess lipid out of our blood stream. LDL contributes to atherosclerosis

160
Q

What waist girth measurements in men and women increase Coronary Heart Disease?

A

32”-35” waist = increased risk of CAD in women

37”-40” waist = increased risk of CAD in men

161
Q

What are the SSX of a Heartattack in women?

A 
shoulder/neck pain
nausea
vomiting
fatigue 
dyspnea
162
Q

When stage of a womens life does Heart Disease increase?

A

Menopause because estrogen decreases and estrogen is known to protect the heart

163
Q

What is the leading cause of death in women?

A

Coronary Heart Disease

  • Twice that of breast cancer
  • Higher risk of death in menopausal women
164
Q

What are the gender related differences in Coronary Heart Disease?

A
  1. Age
  2. Family History of Heart Disease ~ Sudden death before 65 in a
    mother or a sister –> Female
    ~ Myocardial Infarct or sudden
    death before 55 in a father or
    brother –> Male
  3. Hypertension: HTN higher risk factor for women
  4. Smoking: earlier menopause, formation of thrombi, smoking with taking OCA at the same time rises MI risk
  5. Diabetes: Abnormal blood lipid levels and obesity in women
  6. Cholesterol: Low HDL (good cholesterol) is a good predictor of a risk of coronary heart disease in women. Opposite in men
  7. Waist Girth
  8. Atypical Chest Pain: More common in women then men
  9. MI Signs/symptoms: women have a wider variety of symptoms
  10. Ignorance: women are less likely to consider coronary heart disease as a personal health concern
  11. Hormone Replacement Therapy
165
Q

What is HDL

A

Good Cholesterol

Scavenges excess lipids out of our blood stream

LDL contributes to atherosclerosis!

166
Q

Women with “Stable Angina” are more likely to have what..

A

Chest pain at rest or during sleep or during mental stress

167
Q

What does classic triad in pregnancy mean?

A

Hypertension
Edema
Proteinuria

168
Q

what two categories of chest pain is there?

A

1) episodic/recurrent/chronic

2) acute/severe

169
Q

what are the three episodic/recurrent?

A

1) angina pectoris
2) non-angina chest pain
3) “compatible” chest pain

170
Q

what are the 2 acute/severe?

A

1) acute pleuritic chest pain

2) myocardial infarction

171
Q

SX of angina

A
  • predictable
  • Levines sign: fist to the chest
  • abrupt onset, ‘seizes’ the patient
  • lasts 2-3 min
  • relieved by nitroglycerine
172
Q

types of angina:

A

1) Typical(predictable)- exercise induced, relieved by rest, *most common
2) Atypical- not related to stress/exercise, occurs at rest
3) angina equivalent- no chest pain/dyspnea/sweating/vomit/arm-jaw pain
4) mixed angina- related to exercise and stress, also occurs at rest
5) unstable- deterioration of predictable sx
6) silent angina- cardiac insufficiency without pain

173
Q

Non-angina Sx:

A

1) constant chest pain
2) last more than 1 hour
3) lasts one second
4) influenced by respiration
5) affected by posture
6) aggravated by pressure on chest
7) alleviated by lying down

174
Q

Mitral Valve Prolapse Syndrome info:

A

-congenital disorder
-atypical chest pain, palpitations, light-headedness
-6-8% population
DX- auscultation (click->murmur), 2 dimensional echocardiography

175
Q

Compatible Chest pain info:

A
  • episodic chest pain not clearly definable (not angina/non-angina)
  • need further Dx
176
Q

causes of compatible chest pain:

A

1) gastro-intestinal disorders
2) chest wall disorders (pleuritis)
3) psychogenic chest pain (anxiety)
4) cardiopulmonary diseases

177
Q

What are the two types of pleuritis?

A

1) inflammatory pleural effusion

2) non-inflammatory pleural effusion

178
Q

inflammatory pleural effusion sx:

A
  • localized stabbing pain
  • aggravated by coughing
  • shallow, rapid breathing
  • crepitations (crackle sound in LU)
  • absence of tactile fremitus (breathing vibrations)
179
Q

non-inflammatory pleural effusion SX:

A
  • accumulation of fluid in intra-pleural space
    1) hydrothorax (water)
    2) chylothorax (lymph)
    3) pyothorax (pus)
    4) hemothorax (blood)
180
Q

spontaneous pneumothorax info:

A
  • most common in males 20-40
    1) free air in intrapleural space
    2) traumatic
  • open= chest wall penetration
  • closed= blunt chest trauma
  • secondary= most commonly due to lung diseases (emphysema, COPD)
181
Q

what is a Myocardial Infarction

A
  • heart attack
  • irreversible tissue necrosis (DX-blood test enzymes)
  • chest pain that lasts longer than 30 min
  • not alleviated by nitroglycerine
  • SX severity depends on location of tissue involved
  • SX: anxiety, mental confusion, nausea, excessive diaphoresis, palpitations, pallor
  • older patients report dyspnea as chief complaint, not chest pain
182
Q

Myocardial Infarction may or may not have a prodrome….what is a prodrome?

A

predictable symptoms leading up to event, can occur days-weeks prior

183
Q

prodrome SX:

A

1) angina
2) SOB, dyspnea on exertion
3) paroxysmal nocturnal dyspnea
4) palpitations
5) (pre) syncope (feeling faint= anemia/HTN)
6) unexplained diaphoresis (sweating for no reason)
7) TIAs (signs of mini strokes)

184
Q

what percentage of patients report a “silent” MI?

A

25%

185
Q

physical MI findings:

A

1) decreased peripheral pulse
2) HT murmur
3) irregular tachycardia
4) pulse ultermans

186
Q

***most common MI SX:

A

1) dyspnea
2) chest pain
3) pre syncope
4) TIAs (mini stroke sx)
5) fluid retention

187
Q

types of MI dyspnea:

A

1) exertional- *most common
2) paroxysmal nocturnal (PND)- *most specific, more severe, felt when asleep or recumbent pos. for 1hour+
3) orthopnea- felt soon after recumbent pos.
4) at rest- severe, COPD

188
Q

what is pericarditis:

A

inflammation of parietal pericardium

  • sharp, achy
  • radiates (rarely to arm)
  • aggravated by recumbency, inspiration
  • friction rubs often auscultated
189
Q

types of MI syncope:

A

1) orthostatic hypotension- upon standing
2) vasovagal syncope (common)- stress/fear, sudden peripheral vasodilation
3) situational- coughing, defication, excessive vagal tone from physiologic reflexes, increased abdominal pressure
4) recurrent- *immediate concern, may be due to DT Dz/pulmonary embolism
5) cardiogenic- few prodronal sx, spontaneous, palpitations

190
Q

Transient Ischemic Attacks (TIAs) info:

A
  • focal neurologic deficit
  • acute onset
  • 24h
    1) carotid stroke- athlerosclerosis
    2) vertebrobasilar stroke
  • 1/3 TIA patients develop stroke in 5 years
  • 1/3 TIA patients have coronary after Dz
191
Q

compare TIAs carotid VS vertebrobasilar:

A

carotid VS vertebrobasilar
-one eye blind -both eyes blind
-aphasia(loss expression) -ataxia(loss muscle
coordination)
-hemiparesis -cross motor and
sensory deficits
-numb fingers/hand/arm -numb one hand or both
leg/face -vertigo, syncope, nausea, dipolia

192
Q

MI fluid retention:

A
  • late stage
  • increase venous pressure
  • cardiogenic= low extremities, pitting edema
  • sx: weight gain, bloating, vomit, LI/SP hypertrophy, diarrhea, jaundice

Internal Medicine (3 decks)

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