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Complete Physical Diag Review

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PHYSICAL DIAG 1: INTRODUCTION
THE HEALTH HISTORY
1. Demographic data, reliability
2. Chief complaint
3. History of present Illness
4. Past medical and surgical history
5. Family history
6. Personal and social history
7. Review of systems
History section
Demographic data,
reliability
Chief complaint
History of present
illness
PMH and surgical
history
Family history
Personal and social
history
ROS
Questions? Jenny Armstrong | jra2159
A lot of the history is completed at home via online forms. However, history
is still a huge component of the physical exam which helps tailor a Ddx. If you
don’t have a thorough history, you may completely miss the mark. Think
about who the source is, if they are reliable, and who this patient is. Capture,
in quotes, in the patient’s own words, the how and what of the present illness
and chief complaint. Think about if you’d like someone else in the room,
especially if pt is unconscious, a geriatric pt, or someone who may otherwise
need assistance.
Components
Age gender, occupation, marital status
Source of history
o Self vs. others eg. Pt, relative,
stranger, referring doctor
Source of referral
Reliability
o Depends on context seeing and who
is providing the information
Symptoms that brought patient in
In patient’s own words
In quotes
Describes how each symptom developed
What the patient did about these symptoms,
including meds, and other treatment
Seven attributes
= seven sins “liquor saturday” = LQQR SAT
Location
Setting in which it occurs
Quality
Associated manifestations
Quantity or severity
Timing
Remitting or exacerbating factors
Childhood illness
Adult illness
o Medical: cardiac, HTN, DM, asthma
o Obstetric/gynecologic
o Psychiatric
o Health maintenance
o Prior testing
Surgeries
Age, health, or cause of death of close
relatives
Include mental illness, drug and alcohol
addiction
Can use pedigree charts
Life style habits
o Alcohol, drug
o Tobacco use (in pack years)
Occupation, schooling
Exercise and diet
Intertwined with HPI and PMH
Directed questions about organ systems
Anecdotes
There is a way to introduce this which says “this
information is important so I can treat you
better.”
eg. Treating a UPS worker who lifts 100 lbs a day
vs. an old man who is 93 and doesn’t work.
eg. Giving pt a difficult diagnosis and making
sure they have a support system
This is important so we can always refer back.
eg. If CC is nose, but pt has a retrognathic
mandible and we only tx the mandible, it will
mask the nose, but pt may still be unhappy with
their nose
Always use open questions and ask many ways.
Open questions allow discourse, rather than yes
and no answers. Pointing to body parts can also
help.
eg. “What medications do you take vs. do you
take any meds”, “What are you allergic to vs. Do
you have any allergies.”
For the 7 attributes: eg. Bruxism causing pain
and tightness in the am, but symptoms improve
during the day
The OLE LOE down or LOSED
Doctor: “Oh you quit? Great, when?”
Sir smokes a lot: “Last Tuesday ;)”
Subjective findings
Everything the pt tells you = subjective
eg. Pt comes in and complains of nausea =
subjective. You can’t tell from a physical exam
that they have nausea, unless pt is writhing and
gagging. So, ROS is important.
THE PHYSICAL EXAMINATION
General survey
Vital signs
Skin
HEENT
Neck
Back
Posterior thorax and lungs
Breasts, axillae, epitrochlear nodes
Anterior thorax, lungs
Cardiovascular system
Abdomen
Lower extremities
Neurologic
GENERAL SURVEY
Apparent state of health, level of consciousness
Signs of distress: cardiac, respiratory, pain, anxiety, or depression
Height, build, weight, BMI (eg. tall, short, skinny, fat, average, muscular)
Skin color
Dress, grooming, personal hygiene, posture, gait
VITAL SIGNS
Blood pressure
Heart rate
Respiratory rate
Temperature
HEART RATE AND RHYTHM
Radial pulse for 15 seconds and multiply by 4 or better is 30x2– if REGULAR pulse
If irregular pulse:
o 60 second count
o Describe the irregularity (Eg. Thread)
Irregularly irregular = atrial fibrillation
All others need ECG
ROS
General – wt, fever
Skin
HEENT
Neck
Breasts
Respiratory
Cardiovascular
Gastrointestinal
Urinary
Genital
Peripheral vascular
Musculoskeletal
Neurologic
Hematologic
Endocrine
Psychiatric
ROS Cardiac Example
Heart trouble, chest pain, SOB,
palpitations, edema, SOB at night,
exercise tolerance.
ROS Respiratory Example
Cough, sputum, SOB, hemoptysis,
wheezing, exercise tolerance,
pneumonia, TB
Equipment for BP
1.
RESPIRATORY RATE AND RHYTHM
Rate
Adults: Normal is 14-20 (may see other numbers elsewhere)
Rhythm
Depth
Effort of breathing eg. labored breathing or asthmatic having trouble getting air out?
BLOOD PRESSURE
Select the correct size cuff for the patient by measuring arm circ at midpoint of
upper arm (halfway between acromion and olecranon)
o Index line = Perpendicular to length, Range line = parallel to length
o Index within range-line limits, midpoint of bladder over branchial artery
o Undersized overestimate BP
Brachial artery at heart level
Contraindications:
o Axillary node dissection in breast cancer pts
o AV fistula for hemodialysis
o Any deformity or surgical history that interferes with access
o USE CONTRALATERAL ARM OR LEG
Some pre-existing conditions can interfere with accuracy or interpretation of reading
o Aortic coarctation, arterial-venous malformation, occlusive arterial dz,
Antecubital bruit, artherosclerosis (prolonged 4/absent 5), arrhythmias
BP measurement: Find pulse obliteration pressure, and then inflate 20-30 mmHg
above that and deflate 2 mmHg per second while listening for Korotkoff sounds
Korotkoff sounds:
Phase 1: Clear, tapping with appearance of palpable pulse (systolic = pulse appears)
Phase 2: Murmurs
Phase 3 & 4: Muted changes (within 10 mm Hg of diastolic)
Phase 5: Disappearance of sounds = diastolic
Stethoscope
2. Sphygmomanometer
Sphygmomanometer: consists of
a blood-pressure cuff with a
distensible bladder, a rubber bulb
with an adjustable valve for inflation,
tubing that connects the cuff to the
bladder, and a manometer.
1.
2.
3.
4.
5.
View manometer at eye level.
Use bell side of stethoscope to
auscultate low freq sounds.
Regularly inspect and calibrate
equipment.
Position the pt: back and legs
supported, legs uncrossed, feet
resting on firm surface, bare arm
to the shoulder, loose garment
sleeve, supported arm at level of
heart.
Place cuff snuggly 2cm above
elbow crease, with midline of
bladder over brachial artery.
Pulse Oblit - Avoid an ausc gap!
Palpate radial pulse while inflating to
80 mmHg then slow infl to 10 mmHg
every 2-3 sec until pulse disappears,
then deflate and note where appears.
PHYSICAL DIAG 2: HEENT – Head, ears, eyes, nose, throat (neck)
1.
2.
3.
4.
Questions? Jenny Armstrong | jra2159
First, obtain a thorough history
Have a system Stick to a single system until further experience has been gained
Top to bottom
NOTE: Neuro exam beings when interviewing the patient and continues with the head & neck exam
INSPECT THE PATIENT
1. Look at the patient
2. Note asymmetries, steps, malocclusion, bleeding areas, CSF
3. Look for battles sign/raccoon eyes
a. Battle’s sign = mastoid ecchymosis (may be delayed, or bilateral,
fracture of MCF) (B=behind the ear)
b. Raccoon eyes = bilateral periorbital ecchymosis (anterior cranium or
basilar skull fracture)
4. Inspect the scalp
Anecdotes: What symptoms do you see? Inflammation, swelling, tumor, fracture? No! Do not use terms that will
narrow down a diagnosis. Instead, use terms like “young male child with unilateral swelling of the face.” When you
take a history, the patient or parents may mention something and you can put it in quotes, “Pain and swelling on the
side of the face for the past few days” or “fell this morning”.
INSPECTION (=looking)
1. Scalp
2. Pallor (ischemia, or loss of bloodflow can cause changes in pallor)
3. Ecchymosis
4. Bleeding
5. Asymmetries
6. Malocclusion – step in occlusions, normal arches, ask the pt if the occlusion has always been like that or if
changed – you can also ask the patient for a recent picture of themselves or their DL to assess what occlusion
looked like before trauma
7. Battle’s Sign/Raccoon Eyes
PALPATION – feel (start with non-painful and move to areas where there may be pain)
1. Steps
2. TMJ Pain
a. Have pt open (rotation + translation)
b. Feel for clicks, pops, crepice
i. Indicates bone on bone, slipping of disk, arthritis
ii. Note when the click occurs – is it early or late in opening
c. Measure width of opening
3. Depressions
4. Asymmetries
5. Lymphadenopathy
a. Do this on every pt
b. ID cancer, infx
Anecdotes: Pt comes in with trauma, feel for steps or asymmetry in bone. Feel the orbit, look in nose for septal
deviation. If pt punched in nose, and bleeding stops, blood may accumulate in hematoma. Also check the nasal
septum to see if perforated or deviated or necrosed. FUN FACT: cocaine users vasoconstriction can result in
necrosis and perforation of the septum
TOP TO BOTTOM HEENT EXAM: eyes, ears, nose/paranasal sinuses, oral cavity, neck
Eyes – symmetry, how they move, put 1 hand on head to hold still and draw an H with fingers and have pt follow
Nose/paranasal sinuses – nasal septum for perforations, deviations
Neck – lymphadenopathy, changes in feeling (eg. A fracture could displace nerve and cause numbness/tingling)
EYES
1.
Visual fields – Entire area seen by eye when looking at a
central point
2. Pupillary rxn – size change of pupil in response to light and
focusing (CN III)
3. Light rxn – Light in one retina causes constriction of both
ipsilateral and contralateral pupil (consensual reflex)
4. EOM = extra-ocular movements in tact – controlled by 6
muscles, 4 rectus, 2 obliques
EYE EXAM TECHNIQUE (big picture: are eyes working together)
1. Visual acuity = Snellen eye chart
a. 20/200 = what someone with normal visual acuity
can see at 200 ft, 20/20 @20 ft/6m
2. Visual fields = 2 hands at ear width 2 ft from pt. Move
around hand and observe where the pt can see in the field
3. Pupils: Check size and consensual reflex
4. Extra-ocular muscle movements
a. CN III, CN IV, CN VI
5. Check for subconj heme
6. Ophthalmoscope
OPTHALMOGIC EXAM
Visual fields and ocular movement
Diplopia (double vision)
FUNDASCOPE
Hypertension can cause damage to retina
o Hard exudates, cotton wool spots,
EARS
Check the ears in all 3 compartments
1. External ear: auricle, ear canal
2. Middle ear: Ossicles (air filled cavity that transmits
sound)
3. Internal Ear: Cochlea
Pathways of hearing: Vibrations of sound external
meatus vibrate eardrum ossicles move transmit to
cochlea cochlear nerve (CN VIII) transmits info to brain.
1st aspect of hearing = conductive
nd
2 aspect of hearing = sensorineural (secondary)
TECHNIQUE:
1. Inspect the auricle. Check for deformities,
bleeding, masses.
2. Check tympanic membrane with otoscope. Assess
for bleeding, erythema, and perforations.
3. Weber and Rinne tests
Weber test:
256 hz fork, middle of head, if hearing is
symmetric, hear fork in middle of forehead.
Localizes away from sensorineural (inner) and
toward the ear with conductive (middle) loss
Rinne test:
512 hz fork, against mastoid process. When no
longer heard, place it just outside external
auditory canal, normal hearing will still hear
vibrating. (bone and air conduction)
NOSE/PARANASAL SINUS
1. Check anterior and inferior surface of nose. Note lesions,
masses and asymmetries.
2. Test for nasal obstruction by occluding each nasal passage
separately. Listen for poor air movement.
3. Place otoscope with nasal speculum and check for exudates
from septum or turbinates.
4. Check septum for necrosis, perforation or deviation.
5. Palpate area of both max and frontal sinus. Check for pain
or feeling of fullness. Bone of sinus is thin, so you can
occlude the nasal frontal duct and check for pressure or pt
may feel tenderness/pain
Anecdotes: It is difficult to assess sinuses by looking, however, the
maxilla is thin, so if there is sinusitis, it hurts to palpate due to
pressure. Test for nasal obstruction by having the patient occlude
each nostril.
ORAL CAVITY (vestibule, hard & soft palate)
1. Count teeth
2. Check occlusion
3. Look for tooth trauma/mobility
4. Check for mobility of mand/max
5. Check FOM for elevation/ecchymosis
6. Check lateral border of the tongue
7. Check maxillary vestibules for bruising/ecchy
8. Check patient for trismus
Other: See rising and falling of uvula, check for changes in the
OC, such as those caused by ulceration, trauma, smoking,
glands, and salivary flow.
NECK
1.
2.
3.
Survey – inspect the neck. Note symmetry,
masses, scars, enlargement of SM or Parotid and
LAD.
Palpate lymph nodes. Note size, shape,
consistency.
Inspect the thyroid and the trachea. Look for
deviation and symmetry. Inspect for
nodules/masses.
PHYSICAL DIAG 3 – NEUROLOGIC EXAMINATION
Appearance/Behavior
Memory (see insert B)
Orientation
(see insert A)
Level of consciousness
ideas expressed by patient
Thought content = types of
Thought process
Speech
to the examiner
how the patient's mood appears
Affect = objective assessment of
feels
that the patient tells you he/she
Mood = Subjective emotion
Questions? Jenny Armstrong | jra2159
ORGANIZATION:
Mental status
Cranial nerves
Motor function
Sensory function
Reflexes
Cerebellar function
MSE
Physical appearance
Behavior
Attitude
Quality
Appropriateness
Rate (pressured?
Volume
Tone
Tangentiality
Loosening of association
Circumstantiality
Delusions
Clothing, hygiene, posture,
grooming
Good eye contact, mannerisms,
tics
seductive apathetic
Cooperative, hostile, guarded,
shown (flat, blunted, full)
Depth, and range of feelings
subject of the conversation
Is the affect congruent with the
reached; skirting around
Point of conversation never
thought to another
No logical connection from one
after circuitous path
Point of conversation reached
3 other doctors said no.
Seductive - they have an agenda.
Repetitive, intrusive throughts
AAOx3 = alert, awake,
come in or here on own volition.
Cooperative - were the forced to
Obsessions
Repetive behaviors
oriented to peson, place
be changed by reasoning
False, fixed beliefs that cannot
Compulsions
what time is it? and time
Who are you, where are you,
Suicidal/homicidal thoughts
document specifics
Ask person, place, time and
INSERT A: LEVEL OF CONSCIOUSNESS
(=a lertness and a wareness)
Alert: (speak to pt normally) – Opens eyes, looks at
you, responds fully and appropriately
(think: alert and appropriate)
Lethargic: (speak in loud voice) – Appears drowsy,
opens eyes, looks at you, responds, and then falls
asleep
(think: loud, looks, lazy and lethargic)
Obtunded: (shake the patient) – Patient opens eyes
and looks at you, responds slowly. Alertness and
interest in enviro are decreased.
(think: opens but disOriented)
Stupor: (apply a painful stimulus) – 1. Patient
arouses from sleep only after a painful stimulus
(eg. sternal rub, or take thumb and push on buccal
vestibule in mouth on mentalis muscle use this
if pt is heavily sedated and can’t open mouth) 2.
Patient lapses into unresponsive state when the
stimulus ceases. 3. Minimal awareness of self or
the enviro.
(think: stupor stimulus sternal sleepy selfkinda)
Coma: (apply repeated painful stimuli) – Patient
remains unarousable with eyes closed, no
response to external stimuli.
(think: coma closed)
INSERT B: MEMORY
1. Test short term (immediate and at 3 minutes)
a. 3 items: apple, penny, table
2. Recent memory: events of past 3 days
a. Ask questions that you can check
against other sources eg. Weather,
today’s appointment time (don’t ask
what pt had for breakfast unless you
can confirm)
3. Remote memory - Ask about historical events,
schools attended
Attention/concentration: serial 7’s, spell
backwards (W-O-R-L-D)
4.
Neuro exam (cont)
CRANIAL NERVES
#
NAME
I
Olfactory
FUNCTION
Smell
TESTS
Have pt close eyes, occlude one
nostril, and test smell (coffee,
soap, vanilla)
1.Swinging light test for direct
pupillary light reflex: afferent limb
CN II
2.Peripheral vision tests
II
Optic
Visual acuity/
visual fields
III
Oculomotor
EOMI*
1.Motor function tests
2.Swinging light test for
consensual pupillary light reflex:
efferent limb CN III
IV
Trochlear
EOMI
Motor function tests
V
Trigeminal
Sensory &
Motor
1.V1 – Corneal reflex sensory limb
2.V3 – Motor
VI
Abducens
EOMI
VII
Facial
Motor function
Trace an H with your finger and
have pt follow your finger.
1.Motor - Eyebrow raise, close
eyes, tightly smile, puff out cheeks,
blow kiss
2.Corneal reflex motor limb
VIII
Acoustic
Conductive - 1°
Sensorineural - 2°
1.Hearing test
2.Weber test
3. Rinne test
4. Finger rubbing/snapping
IX
Glossopharyngeal
Gag reflex
Say ahhh!
X
XI
Vagus
Spinal accessory
Gag reflex
Motor function
XII
Hypoglossal
Motor
Sah ahhh!
Shoulder shrug = trapezius
Head turn = SCM
Stick tongue out
*EOMI = extraocular movements intact
ANECDOTES
Usually not tested
Pupillary reflex - Senses incoming light. Shine light in
right eye, normal rxn is to have constriction in both
eyes. If no constriction in right eye, indicative of CN
II lesion or intracranial mass.
Swinging light test – examine other eye, assess direct
and consensual.
Peripheral vision tests - Put one or two fingers up
and ask pt to ID how many you are holding up. Pt’s
with pituitary tumors may have impaired vision,
such as reduced peripheral vision, double vision, or
loss of vision.
LR6(SO4)3**
Motor function: Trace an H with your finger, or go
up, down and in oblique directions. Properly
position yourself at a reasonable distance away from
pt so both you and pt can follow movements. Hold
patient’s head, if necessary and ask to follow with
eyes only. Same for CN IV, VI.
Consensual reflex – Shine light in right eye, normal
rxn is to have constriction in both eyes. If no
constriction in left eye, loss of consensual reflex,
indicative of CN III lesion or intracranial mass.
Superior oblique m.; LR6(SO4)3
Same as motor tests for CN III, VI
V1 – Corneal reflex – Look for blinking
Surprisingly tap patient on forehead between eyes
V3 – Teeth clenching, chew, palpate temporalis
bilaterally. It’s nearly impossible to KO all of the
muscles of mastication; lots of compensatory
motion.
Lateral rectus m; LR6(SO4)3
Same as motor tests for CN IV, III
If removing parotid tumor or doing any surgery of
the face or mouth, may dissect out all of the facial
branches, so imp to discuss the possibility of loss of
motor function beforehand. Also, remember 5
fingers on hand along face
Weber's test - tuning fork on forehead.
Loud on one side:
= conductive loss on same side OR
= sensorineural loss on opposite side
Rinne’s test - tuning fork on mastoid, move near ear
Normal = Air louder than bone (+ve rinne's)
Conduction loss = Bone louder than air (-ve rinne's)
Sensorineural = Both the same
Look for rise of soft palate/uvula (uvula towards
normal side), swallow, cough, taste post 1/3
Same as above
Unilateral cortical lesion tongue points towards
affected side. Eg. problem on right, tongue goes to
right, because have an unopposed contralateral side
**(lateral rectus = CN 6, superior oblique = CN 4, the rest are CN3)
Neural exam (cont)
MOTOR FUNCTION
Body position (observe)
Involuntary movements (observe)
Muscle bulk
(compare size and contours of muscles)
Muscle tone
(normal muscle with an intact nerve supply
maintains slight residual tension known as
muscle tone)
Muscle strength
(graded 0-5)
During movement and rest
Resting tremors – slow fine tremor of Parkinson’s
Postural tremors – maintain in active posture, hyperthyroidism, anxiety
Intention tumors – absent at rest, worse when nearing target (Cerebellar disorders)
Tics – brief, repetitive, stereotyped movements at intervals (Tourette’s = tics)
Athetosis – slower, twisting, and writhing (cerebral palsy) (all have w’s cewebwal)
Flattening of thenar eminence: sign of median nerve damage
Flattening of the hypothenar eminence: sign of ulnar nerve damage
Ask patient to relax, put wrist, elbow, shoulder through range
Parkinsonian “cogwheel” rigidity
Flaccid paralysis
0 = no muscular contraction detected
1 = flicker of movement or slight twitch
2 = moves with gravity eliminated
3 = moves against gravity, but not against resistance
4 = moderate movement against resistance (sometimes qualified as 4+ if patient can
generate moderate resistance or 4- if patient can only move against mild resistance)
5 = normal strength or power
Strength can be used to localize lesions
Elbow flexion – Biceps (C5, C6)
Elbow extension – Triceps (C6, C7, C8)
Grip strength – (C7, C8, T1)
Finger abduction – Ulnar nerve (C8, T1)
Opposition of thumb – Median nerve (C8, T1)
Knee, hips, dorsiflexion, plantar flexion
SENSORY FUNCTION
1. Compare symmetrical areas on two sides of the body
HOW TO TEST SENSORY FUNCTION
2. Scatter stimuli to get most dermatomes
a. Both shoulders (C4)
Pain = sharp safety pin, break a q tip
b. Inner/outer forearms (C6/T1)
Temp = tuning fork (often omitted if pain
c. Thumbs and little fingers (C6/C8)
normal)
d. Fronts of both thighs (L2)
Vibes = tuning fork over big toe joint, medial
e. Medial/lateral calves (L4/L5)
malleolus (often first to be lost in diabetic
f. Little toes
peripheral neuropathy)
3. Testing function:
Posish = big toe, up/down
a. Pain and temperature = spinothalamic tracts
b. Position and vibration = posterior columns
c. Light touch = both pathways
REFLEX
Graded 0-4
Biceps (C5, C6)
o 4+ very brisk with Clonus (rhythmic oscillations between flexion and extension
Triceps (C6, C7)
o 3+ brisker than average (not necessarily indicative of dz)
Brachioradialis (C5, C6)
o 2+ normal
Knee (L2, L3, L4)
o 1+ diminished, low normal
Ankle (S1)
o 0 no response
To elicit deep tendon reflexes
o Have pt relax
o Hold hammer between thumb and index finger so it swings freely
The Plantar reflex
o Stroke from heel to ball of foot laterally to medially (normal response is flexion)
o Dorsiflexion of big toe with fanning of the other toes is called Babinski Response
Babinski response indicates a CNS lesion n the corticospinal tract
Clonus – if the pt’s reflexes seem hyperactive, test for clonus (sustained clonus indicates CNS disease)
o Asterixis (metabolic encephalopathy) - Ask pt to “stop traffic” by extending both arms
CEREBELLAR FUNCTION
Heel to shin (legs)
Rapid alternating movements
Finger to nose (point to point): index finger to nose – look for smoothness of movement/watch for tremor
GAIT
Tandem walking: heel to toe
o Ataxic gait is one that lacks coordination
o Ataxia may be due to cerebellar lesion, position sense, or intoxication
Walk on toes, walk on heels
o May reveal distal muscular weakness
o Inability to heel-walk is a sensitive test for corticospinal tract weakness
Hop in place
Shallow knee bend
o Difficulty suggests a proximal muscle weakness (hip extensors, quadriceps)
TESTS OF POSITION
The Romberg Test (from wiki) = RUMberg
o test used in an exam of neurological function, and also as a test for drunken driving
o based on the premise that a person requires at least two of the three following senses to maintain balance while
standing: proprioception (the ability to know one's body in space); vestibular function (the ability to know one's head
position in space); and vision (which can be used to monitor [and adjust for] changes in body position).
o A patient who has a problem with proprioception can still maintain balance by using vestibular function and vision. In
the Romberg test, the standing patient is asked to close his or her eyes. A loss of balance or swaying is interpreted as a
positive Romberg's test.
o THE TEST:
the subject stands with feet together, eyes open and hands by the sides.
the subject closes the eyes while the examiner observes for a full minute.
o
INTERPRETING:
The Romberg test is used to investigate the cause of loss of motor coordination (ataxia).
A positive Romberg test suggests that the ataxia is sensory in nature, that is, depending on loss of
proprioception.
If a patient is ataxic and Romberg's test is not positive, it suggests that ataxia is cerebellar in nature, that is,
depending on localized cerebellar dysfunction instead.
Pronator Drift = Pizza time!
o Ask the patient to extend and raise both arms in front of them as if they were carrying a pizza. Ask the patient to keep
their arms in place while they close their eyes and count to 10. Normally their arms will remain in place. If there is
upper extremity weakness there will be a positive pronator drift, in which the affected arm will pronate and fall. This is
one of the most sensitive tests for upper extremity weakness.
ADDITIONAL RESOURCES:
https://informatics.med.nyu.edu/modules/pub/neurosurgery/motor.html
http://geekymedics.com/2012/12/12/cerebellar-examination-osce-guide/
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• P#wave#in#the#same#direction#as#QRS#
Rhythm&
#
#
$
Axis#
%30#to#+90#is#normal$
Right#Axis#Deviation=#Right#
Ventricular#Hypertrophy$
Ischemia!
• Usually#indicated#by#ST$
o Elevation=#Acute#infarct$
o Depression=#ischemia$
• Can#manifest#as#T#wave#changes$
• Remote#Ischemia#shown#q#waves$
•
•
Remember:!
• Myocardial#ischemia#=#T%wave#inversion$
• Subendocardial#Infarct#=#ST#depression$
• Acute#MF#=#ST#Elevation$
Where’s$the$Lesion?$
• ST#Depression#$
o Lead#II,#III,#aVF#!#inferior#wall$
o Lead#V3%V6#!#Anterior%#lateral#$
• So….Inferior,#Lateral$
$
EKG$$
• First&Degree&Block&
$
$
Common$EKG$(Abnormal)$Patterns$
Atrial&Fibrillation&
• Irregular&Irregular&
Atrial$Fibrillation$
o Irregularly#irregular#
Multi7ectopic&Foci&
&o Multi%ectopic#foci#
AV$Blocks#
• Prolong&PR&Interval&&
PR!interval!prolongation!
• First$Degree$Block$$
o PR#interval#fixed,#but#prolonged#(>0.2#sec)#
I&
Type&1&Second&Degree&AV&Block&
•
Second$Degree$Block,$Mobitz$Type$1$$
o PR#gradually#lengthened,#then#drop#QRS#
#
Type&II&Second&Degree&AV&Block&
Fixed PR Interval
QRS Dropped Randomly
•
Second$Degree$Block,$Mobitz$Type$2$
o PR#fixed,#but#drop#QRS#randomly#
Third&Degree&Block&
•
Type$3$Block$$
o PR#and#QRS#dissociated#
Atrial&Flutter&
• Irregular&Regular&
Atrial$Flutter$
& o Irregularly#Regular##
#
Look At All These Teeth
#
#
Ventricular&Fibrillation&
•
$
$ No relation between p-waves and the (nodal) QRS
$ complexes.
$
$
$
$
$
$
$
$
$
$
$
$
$
$
$
$
$
$
$
$
$
$
$
$
$
dad2165$
Ventricular$Fibrillation$
#
#
Ventricular&Tachycardia&
•
Ventricular$Tachycardia$
$
#
#
#
#
#
###
#
#
#
#
#
&
(
(
(
(
(
(
dad2165&
The(Cardiac(Cycle(
(
•
•
•
•
•
•
normal(
•
abnormal(
CARDIAC&PHYSICAL&DIAGNOSIS&&
&
!
History(Taking(
Previous)hx)of?)
• Myocardial(infarction(
• Arrhythmias(
• Endocarditis/Rheumatic(heart(disease(
• Coronary(artery(bypass(
• Valve(repair/replacement(
• Pacemaker/AICD(
Exam(Technique((
(do)it)the)same)way)every)time))
Inspect(
How(does(the(patient(look?(How’re(
they(sitting?(Are(they(cyanotic?(
Palpate((
(
Percuss(
Chest(wall,(determines(airIfilled,(
fluidIfilled,(or(solid(
Auscultate(( Listen(on(the(skin((no(clothes(or(
hair)(
• Examine(for(jugular(venous(distension(
• Palpate(the(carotid(pulsation((
• Listen(for(carotid(bruits((
• Examine(the(posterior(chest(sitting(up(
o If(pt(can’t(sit,(roll(side(to(side(
Circumferential Landmarks
• Examine(the(anterior(chest(with(pt(supine(
• Use(vertical(and(
circumferential(
landmarks(to(
describe(
abnormalities((
o Rib(or(
vertebral(
level(
o Midaxillary,(
Anterior(axillary(
• (Cardiac(sequence(of(auscultation(
o Right(second(interspace((aortic)(
o Left(second(interspace((pulmonic)(
o Left(fourth(interspace((tricuspid)(
o Left(fifth(interspace((mitral)(
(
(
(
(
(
(
(
(
(
Atrial(systole((
o Preceded(by(the(P(wave((atrial(depolarization)(
o Increase(atrial(pressure(by(atrial(kick((S4)(
Isovolumetric(Ventricular(Contraction(
o After(onset(of(QRS((ventricular(depolarization)(
o VP>AP(!(Closure(of(the(AV(valve((S1)(
o Pressure(increases(but(no(change(in(volume(b/c(
AV(&(aortic(valves(are(closed(
Rapid(Ventricular(Ejection(
o VP(reaches(max(
o VP>(Aortic(P(!(Aortic(valve(opens((
o Most(stroke(volume(is(ejected(
o Atrial(filling((begins((
o T(wave(=(end(of(ventricular(contraction(
Reduced(Ventricular(Ejection((
o VP(decreased(
o Left(Atrial(filling(
o Aortic(Pressure(decreases(as(blood(runs(off(
Isovolumetric(Ventricular(Relaxation(
o Complete(Ventricular(repol.((end(of(T(wave)(
o Closure(of(aortic(valves((S2):(VP<(Aortic(
Rapid(Ventricular(filling(
o VP<AP(!(AV(valves(open((S3)&if(present,(blood(
flows(from(atria(to(ventricle((
Diastasis(
o Slow(ventricular(filling((
o HR&dependent!!!!&
S1( AV(closing,(beginning(of(systole(
S2( Semilunar(closing,(beginning(of(diastole;(normal(
splitting(between(A2(&P2(during(inspiration(
(pathologic(widening(splitting=(pulmonary(stenosis,(
pathologic(reversal=aortic(stenosis)(
S3(( Turbulence(within(the(ventricle(during(early(diastole,(
rapid(filling,(normal(in(children(but(also(HF(
S4( Atrial(systole((“kick”),(Vent(resistance(to(filing(due(to(
decreased(compliance((HTN,(LVH)(
CARDIAC&PHYSICAL&DIAGNOSIS&&
&
)
Additional)Heart)Sounds) ! Consistent distance
• Murmur:(turbulent(flow(through(a(valve(
between R-waves
• Rub:(Inflamed(pericardial(sac(
• Gallop:(Triple(cadence(including(S1IS2IS4(
(
Normal((Regular)(Rhythm(
&
dad2165&
Wave forms are similar
Systolic&
Diastolic&
! Normal
sinus rhythm
Start)with)S1)
Start)with)S2)
Mitral/Tricuspid(
Early(( originates
Aortic/Pulmonary( in SA
since
Regurgitation(
Regurgitation(
#bloodflowprobs,(anemia,( node
Mid( Turbulent(flow(across(
!
Types&of&Murmurs&
Early(
Mid(
Late(
Pan(
thyrotoxicosis,(AORTIC(
STENOSIS((
Crescendo;(Mitral(Valve(
Late(
Prolapse((MVP)((
Vent.(Septal(defect(
(
Continuous(
Mitral(Stenosis(
(
! Ischemia is characterized
by inverted T-waves
(
Myocardial(Ischemia((TIwaves)(
! May vary from slightly
flattened to deep inversion
! Inverted T-waves may
indicate ischemia in the
absence of myocardial
infarction
! T-wave changes are most
pronounced in the chest
leads (V1 - V6)
&
Grading&Murmurs(
1.Very(faint((
2.(Quiet(but(easily(heard(
(
3.(Moderately(loud(
(
• Consistent(distance(between(R(waves(
• Wave(forms(are(similar((
• Normal(sinus(rhythm(since(originates(in(the(SA(node(
Myocardial
Ischemia
(T-waves)
AV(during(rapid(filling,(
4.(Loud((
5.(Heard(when(stethoscope(is(((
((((partially(off(chest((
6.(Heard(with(stethoscope((
((((entirely(off(chest(
(
(
•
•
•
•
Ischemia(is(characterized(by(inverted(TIwaves(
May(vary(from(slightly(flattened(to(deep(inversion(
Inverted(T(waves(may(indicate(ischemia(in(the(absence(of(
myocardial(infarction(
T(wave(changes(are(most(pronounced(in(the(chest(leads(
(v1Iv6)(
Distinguishing(Cardiac(v.(NonICardiac(chest(pain?(
(
ST Segment Depression
• General(Appearance(
ST(Segment(Depression(
o May(suggest(seriousness(of(symptoms((
ST segment depression
usually signifies
• Vital(signs(
subendocardial infarction
Stressed patients with
o Marked(difference(in(BP(between(arms(suggests(
ischemia may demonstrate
ST
Segment
ST
segment
depression Elevation
such as stress testing
aortic)dissection(
Subendocardial infarction
is usually non Q-wave
• Palpate(the(chest(wall(
(
May be sign of impending
myocardial infarction
o Hyperesthesia((hypersensitivity)(may(be(due(to(
• Signifies(subendocardial(infarction(
herpes(zoster( ! ST segment elevation gives
• Stressed(patients(with(ischemia(may(demonstrate(ST(
evidence of an acute
• Complete(cardiac(examination(
depression(during(stress(test(
o Pericardial(rub( myocardial infarction
• Subendocardial(infarction(is(usually(non(QIwave(
ST Segment Elevation
o Signs(of(acute(aortic(insufficiency(or(stenosis(
! ST segment rises above the
• May(be(sign(of(impending(myocardial(infarction(
o Ischemia(may(result(in(MI,(murmur,(S4(or(S3(
baseline with acute
(
• Determine(if(breath(sounds(are(symmetric(and(if(
infarction and later returns
ST(Segment(Elevation(
! ST segment
elevation gives
wheezes,(crackles(or(evidence(of(consolidation(
to baseline level
evidence
of
an
acute
(
! ST elevation require
myocardial infarction
(
enzyme studies and close
! ST segment rises above the
(
observation
baseline with acute
(
! Rule out pericarditis
infarction and later returns
&
(
to baseline level
• Gives(evidence(of(an(acute(MF((
(
! ST elevation require
• ST(segment(rises(above(the(baseline(with(acute(infarction(
enzyme studies and close
(
and(later(returns(to(baseline(
observation
(
• ST(elevation(requires(enzyme(studies(and(close(
! Rule out pericarditis
observation((
!
!
!
!
(
(
(
(
(
(
(
•
&
Need(to(rule(out(pericarditis((
Pulmonary**
Anatomical'planes:'Picture''
'
Basic*anatomy:*
Left'lung'='2'lobes'
' Upper'
' Lower'
Right'lung'='3'lobes''
' Upper''
' Middle'
' Lower'
Ribs:''
'''''1stB7th'attach'to'sternum'
'''''8thB10th'attach'to'costal'cartilage'above'them'
'''''11th'and'12th'ribs'='“floating'ribs”'
No'anterior'attachments'''
Fissures:'''''''''''''
'''''Both'lungs'='oblique'fissures'
'''''Only'right'lung'has'a'horizontal'fissure''
'
RATE*OF*BREATHING*
Normal'
RR'='12B20''
Tachypnea'
Hyperpnea'
(hypervent)'
Apnea'
Bradypnea'
'
Cessastion'of'
breathing'
Slow'breathing'
'
'
'
'
'
HISTORY/ROS*
History*of*Pulmonary*Disease:*
Cough'
Asthma'
Sputum'production'
DVT/PE'
Hemoptsis'
Cancer'
Dyspnea'
Occupational'Exposures'
Wheezing'
TB'exposure'
Cyanosis'
Sleep'patterns'
Sleep'apnea'
Recurrent'infections:'pneumonia'or'
'
bronchitis'
Respiratory'Assessment'Essential'Parameters'
' Rate:'12B20'breaths/min'
' Regularity:'steady'pattern'of'inspiration'and'expiration'
' ' Inspiration:expiration'ratio'='1:2'in'terms'of'length'
' Effort:'none'at'rest'
Recognize'airway'problems'that'indicate'respiratory'
distress'
*
Irregular*respiratory*pattern*
Significant'until'proven'otherwise'
* How'patient'compensates'for'the'inability'to'breathe:'
' ' ' *Upright'sniffing'–'head'tilted'back'
' ' ' *Tripod'–'leaning'forward'on'arms'(COPD)'
' ' ' *SemiBFowlers'
Lying'supine'worsens'their'respiratory'distress'
because'the'abdomen'pushes'up'into'the'lung'
space'making'it'more'difficult'to'breath''
*
BODY*TYPE*
* Barrel'shaped'–'increased'anterior'posterior'diameter'
' ' B'COPD'patients'–'this'is'secondary'to'air'trapping'
Pink'puffer'–'emphysema'is'primary'underlying'
pathology'
' Pink'complexion'–'less'hypoxemia'
Blue'bloater'–'chronic'bronchitis'is'the'primary'
underlying'pathology''
Cyanotic'because'of'worse'hypoxemia'than'pink'
puffers'and'therefore'get'bluish'lips'and'faces'
*
SEVERE*RESPIRTAORY*DISTRESS:*
Tripod'position,'cannot'speak'in'complete'sentences'
and'breathlessness'at'rest'
'
RESPIRATION'
Automatic,'controlled'in'brainstem;'mediated'by'
muscles'of'respiration:'diaphragm'and'ICM'
Accessory'muscles:'SCM,'scalenes,'and'abdominals''
BREATHING'
' Gas'exchange'of'O2:CO2'
' Controlled'in'medulla'
' Mediated'by'muscles'of'respiration'+'accessory'm.'
' Thorax'enlarges'by'75%'='diaphragm'descends'in'chest'
Upper'respiratory'passages:'Warmed,'humidified'and'
filtered'air'
Pathway**
' '
Larynx'
Thoracic'enlargement'decreases'
' '
'
Trachea'
'
'
When'inspiration'stops:'Chest'
Left'and'Right'Bronci'
'
wall'and'lungs'recoil'!'
'
diaphragm'rises'!'CO2'expired'
Bronchioles'
'
'
'
Right*main*bronchus*=*more*vertical*–*
Alveolar'duct'
'
if*something*is*aspirated*it*is*more*
likely*to*be*in*right*lung*
'
Alveolar'Sacs'
*
'
kdc2124'
Rapid'shallow'
breathing'
Rapid,'deep'breathing'
'
' 1'
EXAMINATION*TECHNIQUE*
Examine'posterior'chest'with'patient'upright;'anterior'
chest'with'patient'supine.'If'patient'cannot'sit;'roll'to'side'
PERCUSSION*SOUNDS*
Dullness'
Hyperresonance'
Lobar'pneumonia'
Hyperinflated'lung'
Pleural'effusion'
Emphysema'
Blood'(hemothorax)'
Pneumothorax'
Pus'(empyema)'
Bulla'
Fibrous'tissue'
Tumor'
BREATH*/*LUNG*SOUNDS*
Absent'
Complete'airway'obstruction'
Diminished''
Condition'that'lessens'airflow,'some'
portion'of'alveolar'tissue'is'not'
ventilated'
Adventitious'
Discontinuous'and'continuous;'
Usually*inspiratory'
Large'or'small'airway'obstruction''
Wheezes'
Continuous,'high'pitched'hissing'or'
shrill'quality'
Usually*expiration'
Rhonchi'
Low'pitched'and'snoring'sounds'
Suggest'secretions'in'large'airways'
Usually*expiratory'
Crackles'(rales)' High'pitched,'discontinuous'sound'that'
is'intermittent'nonmusical'and'brief'
End*or*inspiration**
Fine'or'course'
Suggestive'of'fluid,'atelectasis'
(alveolar'collapse),'or'pneumonia''
Stridor'
Inspiratory'wheeze'that'indicates'
partial'obstruction'of'larynx'or'trachea'
Pleural'rub'
Produced'by'the'rubbing'of'inflamed'or'
rough'pleural'surfaces'
Mediastinal'
Heard'over'precordium,'synchronous'
crunch'
with'heart'beat'and'due'to'mediastinal'
emphysema''
Egophany*
Transmitted'voice'sound'
Ask'patient'to'say'“ee”''
Normally'head'as'muffled'long'E'
If'“ee”'is'heard'as'“ay”'then'
Egophany'is'present'
Whisper*
Have'patient'whisper'“99”'
pectoriloquy*
Normal'='faint'and'indistinct'
Loud'or'clear'sounds'suggest'normally'
air'filled'lung'!'airless'
Fluid'filled'sound'is'louder'because'
sound'transmits'better'through'a'
solid'medium'
IMMENINET'RESPIRATORY'FAILURE'
Bradycardia'
Bradypnea'
Agonal'respirations'
Apnea'
Resonance'
Normal'
1. Inspect'
a. How'does'patient'look'
i. Flaring'nostrils'to'increase'O2'consumption'
with'minimal'effort'
ii. Pursed'lips'–'emphysema''
b. Rate,'rhythm,'depth'and'comfort'
c. Can'they'speak'full'sentences'
d. Examine'fingernails:'clubbing*=*COPD'
e. Shape'of'chest'
i. Barrel'chest'='COPD'patients''
ii. Pigeon'chest'='displaced'sternum'
iii. Funnel'chest'='depression'in'sternum'
2. Palpate'
a. Identify'tender'areas'
b. Assess'abnormalities'–'masses,'sinus'tracts'
c. Assess'respiratory'expansion'
d. Assess'tactile'fremitus'
i. Palpable'vibrations'transmitted'through'
bronchopulmonary'tree'to'chest'wall'
ii. Use'ball'or'ulnar'surface'of'hand'
iii. Ask'patient'to'say'“ninetyBnine”''
Fremitus**
Decreased'
Increased'
Soft'voice/thick' Consolidated'
chest'
Pneumonia'
Bronchial'
obstruction'
COPD'
Pleural'effusion'
Fibrosis'
Air'
Tumor'
'
3. Percuss'
a. Producing'audible'sounds'and'palpable'vibrations'
b. Determines'whether'tissues'are:'
i. AirBfilled'
ii. Fluid'filled'
iii. Solid'
4. Auscultate''
a. Listening'to'the'sound'of'breathing'
b. Listening'for'extra'sounds'
c. Egophany'if'abnormalities'are'suspected'
i. Increase'resonance'of'voice'sounds'heard'by'
lung'consolidation'and'fibrosis'
Tips:'always'listen'on'the'skin'!'not'clothing'and'avoid'
hair,'tell'the'patient'to'use'their'mouth'
Describe:'PITCH,'INTENSITY,'DURATION'
kdc2124'
'
' 2'
PHYSICAL DIAG 7: ABDOMINAL EXAM
Questions? Jenny Armstrong | jra2159
4 QUADRANTS: RU, RL, LU, LL
9 SECTIONS: Epigastric, Umbilical, Hypogastric/suprapubic
LOCATIONS OF ORGANS:
Normal liver - RUQ; often extends down just below the right costal margin
Stomach - epigastric
Gallbladder – RUQ; deep to liver
Appendix – RLQ
Spleen – LUQ
Kidneys – posterior, CVA angle (costo-vertebral angle), 12th rib
Abdominal aorta - pulsations visible/palpable in upper abdomen
TECHNIQUES
Drape – cover breasts and groin
Arms at side
Before exam, ask patient for painful areas and exam those LAST
Monitor exam by watching patient’s facial expressions
Warm hands, clean stethoscope
Inspect, Auscultate, Percuss, Palpate
INSPECTION (U COPS)
Umbilicus
o Hernia
Contour
o Flat, rounded, protuberant, scaphoid
o Bulging flanks
Ascites
o Suprapubic bulge
Distended bladder, pregnant
uterus, hernias
Symmetry
o Enlarged organs, masses
Pulsations
o Aorta may be visible
Obese
AUSCULTATION (DBB = DEEP BASS AND BEATS)
Diaphragm of stethoscope
Bowel sounds
o Clicks & gurgles 5-34/minute
o Diarrhea, intestinal obstruction,
paralytic ileus, peritonitis
Bruits
o Renal artery stenosis
o Vascular occlusive dz
PERCUSSION
Helps assess amount and distribution of gas
Identify masses
Estimate size of liver and spleen
Intestinal obstruction
o Protuberant
o Tympanic
Flank dullness
o Ascites
PALPATION
Light palpation
o Identifying abdominal tenderness,
muscular resistance
o Keep hand and forearm on a horizontal
plane, fingers together, flat
o Light, gentle, dipping motion
o Persistent involuntary rigidity (muscular
spasm)
Peritoneal inflammation
Deep palpation
o Delineate abdominal masses
o Identify any masses and note location,
size, shape, consistency, tenderness,
pulsation, mobility
o When difficult (as in obesity) use two
hands, one on top of the other
Disease
Hepatic disease
Intestinal obstruction
Renal disease
Appendicitis
Gallbladder Dz
Gastroenteritis
Findings
Palpation
Enlarged, hard
o cirrhosis
Ascites
Indicative of end stage liver dz
Distended, fluid filled abdomen
Shifting dullness
o In dependent areas
Fluid waves
Caput medusa
Periumbilical varicosities
(image to the right)
Spider hemangiomas
Bilious vomiting, nausea, pain
Distended abdomen
Abdominal radiographs
Air/fluid levels
Dilated loops of bowel
History of abdominal surgery, gastrointestinal cancer
Pyelonephritis
Costovertebral angle tenderness
Pyuria, fevers, elevated WBC
Urinary tract infection
Dysuria
o Burning on urination
Cystitis
Classically, pain begins near umbilicus and then radiates
to RLQ McBurney’s Point
Ruptured appendix
May lead to peritonitis
o Rigid abdomen with rebound tenderness
Elevated WBC, fever, nausea
May be elucidated by CT or ultrasound
Usually is clinical diagnosis
Differentiate from tubo ovarian abscess or ovarian torsion
Acute cholecystitis
Murphy’s sign
o Sharp increase in tenderness with a
sudden stop in inspiratory effort
Cholecystitis
Fertile, fat, forty, female
Usually viral, or “food poisoning
Self-limited
Focus on avoiding dehydration
Vomiting, diarrhea
Diffuse abdominal tenderness
Image
(caput medusa + ascites)
Colon cancer
Pyloric stenosis
Intussuception
Hernias
May present with intestinal obstruction
Family history
May be palpated on rectal exam
Occult bleeding on rectal exam
o Guaiac exam
Newborn
May be present at 3-7 weeks
Classically described as projectile vomiting
May palpate abdominal mass = OLIVE SIGN
Easily corrected with pyloromyotomy
Bowel telescopes itself
Infants
Colicky, intermittent pain
Classic sign is bloody diarrhea
Air enema, diagnostic and therapeutic
Incisional
Umbilical
Inguinal
Bowel contents extruding through muscular wall
defect
Emergency if incarcerated/strangulated
Usually gentle attempt at reduction by physician
If incarcerated and forced reduction
o Bowel contents may spill into abdominal
cavity, causing peritonitis
Surgical repair
PHYSICAL DIAG 8A: EVALUATION AND MANAGEMENT OF THE PREGNANT PATIENT
CLINICAL SX
ZEE BABY
DENTAL CARE?
1ST TRIMESTER
Cessation of menstrual flow
N/V (nausea/vomiting)
Breast enlargement
SUM: wanna vom, but at least you have
big boobs & don’t have your period.
Tendency toward:
o Fatigue
o Syncope
o Postural HYPOtension
FPS = feeling pretty shitty
(fatigue & fainting are common when
you have low BP)
Organogenesis
Highly sensitive to exogenous insult
May undergo morphologic changes
Rate of spont. abortion: 15%
Elective dental care best avoided
2ND TRIMESTER
Patient develops a sense of
well being
Fetal heart sound audible
Skeleton demonstrated
radiographically
Fetus less sensitive to
morphological changes
Changes in functional
capacity may occur (intellect,
reproduction? – not sure if
this is about mom or fetus)
Safest period to provide routine
dental care
Questions? Jenny Armstrong | jra2159
3RD TRIMESTER
Pronounced breast and
abdominal enlargement
Fetal movement and heart
sound felt
Fetal movement and heart
sound
Fetus becomes sensitive to
transplacental carcinogens
Initial period still good time to
provide routine dental care, but
after the second trimester,
elective dental care best
postponed.
ORAL MANIFESTATIONS
MYTH:
THEORY:
REALITY:
Tooth loss! “A woman loses a tooth for every baby she bears!!”
Calcium taken from mother’s teeth and given to fetus
Not possible. Calcium within the teeth is stable, crystalline form NOT accessible to rest of body.
Gingivitis
Pregnancy
Granuloma
ORAL
MANIFESTATIONS
Tooth Mobility
Perimyolysis
NINJA SLIDE! = Theories of gingivitis in pregnancy
1.
Hormones encourage proliferation of anaerobic organisms: Bacteroides intermedius & Prevotella. Results in: 1.
Adult periodontitis. 2. ANUG. 3 Localized juvenile periodontitis
2. Gingiva contain receptors for estrogen and progesterone. Elevated levels of these hormones inc prostaglandins, and
mediate inflammation. Progesterone also causes dilation of capillaries in gingiva which results in swelling.
3. Estrogen and progesterone alter structure of gingiva. Reduced keratinization, reduced protective barrier.
4. Estrogen and progesterone decrease performance of immune system.
(rare)
Gingivitis
Starts in 2nd month, peaks in 8th month, decreases in 9th month
May be severe irrespective of plaque amnt or OH habits
Hormone levels are much higher Gingival response to bacteria and plaque are exaggerated
Many theories how elevated levels of hormones promote gingivitis
Pregnancy Granuloma (pyogenic granuloma)
5% of pregnant women
Location: labial aspect of max ant region, usually in interdental papillae
Starts in area of inflammatory gingivitis, grows rapidly to <2cm
Color: Purplish red to deep blue, depending on vascularity
Regresses post-partum
Surgical excision often required for COMPLETE resolution either DURING or AFTER pregnancy
Before parturition, s/rp (scaling and root planing) and OHI to reduce plaque retention
Tooth mobility
Looser during pregnancy, disappears after parturition
Perimyolysis (rare)
Acid erosion of teeth caused by repeated vomiting of gastric contents assc w/ morning sickness or GERD
PHYSIOLOGICAL CHANGES: Cardiovascular, respiratory, hematological, GI, renal, immunologic
CARDIOVASCULAR
o Facilitates maternal and fetal xchange of respiratory gas, nutrients and metabolites
o Reduces impact of maternal blood loss at delivery (body compensates)
Dilutional anemia and decreased plasma colloid
o Hematocrit: 31-33% normal
o Hemoglobin: 11g/dL normal; If <11, iron deficiency anemia
o Dilutional anemia results from inc plasma volume, therefore, RELATIVE, not absolute decrease in Hb
Blood pressure: Systemic BP remains same, but decreased TPR, myocardial hypertrophy and inc total BV
TRIMESTER SPECIFIC OCCURENCES:
1st trimester
o Increased pulmonary blood volume
o Increased vascular markings and signs of enlarged heart on CXR
o Systolic murmur
Late pregnancy
o In supine position:
Enlarged uterus compresses the IVC
venous return and CO
Enlarged uterus compresses aorta
blood flow to common iliac
SUPINE HYPOTENSION SYNDROME
Lightheadedness, tachycardia, loss of consciousness
If lying flat too long, symptoms result from decreased blood return
After the 1st trimester, avoid supine position for more than a few minutes
Aortocaval patency regained by placing pt in left lateral position
SUM: You have increased plasma volume, which increases the total blood volume. Due to the inc plasma volume, pregnant ladies
may have dilutional anemia. Despite this increase in BV, TPR is decreased, so systemic BP is the same. There are some changes that
occur throughout pregnancy, such as in the first trimester where SV, HR, and CO are increased. This can result in inc markings and
signs of an enlarged heart as well as a systolic murmur. Avoid being supine after 1st trimester to prevent compression on the IVC and
aorta. Pregnant women are advised to lay on their left side, instead.
FUN FACT: In yoga, they tell you to roll to your right side after shavasana, but if you are pregnant they will tell you left side. I asked about this once
after a class since left side seems more natural to me. Read more: http://blog.lululemon.com/why-the-right-side/
RESPIRATORY
1. Changes in O2 and lung capacity:
o
Total lung capacity decreases only slightly (appx 5%)
o
FRC ERV RV
O2 reserve (FRC = functional residual capacity, ERV = expiratory residual v, RV = residual v)
o Two images. The one below is the one he provided, and the one at the bottom explains it better I think.
2.
3.
Changes in airway resistance:
o Capillary engorgement and swelling of lining of nose, oropharynx, larynx, and trachea
Results in:
Nasal congestion, voice change, upper respiratory infx
May be exacerbated by fluid overload associated with preeclampsia (high BP when preg)
Manipulation of airway can result in PROFUSE bleeding as a result of cap
Endotracheal intubation difficult
o
Airway resistance
Hypoxia
o During apnea/after induction of GA (general anesthesia) Hypoxia and hypercarbia due to FRC
o Supine position aggravates hypoxic episodes
Changes that occur during pain/labor
o
HYPOcarbia and alkalosis
Results in:
o
o
left shift of O2 dissociation curve
Therefore, allow adequate preoxygenation for 32 or apply
(VC breaths = amnt of air a person can expel after maximum inhalation) (vital capacity)
HEMATOLOGIC
Hypercoaguable state: INCREASED I, VI, VIII, IX, X, fibrinogen, and DECREASED fibrinolytic activity
Therefore, INCREASED risk of clots, DVT, and PE
o 1-5x higher risk of DVT and PE in 1st trimester than a person who is not preggers
o Supine position avoided: Compression of the IVC increases venous stasis, and risk of clot formation
**Platelet levels = normal**
SUM: In a hypercoaguable state, so you have an increased risk of clots, DVT, and PE despite normal plt levels. Avoid supine posish.
GASTROINTESTINAL
peristalsis (may vomit or aspirate gastric contents – so gross to think about)
gastric motility and absorption associated with delayed gastric emptying which can lead to reflux
o Mechanism: progesterone inh motilin
o Reflux more prevalent later in pregnancy
placental gastrin
stomach pH
o All pregnant women are considered to have a full stomach
o Antacids (sodium citrate, bicarbonate) are used to decrease reflux and acidity of contents being refluxed
As a result of all of the above, anesthesia is more hazardous. Regional anesthesia and blocks > general anesthesia
SUM: Less esophageal tone, peristalsis, and gastric motility results in inc stomach volume and lower pH. Take antacids to control
stomach acidity, vomiting, and GERD. Caution with anesthesia, and use localized blocks rather than general anesthesia.
RENAL
Progesterone dilates ureters, renal pelvises and calyces
This
(not in lecture but this likely contributes to why women have to pee a lot when preggo)
o results in
increased creatinine clearance, mild glycosuria, and proteinuria
increased filtered Na, but tubular absorption increased due to aldosterone via RAS
Enlarging uterus can compress ureters as they cross the pelvic brim increased dilation by obstructing flow
o Results in:
increased risk of UTI’s
urinary stasis
asymptomatic bacteriuria pyelonephritis
In supine position: RBF
GFR
urine output
Placement of urinary catheters contraindicated
SUM: Hormones, like progesterone, dilate your ureters, renal pelvis and calyces resulting in increased GFR and RBF. The uterus
compresses against the ureters and can obstruct flow, making pregnant women susceptible to infection of the urinary tract and
kidney. Avoid supine position, because this compresses the vascular system, resulting in decreased blood flow, GFR, and urine
output (even though pregnant women have to pee a lot at night, likely due to uterus pushing on bladder). Don’t use catheters.
IMMUNOLOGIC
Suppression decreased chemotaxis and NK Cells
Neutrophilic leukocytosis
-
SUM: Your immune system is suppressed, but you have elevated neutrophils.
3
)
NUTRITION, XRAYS, SURGERY AND DRUGS
MATERNAL NUTRITION
Inc need for Vit A, folic acid, Vit D, calcium phosphorus, iron, magnesium and zinc
WHY? Inc red cell mass, maternal skeleton, megaloblastic anemia
Inc caloric and protein intake to prevent LBW
DENTAL RADIOGRAPHY:
Not contraindicated, but especially avoided during 1st trimester
o If someone comes in with a broken tooth or something really wrong, take an xray
Use lead of lead apron, rectangular collimation, E-speed films, or faster is BENEFICIAL
in utero
o Fetus is exposed to more radiation naturally
BW, pan, selected periapicals recommended
SURGERY
Detailed questionnaire of pregnancy state (how far along, any complications, who is OB-GYN?)
If unsure, tx should be delayed and pt referred to her physician to confirm
Urgent/emergency situation: always ask when last menstrual cycle was
THERE IS NEVER A TOTALLY SAFE PERIOD TO UNDERGO OS TX DURING PREGNANCY.
Fetus is MOST susceptible to harmful effects of teratogens, carcinogens, and maternal stress during 1st and 3rd trimester.
Most surgeries are deferred to 2nd trimester.
Orthognathic/cosmetic procedures
o All elective tx delayed until after delivery
o Initiation of tx not until return of maternal normal state of health
Maxillofacial infections
o Not logical to delay tx
o Remember hormonal and vascular changes
o Systemic effects of infx harmful to both mother and fetus
o Disruption of normal physical barriers to bacterial infx lowers host defense
o Neutrophil chemotaxis and adherence, cell mediated immunity, and NK cell activity all DECREASED
DRUGS
A = no risk in controlled human studies
B = no risk in animal studies
C = teratogenic in animal studies
D = positive evidence of human fetal risk; benefits may outweigh the risks if life threatening situation
E = positive human fetal risk
LOCAL ANESTHETICS (see table)
Safe
More rapid onset and longer duration of action
Avoid significant dose of epi to preserve placental perfusions
Use lidocaine whenever you can without epi and then use half a carpule of one with epi to get proper anesthesia
GENERAL ANESTHETICS (see table)
Nitrous oxides
o One of most common inhalation agents used by oral surgeons
o Associated with spontaneous abortion rate in OR personnel with chronic exposure (DNA synth)
Eg. Anesthesiologists who are always around it!
o Toxic effect on hematopoietic tissue in humans
NSAIDS
Constriction of ductus arteriosus fetal pulmonary hypertension
3rd trimester: inhibition and prolongation of labor and reduction in amniotic fluid volume
Should be avoided in 3rd trimester or near delivery!
Acetaminophen is the ‘go to’ choice for pregnant pt who need pain mgmt.
Category
Local anesthetics
Analgesic agents
Drug name
Xylocaine (lidocaine)
Side effects/evidence
Category B
compatible with breast feeding
Bupivicaine (Marcaine)
Category C
Hypotension, cardiac arrest, convulsions
Category C
Category C
ADME similar in pregnancy and nonpregnancy states
Anemia, antepartum/postpartum
hemorrhage, inc gestation, labor
1 w before delivery: intracranial
hemorrhage in premature infant
Congenital abnormalities
Poor maternal and fetal weight gain
Neonatal addiction
No congenital defects
No depression of RR, HR, or BP
Respiratory depression
Therapeutic effects on mother/fetus
Not associated with congenital defects
Septocaine (Articaine)
Mepivacaine (Carbocaine)
Acetaminophen
Aspirin
Codeine
Morphine
Fentanyl
Antibiotics
Penicillin
Cephalosporin
Erythromycin
Clindamycin
Aminoglycoside
Tetracycline
Metronidazole
Sulfonamide
Anxiolytic agents
Diazepam
General
anesthesia
Nitrous oxide
Halogenated agents
eg. Halothane, Isoflurane,
enflurane, desflurane
Fetal toxicity
Nephrotoxicity
Permanent discoloration of fetal teeth
Maternal liver toxicity
Congenital defects
Studies show its carcinogenic in rodents
When administered close to delivery, persist in
fetal blood for 2-3 days after birth.
May result in jaundice, hemolytic anemia, and
kernicterus in newborn.
Cleft lip/cleft palate?
Cranial anomalies?
One of most common inhalation agents used
Toxic effect on hematopoietic tissue in human
Assc w/ spont abortion rate in OR personnel
with chronic exposure.
Safe in low-moderate doses
High doses maternal HYPOtension,
placental HYPOperfusion, fetal asphyxia
Contraindicated or choice?
Local anesthetic of choice,
give w/o epi + half a carpule
with epi.
Drug of choice
Contraindicated
Contraindicated
Pens are safe!
Category D, so don’t use
unless absolutely necessary
Contraindicated
Controversial
AVOID DURING 3rd trimester
NOT recommended
Safe in low-moderate doses
REMINDER:
DRUGS
A = no risk in controlled human studies
B = no risk in animal studies
C = teratogenic in animal studies
D = positive evidence of human fetal risk; benefits may outweigh the risks if life threatening situation
E = positive human fetal risk
QUESTIONABLE OR CONTRAINDICATED? SAM D. CAT
S = sulfonamide
D = Diazepam
A = Aminoglycoside
M = metronidazole
C = codeine
A = Aspirin
T = tetracycline
PHYSICAL DIAG 8b: EXTREMITIES
Questions? Jenny Armstrong | jra2159
2 PARTS: Inspect & Palpate
INSPECT
PALPATE
Pulse – note rhythm and rate
o Radial, ulnar, carotid, brachial, femoral,
popliteal, posterior tibial, dorsalis pedis
o If not palpable, Doppler ultrasound
Skin
o Cool vs. warm
o Dry vs. moist
o Coarse vs. smooth
Capillary refill
o May be due to heart or vascular probs
Sensory
o Diabetic neuropathy (chronically, DM has not
been well controlled)
Eh sun or Sun eh
Edema
o Hepatic dz, venous incompetence, fluid
overload, CHF
Hair
o Thin or missing with poor perfusion
Skin
o Course or smooth
Ulcers
o Arterial insufficiency, diabetes
Nodular
o RA, gout
INSPECT
Lecture focused on EDEMA for the inspect section
EDEMA
Compare one side of the foot and leg with the other
Size, prominence of veins, tendons, bones
Check for PITTING EDEMA
o Dorsum of foot
o Behind medial malleolus
o Up the shin
Think of causes:
o Deep vein thrombosis
o Chronic venous insufficiency from prior DVT
OR incompetence of the venous valves
o Lymphedema
Pitting Edema
A couple of facts re: Edema
1. Edema is a common physical exam finding.
2. Pitting edema is extravasation of fluid from blood vessels
or lymphatic vessels.
Pop Quiz:
Q: What is a common cause of chronic venous insufficiency?
A: 1. Pregnancy
-causes dilation of the veins and can lead to venous
insufficiency
2. Lymphedema
Lymphedema
Venous Stasis Ulcer
Red mass, erythema in the area of the
shin by malleolus
1.
2.
Push finger if pit persists, its
pitting edema.
Can be classified as 1+, 2+, 3+
depending on how long it takes
before it is normal.
Can be unilateral or bilateral
INSPECT ALL EXTREMITIES AND LIMBS
Note:
1. Size, symmetry, and any swelling
2. The venous pattern and any venous enlargement
3. Any pigmentation, rashes, scars, or ulcers
4. Color and texture of skin, color and texture of nail beds, and the distribution of hair on
limbs and fingers/toes
TX: Start by cleansing out ulcer and
then put compression stocking to
treat cause (insufficiency of vein
causing back up of fluid and
ulceration). Can correct by self if
correct cause, or may be corrected
surgically by stripping out the veins
that are causing the problem.
PALPATE – PULSE, SKIN, CAPILLARY REFILL, SENSORY
PERIPHERAL ARTERY SYSTEM
Used to measure upper
extremity BP
If normal femoral and popliteal,
and decreased foot pulses,
indicative of occlusive disease
often seen in diabetes. If
occluded here, everything below
is also occluded.
Commonly used for pulse
Important to palpate foot pulses for occlusive disease,
commonly seen in diabetes
PERIPHERAL VASCULAR SYSTEM: PULSE PALPATION
ARMS
Radial pulse – the radial pulse is felt on the wrist, just under the thumb (proximal)
Brachial pulse – 3 cm above the medial epicondyle between biceps and triceps groove
o Palpate before take BP so know where to place the stethoscope
Anecdotes: The radial pulse is felt for a count of (30x2 or 15x4). Note if regular, thready, irregular, etc. If irregular, note
irregularity. Irregularly irregular = afib. All others use ECG. Normal BP 120/80.
LEGS
Femoral – press deeply below the inguinal ligament, midway between the anterior and superior iliac spine and symphysis
pubis. Use two hands if necessary as in a deep abdominal exam.
Popliteal – Pt knee flexed. Use two hands in the midline of the popliteal fossa. Often difficult to find
Anecdotes: Widened femoral or popliteal pulse is suggestive of an aneurysm (not common). Lessened pulse is indicative of
atherosclerosis and would be often accompanied by postural skin color changes.
FEET
Dorsalis Pedis Pulse – dorsum of foot just lateral to the extensor tendon of the great toe. (Between 1st 2nd second toes, but a
bit higher up on the foot)
Posterior tibial pulse – slightly below the medial malleolus of the ankle.
Anecdotes: Decreased foot pulses with normal femoral and popliteal suggests occlusive disease in the lower popliteal or
branches – often seen in diabetes. If you cannot palpate a pulse, get a Doppler. It is more sensitive at taking the pulse. If it is
not “Dopplerable”, there is no flow through the artery and you can investigate further by going up the vascular system. So, if
there is nothing at dorsalis, then check the popliteal, and if there is a pulse there, you know block is between these two. If
there is no pulse at popliteal, then continue up and so on.
GRADING PULSES
3+ Bounding
2+ Brisk, expected (normal)
1+ Diminished, weaker than expected
0 Absent, unable to palpate
PERIPHERAL VASCULAR EXAM
TEMPERATURE
Use back of fingers
Bilateral coldness:
o Due to cold environment or anxiety
Unilateral coldness:
o When associated with other signs, suggests arterial insufficiency
ALLEN TEST
Examine for collateral perfusion between the radial and ulnar arteries (normal finding)
If no collateral perfusion, heightened risk of ischemic hand with interventions such as arterial blood draws
HOW TO DO THE ALLEN TEST
1. Ask pt to make a tight fist with one hand for appx 30 sec
2. Compress both the radial and ulnar arteries firmly between your
thumbs and fingers
3. Ask the pt to open their hand into a relaxed, slightly flexed
position. The palm is pale. Extending the hand fully may cause
pallor and a false positive.
4. Release pressure in the ulnar artery. If the ulnar artery is patent,
the palm flushes within about 5 seconds.
5. You can also check patency of the radial artery by releasing the
radial while compressing the ulnar.
6. Interpreting results: persisting pallor indicates occlusion of the
ulnar artery or distal branches. May be a sign of inadequate
collateral circulation and you don’t want to do whatever
intervention/blood draw you were planning on doing.
ANKLE/BRACHIAL INDEX
Ratio of systolic BP of ankle:arm
o Normal > 1.0
o Claudication 0.8-1.0
o Ischemic rest pain <0.8
compromised flow to foot
common in many severe dz’s
PERIPHERAL ARTERIAL INSUFFICIENCY
Claudication: pain that worsens with movement, relieved by rest
Treatment: initially medical, use anticoagulants (ASA, Plavix), exercise,
surgery.
Surgical options: Arterial bypass, shunting
**COLD FOOT = EMERGENCY**
DEEP VEIN THROMBOSIS = clot in deep veins
Classically associated with extended hospitalization, bedridden patients, hypercoagulopathies, cancer, international flights
Calf pain upon dorsiflexion (Homan’s sign) may be present (knee is extended, test has fallen out of favor)
Asymmetric edema
May embolize to lungs, brain
Treatment is anticoagulation, Greenfield filter (not commonly used, inserted in IVC, indicated if can’t take antiocoags)
Tests not mentioned that are more favorable and commonly used: D-dimer, ultrasound
HOW TO MEASURE DVT
Measure diameter in both legs to ID edema and follow course
Measure at different locations
o Eg. forefoot, smallest circ above ankle, largest circ at calf, midthigh
Interpreting results: A difference of +1 cm at ankle or +2 cm at calf is unusual
SUPERFICIAL VEINS (image to the right): Greater saphenous, lesser saphenous so technically
Not a “deep vein thrombosis” since it is a superficial clot.
HEAD, SHOULDERS, KNEES AND TOES, KNEES AND TOES! KNEES AND TOES (AND WRISTS AND BACKS AND LEGS!)
KNEE EXAM
1. Range of motion
a. Active and Passive
b. Extension (0 to -10) (may not get any extension unless upper flexible and athletic)
c. Flexion (100 to 150 degrees)
2. Check for effusions
a. Apply pressure on the suprapatellar pouch
b. Tap and watch/feel for fluid wave
3. Tears + Tests
DRAWER TEST: pt is supine with hips flexed to 45 deg, knees flexed to 90, feet flat on table. Tibia drawn fwd and back.
a. Anterior drawer sign: A forward jerk showing the contours of the upper tibia is a POSITIVE anterior drawer sign
i. POSITIVE ANTERIOR DRAWER SIGN = ACL TEAR (more common than PCL tear) (goes too far forward)
b. Posterior drawer sign: Tibia goes too far back and there is excessive posterior movement
i. POSITIVE POSTERIOR DRAWER SIGN = PCL TEAR (more rare) (tibia goes too far back)
VARUS TEST: LCL (VaRus = LateRal)
VALGUS TEST: MCL
ADDUCTION TEST: LCL
ABDUCTION TEST: MCL
These tests are similar to the drawer test, but instead of going forward and back, abduct/adduct with pressure at
medial thigh with one hand and use the other hand to apply OPPOSITE pressure from the lateral ankle with the
other hand. Eg. If you are abducting at the medial thigh (outward pressure), then adduct at lateral ankle (inward
pressure).
PS. Where’s Dr. Bernd when you need her to explain something.
ABDUCTION TEST (I think): MCL
KNEE ANATOMY:
ADDUCTION TEST (I think): LCL
CARPAL TUNNEL SYNDROME
Pain and numbness of the hand, especially at night, suggest compression of the median nerve in the carpal tunnel.
o Recall: The median nerve runs through carpal tunnel and gives sensation to the first 3.5 fingers.
o If compressed numbness
Two tests: Phalen’s test + Tinel’s sign
PHALEN’S TEST
Flex wrists for 60 seconds in an upside down prayer. If elicits
pain or tingling, it is a positive Phalen’s test.
Phalen’s prayer pain
TINEL’S SIGN
Percuss wrist over the course of the median nerve. If elicits
symptoms of pins and needles or tingling, then positive test.
Tinel’s tingles thumbs (and along nerve)*
LAST LEG (phew!) My neck…my back...my lala and my…
LOW BACK PAIN
Test for low back pain with radiation into the leg: Straight leg raise
Anecdotes: Low back pain is very common – we do this test to rule out a heniated disc.
HOW TO DO THE STRAIGHT LEG RAISE
1. Patient supine
2. Raise leg until pain, then dorsiflex the foot
RESULTS: Sharp pain radiating down the leg in L5/S1 distribution suggests tension or compression on nerve roots (often caused
by a herniated lumbar disc)
LECTURE 9: ELECTROLYTES & ACID BASE BALANCE
Questions? Jenny Armstrong | jra2159
HOMEOSTASIS
Stable internal environment
Proper fluid balance, electrolyte levels, and acid-base balance
Many body systems involved in this process
o Kidneys, GI tract, lungs, skin, nervous system
Illness, injury, surgery and treatments can disrupt fluid, electrolyte, and acid base balance
BODY FLUID COMPOSITION
Water, proteins, electrolytes
Water 60% of body weight
o Varies with age, gender, body mass
Proteins
o Albumin, globulin, fibrinogen
o Albumin helps hold water/plasma in
Electrolytes
o Substances which acquire a “charge”
when dissolved in H2O
o Help with fluid shifts
BODY FLUID COMPARTMENTS
Intracellular (2/3)
o Inside the cells – 40% of body weight
Extracellular (1/3)
o Outside the cells – 20% of body
weight
o Interstitial – tissue space – 15% of bw
o Plasma – in blood vessels – 5% of bw
Transcellular – trace amnts - CSF, lymph, joint
fluid, pleural fluid, etc. –
REGULATORS OF FLUID BALANCE: Thirst (dipsogen), ADH, aldosterone, lymphatic system, kidneys, RAAS, ANP
ADH Secreted from post pituitary. Hold water because sensing you are volume depleted. Sensor is in the
carotid bodies and macula densa. This will also tell you that you are thirsty and should drink more fluid
ANP Vasodilator, makes you urinate
I’S AND O’S – AVERAGE ADULT (salt will change this balance)
Intake
Output
1300 cc = ingested H2O
1500 cc = kidneys
1000 cc = ingested food
600-900 cc = skin (insensible); sensible varies
300 cc = metabolic ox
400 cc = lungs
100 cc = GI tract
2600 cc = TOTAL INTAKE
2600-2900 cc = TOTAL OUTPUT
ALTERATIONS IN FLUID BALANCE
a. Why do fluids relocate?
1. Changes in hydrostatic pressure
pushing force of water on walls
2. Changes in oncotic pressure dependent on osmolality
3. Filtration
b. Edema (next page)
EDEMA
Expansion of the interstitial fluid volume
o Fluid moves from vascular space to interstitium
Third space fluid shifts
o Skin
o Peritoneum
o Pleural or pericardial
o Pulmonary edema
To assess clinically: +2-3 liters
ANECDOTES: You need extra fluid to get
puffy. If you give a hypo-osmolar solution, it
will flow INTO the tissues.
MECHANISMS LEADING TO EDEMA (hydrostatic pressure + oncotic pressure)
MECHANISM:
1. Decreased Colloid Osmotic Pressure (COP)
a. Low levels of protein (esp albumin) in blood
b. Less inward “pulling” force for fluids
c. Fluids move into tissues
d. Result = low plasma volume
e. Kidneys respond
f. Edema worsened until protein problem
corrected
2. Increased Capillary Hydrostatic Pressure
a. Elevated pressure in veins “pushes” fluids out
and keeps fluids from moving back in
b. Volume overload
c. Pump (heart) failure
3. Increased Capillary Permeability
a. Fluids leak out of capillaries
b. Direct damage to blood vessels
c. Inflammatory response
4. Obstruction of Lymphatics
a. Lymphatic system removes excess proteins
and fluids from tissues
b. If lymphatic system is blocked, protein and
fluid remain in tissue
CLINICAL REASONS:
Liver failure (body’s “protein factory”)
Protein malnutrition (decreased intake of protein)
Nephrosis
o ‘leaky’ kidneys due to dz
o Protein usually NOT lost in urine
Burns
o Proteins lost to environment)
CHF
Local venous obstruction
Prolonged standing
Pregnancy
Burns
Allergic rxns
Inflammation
Sepsis
Surgical removal of LN (prevent spread of cancer)
Radiation therapy
Trauma
Filariasis
MANIFESTATIONS OF EDEMA
Distribution
o Localized – where?
o Generalized
o Anecdotes: Swelling drains towards gravity. Characterize it as asymmetrical or post-surgical, or infx. If
you sleep on one side, it will go towards that side. Otherwise, it will go toward feet and legs or hands.
Pitting vs. non pitting
o Put finger in and it stays depressed
o If it is in tissue and you press, the tissue will collapse
Stasis dermatitis
o skin changes that occur as a result of stasis/blood pooling from insufficient venous return
Brawny edema
o common in non-pitting edema; brawny color from lysed RBC’s, skin atrophies, necrosis, dry scaling
pruritic skin
WATER DEFICITS AND EXCESSES
Que es esto?
Causes
Clinical manifestations
Hypovolemia
Depletion of extracellular volume
H2O and electrolytes lost in = proportion
Eventual depletion of cellular fluid
Decreased fluid intake
Hemorrhage
Diarrhea
Excessive sweating (‘diaphoresis’)
Vomiting
DM
Excessive wound drainage
Weight loss
Tachycardia
Thirst
Dry mucous membranes
Orthostatic hypotension
Poor skin turgor
Hemoconcentration
Concentrated urine
Decreased level of consciousness
Flat neck veins
Hypervolemia
Excess extracellular volume
Water and electrolytes gained in = proportion
Circulatory overload
Too much IV fluid
CHF
Renal failure
Liver failure (ascites)
Too much aldosterone
Weight gain
Ascites (fluid in abdomen)
Hypertension
Hemodilution
SOB
Distended neck veins
ALTERATIONS IN ELECTROLYTE BALANCE
MAJOR ELECTROLYTES
Electrolytes:
o Cations: Na+, K+, Ca++, Mg+
o Anions: HCO3-, Cl-, PO4ICF: K+ is the major electrolyte IN the cells
ECF: Na+ is the major electrolyte OUTSIDE the cells
NORMAL ELECTROLYTE LEVELS
INTRACELLULAR (can’t usually be measured directly)
EXTRACELLULAR (measured in pt’s blood)
Na = 10 mEq/L
K = 140 mEq/L
Ca = 10 mEq/L
Mg = 40 mEq/L
Cl = 4 mEq/L
PO4 = 100 mEq/L
Na = 135-145 mEq/L
K = 3.5-5.0 mEq/L
Ca = 9 – 10 mEq/L
Mg = 1.2 -2 mEq/L
Cl = 90-110 mEq/L
PO4 = 2.0-4.5 mEq/L
OSMOLALITY
Concentration of particles in solution
Normal serum (blood) osmolality 275-295 mOsm/L (normal osmolality to maintain oncotic pressure)
o Iso-osmolar – same osmolality as blood and body fluids
o HYPERosmolar – greater osmolality than blood and body fluids
o HYPO-osmolar – lower osmolality than blood and body fluids
SODIUM: Na+ = 135-145 m mEq/L
Major cation of the ECF
Essential for proper neuromuscular function
Regulates osmotic pressure
o Close relationship between sodium and water balance
Obtained through diet
Hyponatremia (Na + < 135 mEq/L)
Hypernatremia (Na+ >145 mEq/L)
Can be due to:
Can be due to:
1. Loss of sodium OR
1. Decreased H2O intake
2. Gain of water
2. Excess water output
Cells swell because water moves into cells to
3. Excess sodium intake
equalize the concentration
Fluid moves out of cells, causing them to shrink
Causes
Giving the pt IV fluids that don’t have Na
Too little secretion of ADH
Heart failure - weak pump leads to sluggish
Excess administration of Na, either in diet, or by
blood flow and poor filtration dynamics
concentrated by IV solutions with NaCl or
NaBicarb, etc.
Burns – leads to loss of body fluids
Decreased oral intake of water
Psych disorders – pt obsessively drink H2O
Elevated levels of aldosterone
Excessive sweating followed by drinking plain
H2O
Over-secretion of ADH
Clinical
Cell swelling
Thirst
manifestations
Swelling of brain cells, cerebral edema*
Nausea and vomiting
Neurologic signs and symptoms
Shrinking of brain cells leading to:
Headache, stupor, coma
Irritability, lethargy, weakness, convulsions,
Peripheral and pulmonary edema
coma, and if xtreme, death
Nausea and vomiting
Low BP
Muscular weakness
Decreased urine output
Elevated BP
Elevated urine output
* Common in elderly pt where kidney’s not working well and not eating properly. Can result in neurologic consequences – confused,
weak.
Que es esto?
POTASSIUM (K+ = 3.5 – 5.0 mEq/L)
Anecdotes: If K too high or low, it can kill you.
Major intracellular cation
Heart needs Na/K to fire, and if K is out of
Imp for skeletal/cardiac muscle activity and neuromuscular excitability
whack, causes arrhythmia. It is critical to
Important for maintaining acid-base balance
monitor in renal pts.
Obtained through diet
Excreted through kidneys
Hypokalemia (K + <3.5 mEq/L)
Hyperkalemia (K+ > 5 mEq/L)
Que es esto?
Affects every body system
Main effects are seen in cardiovascular system
Human body very good at excreting K, but not
Effects can be life threatening
conserving.
Usually due to kidney problems
Depletion can occur in a matter of days if dietary
intake is inadequate (imp in hospitalized pts)
Causes
Poorly functioning kidneys
Renal failure
Loss through GI tract (N/V, laxative abuse)
Hemolysis of RBC’s (K in cells released in blood)
Certain meds (diuretics, esp loops, like Lasix)
Under-secretion of aldosterone
Excessive sweating
Metabolic acidosis (High H+ Kidneys excrete H+
instead of K+ and accumulates in blood
Poor oral intake
Certain meds
Excessive secretion of aldosterone
Clinical
Muscular cramping
Cardiac dysrhythmias
manifestations
Fatigue, weakness
Cardiac arrest
Disruption of cardiac rhythm
Muscle weakness
Vomiting
Numbness and tingling of face, feet, hands
Decreased intestinal paralysis
Nausea and diarrhea
Low BP
Dilute urine
CALCIUM (Ca2+ = 9.0 – 10 mg/dL)
Along with phosphorus, mainly found in bones and teeth
99% of body’s Ca2+ in bones and teeth
1% circulating in blood
o 45% of that bound to protein – not “free”
o 50% is ionized – active
o 5% complexed with other substances
Needed for cell membrane integrity, blood clotting, and muscle contraction
Que es esto?
Causes
Clinical
manifestations
*Trousseau
**Chvostek
Hypocalcemia (Ca++ <9 mg/dL
Effects usually seen in muscular system and cardiac contractility.
Need to check pt’s protein levels before assuming calcium levels are altered, since so much Ca is
bound to protein.
Hypoparathyroidism, elevated PO4, low Mg (PTH)
Too little vit D or Ca in diet
Low protein
Transfusion of blood w/ citrate added (binds Ca)
Alcohol abuse, malnutrition, altered abs in GI
Muscle spasms, inc muscle excitability, tetany
Positive Trousseau* and Chvostek signs**
Intestinal cramping and diarrhea
Cardiac changes – decreased contractility of heart m.
latent tentany – looks like someone holding a napkin and dangling it. Take a BP cuff, inflate over systole, and hold for 3 min.
abnormal rxn to stimulation of facial nerve. Tap along CN7.
PHOSPHATE (PO4- = 2.5 – 4.5 mg/dL)
Along with calcium, important for bone formation
o 85% in bone
o 15% intracellular
Obtained from diet – dairy, meat, eggs
Needed for function of muscle, RBC’s, formation of ATP, and maintenance of acid/base balance
Mainly excreted by kidneys
Que es esto?
Causes
Clinical
manifestations
Hypophosphatemia (PO4- <2.5 mg/dL
Decreased intestinal absorption
Increased urinary excretion
Enhance uptake into bone
Overuse of antacids which bind phosphate
Burns
Alcohol withdrawal
HYPERparathyroidism
Bone pain
Anorexia
Muscle weakness
Tremors, reflexes, confusion, seizures, coma
Hyperphosphatemia (PO4- > 4.5 mg/dL
Closely related to Ca levels
Rarely occurs if kidneys are functioning properly
Renal failure
HYPOparathyroidism
HYPERthyroidism
Some meds – chemo, laxatives with
phosphate (Fleets phosphosoda)
Low serum Ca levels in response to elevated PO4
Kidneys stones composed of Calcium Phosphate
Tingling of mouth, fingers, and toes
Cardiac rhythm disturbances
CHLORIDE (Cl- = 98-106 mEq/L)
Main anion of the ECF
Amount of chloride closely matches amnt of Na (NaCl)
Amount of chloride inversely related to bicarbonate levels
Coupled with H+ in the stomach to form HCl
Que es esto?
Causes
Clinical
manifestations
Hypochloremia (Cl < 98 mEq/L)
Most commonly seen in patients exhibiting
metabolic alkalosis
Hypercholermia (K+ > 110 mEq/L)
Usually associated with hypernatremia
Commonly seen in dehydrated pts
Loss through GI tract: N/V, diarrhea,
nasogastric suctioning
Burns
Fever
Use of meds like diuretics
Hyperexcitability of the CNS
Tremors
Metabolic alkalosis
Manifestation of hyponatremia concurrently
MAGNESIUM (Mg+ = 1.5-2.5 mEq/L)
Mainly found in bones and ICF
Important for enzyme systems
Important for synthesis of proteins, DNA, and RNA
Needed for normal cardiovascular function
Closely related to Ca and K levels
Causes
Clinical
manifestations
Hypomagnesemia (Mg + <1.5 mEq/L)
Poor absorption from GI tract
Diarrhea
Renal failure
Alcoholism
Malnutrition
Drugs
Muscle tremors and tetany
Anorexia, nausea, vomiting
Hyperactive reflexes
Difficulty swallowing
Numbness/tingling of extremities
Hypermagnesemia (Mg+ > 2.5 mEq/L)
Renal failure
Dehydration
Intake of medications containing Mg (milk of
magnesia)
Lethargy and drowsiness
Flushing of skin
Low BP
Nausea and vomiting
Decreased HR
Slurred speech
ALTERED ACID-BASE BALANCE
HOMEOSTASIS
Balance of acids and bases
Stabilization of H+ ion concentration
Metabolic and respiratory processes work together
Anecdotes: K is a cation. If excess K outside of
cell, all of the sudden H+ is pushed into cell and
acid-base balance is more basic in ECF. Na is an
electrolyte. Look at compensations between
respiratory and metabolic for final exam!
The normal pH of blood is 7.35 to 7.45. This is a slightly ALKALINE pH.
ACIDOSIS
pH < 7.35
Results from high H+ concentration or low
bicarbonate concentrations
Due to
o Excessive acid
o Not enough base
ALKALOSIS
pH > 7.45
Results from low concentration of H+ or high
concentration due to bicarbonate
Due to
o Excessive base
o Not enough acid
ACIDS AND BASES
Principal acid in the body = CO2
o The RESPIRATORY parameter
o Controlled by lungs
o Combines with water to form carbonic acid
Principal base in the body = HCO3- (bicarb)
o The METABOLIC parameter
o Primarily controlled by kidneys
o Binds with free H+ to reduce its level
EFFECTS OF pH ON ELECTROLYTES
Changes in pH affect K+ and Ca2+ balance
Kidney’s excrete H+ to maintain proper blood pH
o For every H+ excreted by kidney, a positive ion is retained
o When H+ excretion is elevated (as in acidosis), extra K+ is retained leading to hyperkalemia
Calcium in the bloodstream is affected by pH
o When the blood is alkalotic, calcium binds more proteins in the blood, leading to hypocalcemia
o When the blood is acidotic, calcium is released from the blood proteins leading to hypercalcemia
From Anne Hollands aah2150 2013 SSN Review sheet
Metabolic = all in same direction; Respiratory = HCO3 and PCO2 opposite from pH
CLINICAL MANIFESTATIONS OF ACIDOSIS AND ALKALOSIS
1. Respiratory Changes
a. CO2 is the acid
b. Normal PaCO2 = 35-45 mm Hg
c. Respiratory acidosis = too much retained CO2 = hypoventilation (low pH, high CO2)
d. Respiratory alkalosis = too little retained CO2 = hyperventilation (high pH, low CO2) (alkerlemia)
CAUSES OF RESPIRATORY CHANGES
Acidosis
Respiratory failure or respiratory arrest
Drug OD
Chest trauma
Pulmonary edema
Airway obstruction
Neuromuscular Dz
COPD, asthma
Alkalosis
Hyperventilation
o Anxiety
o High altitude
o Pregnancy
o Fever
o Hypoxia
o Pulmonary embolus
o Large TV in vented patients (wtf?)
2. Metabolic changes
a. HCO3- is the base
b. Normal HCO3- = 22 to 26 mEq/L
c. Metabolic acidosis = decreased levels of bicarb
d. Metabolic alkalosis = increased levels of bicarb
CAUSES OF METABOLIC CHANGES
Acidosis
Diarrhea
Renal disease
Diabetic ketoacidosis
Shock
Salicylate (aspirin) OD
Sepsis
ACID-BASE PARAMETERS
Acid
pH
<7.35
PaCO2
>45
HCO3
<22
Normal
7.35-7.45
35-45
22-26
Alkalosis
Prolonged periods of vomiting
Diuretic use
Overuse of antacids
Alkaline
>7.45
<35
>26
HOMEOSTASIS = body’s attempt to normalize pH
Sometimes cause of acid/base imbalance cannot be corrected and the renal & respiratory systems will try to
compensate for change.
COMPENSATION EXAMPLES
Person w/diabetic ketoacidosis (metabolic prob) respiratory sys compensates
o HYPERVENTILATES to “blow off” excess CO2
Person with COPD (respiratory prob causing respiratory acidosis) renal system compensates
o INCREASES secretion of H+
o INCREASES reabsorption of bicarb
ANALYSIS OF ABG
Allows one to analyze the acid-base imbalance that the patient is exhibiting
Allows one to determine if any compensation or correction has occurred
STEPS IN ABG
Look at pH acidotic, alkalotic or normsies?
Look at CO2? high, low, or normsies?
Look at the HCO3 high, low, or normsies?
WHAT IS THE CAUSE OF IMBALANCE?*
If pt is acidotic, which of the two parameters – the CO2 or the HCO3 is consistent with the finding?
o Elevated CO2 – respiratory acidosis (from hypoventilation)
o Decreased HCO3 – metabolic acidosis
If the pt is alkalotic, which of the two parameters – the CO2 or the HCO3 is consistent with the finding?
o Decreased CO2 – respiratory alkalosis (from hyperventilation)
o Increased HCO3 – metabolic alkalosis
COMPENSATION
The pH is within normal range, but both the CO2 and the HCO3 are abnormal. This indicates that BOTH
parameters have been modified
One of the modifications was the primary CAUSE of the imbalance
The other modification with the RESPONSE to the imbalance
THE BODY DOES NOT OVER COMPENSATE
Look again at the pH
Is it closer to the alkaline range or the acidotic range?
If it is closer to the acidotic, the imbalance started out as an acidosis
If it is closer to the alkalotic, the imbalance started out as an alkalosis
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