Physical

 examina.on  methods  
General  examina.on  
Dr.  med.  Aiga  Staka  
University  of  Latvia,  Faculty  of  Medicine  
 
 Physical  examina.on  methods  
•  Inspec.on  (looking);  
•  Palpa.on  (feeling);  
•  Percussion  (tapping);  
•  Ausculta.on  (listening).  
 Inspec.on  
 Seeking  and  detec,on  physical  signs  by  
observing  the  pa,ent:  
ü yields  most  physical  signs;  
ü more  diagnosis  is  made  by  inspec.on  than  by  
all  other  methods  combined;  
ü Depends  en.rely  upon  the  knowledge  of  the  
observer.  
Inspec.on  
 Palpa.on  
 Act  of  touching  a  pa.ent  in  a  therapeu.c  manner  
to  elicit  specific  informa.on:  
ü Inform  the  pa.ent  where,  when  and  how  the  
touch  will  occur;  
ü Short  fingernails  to  avoid  hur.ng  the  pa.ent;  
ü Warm  your  hand  prior  placing  them  on  pa.ent;  
ü   Encourage  pa.ent  to  con.nue  breath  normally  
throughout  examina.on;  
ü   Discon.nue  palpa.on,  if  pain  occurs;  
ü Gloves  must  be  used  when  examining  any  open  
wounds,  skin  lesions,  a  body  part  with  discharge,  
internal  body  parts  (mouth  and  rectum).  
 Palpa.on    
Palmar  surface   Dorsal  surface  

•  U  

Copyright  2006  Thomson  Delmar  Learning  

 Light  palpa.on  
•  Done  more  frequently  
than  deep  palpa.on,  
always  before  deep  
palpa.on;  
•  Superficial,  gentle,  
delicate,  finger  pads  are  
used;  
•   Depth  of  palpa.on  
approx.  1  cm  below  
surface;  
•  Palpa.on  of  a  tender  area   Reveals  informa,on    on  skin  texture  
in  the  abdomen  should  be   and  moisture,  overt,  large,  or  superficial  
performed  last.   masses,  fluid,  muscle  guarding  and  
superficial  tenderness  
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 Deep  palpa.on  
•  Use  hands  to  explore  
body’s  internal  
structures  to  a  depth  4-­‐5  
cm  or  more;  
•  Most  oSen  used  for  the  
abdominal,  male  and  
female  reproduc.ve  
assessments;  
Reveals  informa,on    about  the  
•  Varia.ons:  single-­‐ posi,on  of  organs  and  massess,  
handed  and  bimanual.   their  size,  shape,  mobility,  
consistency    

Copyright  2006  Thomson  Delmar  Learning  

 Percussion  
 The  technique  of  striking  one  object  against  
another  to  cause  vibra.ons  that  produce  sound:  
ü The  density  of  underlying  structures  produces  
characteris.c  sounds;  
ü These  sounds  are  diagnos.c  of  normal  and  
abnormal  findings;  
ü Any  part  of  body  can  be  percussed,  most  
frequently  –  thorax  and  abdomen;  
ü The  sounds  are  generated  from  body  .ssue  up  to  5  
cm  below  surface  of  the  skin.    
   
 Out  of  history.......  
Leopold  Auenbrugger  
(1722-­‐1809)  
•  Invented  percussion  as  
a  diagnos.c  technique;  
•  One  of  founders  of  
modern  medicine.  
 Percussion  
   Can  confirm:  
1.  The  presence  of  air,  fluid  and  solids;  
2.  Organ  size,  shape  and  pos.on.    
 Percussion  sounds  analysis  
1.  Intensity  (rela.ve  loudness  or  soSness),  also  called  
amplitude;    
2.  Dura.on  –.me  period  over  which  sound  ir  heard;  
3.  Pitch  (amplitude  frequency)  –  caused  by  sound’s  
vibra.ons  (highness  or  lowness    of  a  sound);  
4.  Quality  –  its  .mbre  or  musical  percep.on.  
Percussion  sounds  classifica.on  
 Percussion  techinques  

Direct  fist  percussion  

Immediate  percussion   Mediate  percussion    

Copyright  2006  Thomson  Delmar  Learning   Indirect  fist  percussion  

Mediate  percussion  technique(I)  
1.  Nondominant  hand  is  lightly    
 placed  on  the  surface  to  be  percussed;  
2.    Extend  middle  finger  (pleximeter)  and  press  
its  distal  phalanx  and  DIP  joint  firmly  on  the  
loca.on  of  percussion;  
3.    Spread  other  fingers  of  nondominant  hand  
slightly  off  the  surface  (prevents  dampening  
of  vibra.ons);  
Mediate  percussion  technique  (II)  
4.    Flex  the  middle  finger  (plexor)  of  the  dominant  hand  and  
place  the  wrist  directly  over  the  pleximeter  finger;  
5.    Strike    the  pleximeter  with  the  plexor  with  sharp,  crisp,  
rapid  movement  from  the  wrist  of  dominant  hand;  
6.    As  soon  as  the  plexor  strikes  the  pleximeter,  withdraw  
the  plexor  to  avoid  dampening  the  resul.ng  vibra.ons;  
7.    Note  the  sound  produced  from  percussion.  
 Recognizing  percussion  sounds  
 The  change  from  resonance  to  dullness  is  more  
easily  recognize  than  change  from  dullness  to  
resonance  (liver  borders,  lower  lung  border,  
diaphragma.c  excursions);  
 
N.B.  
 The  percussion  technique  can  take  
considerable  4me  to  develop  and  perfect.    
 Ausculta.on  
 Ac.ve  listening  to  the  body  organs  to  gather  
informa.on  on  a  pa.ent’s  clinical  status.  
Includes:  
ü Listening  to  involuntary  sounds  (heart  sounds,  
bowel  peristalsis);  
ü Listening  to  voluntary  sounds  (lung  sounds  
with  a  deep  inspira.on).  
Quiet  environment  is  necessary.    
 Again  out  of  history.....  
René  Laennec  
(1781-­‐1826)  
•  French  physician,  who  
invented  stethoscope  
(1816.);  
•  Classified  the  terms  –  rales,  
rhonchi,  crepitance,  
egophony;  
•  Developed  the  
understanding  of  
peritoni.s  and  cirrhosis,  
coined  the  term  melanoma.  
 Ausculta.on  
Direct   Indirect  ausculta,on  
ausculta,on:  
•  Listening  with  the  
unaided  ear  from  
some  distance  away  
or  placing  the  ear  
directly  on  the  
pa.ent’s  skin  
surface.  
Example  –  wheezing  in  
a  person  with  
severe  asthma  
 
Copyright  2006  Thomson  Delmar  Learning  
Pa.ent’s  posi.ons  (I)  

Copyright  2006  Thomson  Delmar  Learning  

Pa.ent’s  posi.ons  (II)  

Copyright  2006  Thomson  Delmar  Learning  

 General  visual  inspec.on  
Status  praesens  obiec4vus  communis  

•  Inspec.on  of  the  person  as  a  whole;  

•  Starts  at  your  first  encounter  with  the  pa.ent;  
•  Watch  how  the  pa.ent  walks  when  moving;  
•  Note  how  he  is  dressed  and  groomed;  
•  Whether  eye  contact  is  established;  
•  Tone  and  paeern  of  speech;  
•  Facial  expression,  nutri.on,  specific  behaviour  
etc.;  
Pa4ent’s  posture  
 Abdominal  pain  
•  Pancrea44s  –  lie  in  fetal  pos.on:  on  one  side,  
with  knees  and  legs  bent  over;  
•  Peritoni4s  –  very  s.ll  and  avoid  any  movement  
that  might  worsen  the  pain;  
•  Intes4nal  obstruc4on  (ileus)  –  quite  restless;  
•  Renal  or  perirenal  abscess  –  bend  toward  the  
side  of  lesion;  
•  M.  psoas  sign  –  lie  supine,  with  one  knee  flexed  
and  the  hip  externally  rotated  (reflect  local  
abnormality  around  the  iliopsoas  muscle  –  
appendici:s,  diver:culi:s,  terminal  ilei:s  in  
Crohn’s  disease).  
S.  Mangione.  Physical  diagnosis  secrets,  Elsevier,  second  edi:on,  2008,  p.10.  
 Postures  of  pa.ents  with  dyspnea  
•  Chronic  obstruc,ve  pulmonary  disease  –  sit  
up,  lean  forward  (to  improve  accesory  
respiratory  muscles  contrac.lity)  by  res.ng  
hands  or  elbows  against  the  thighs  (Tripod  
pos.on);  
•  Conges,ve  heart  failure  –  breathlessness  in  
lying  posi.on,  relieved  by  sifng  or  standing  
(pa.ents  spend  during  night  in  sifng  posi.on  
and  many  pillows  behind  back  ).    

S.  Mangione.  Physical  diagnosis  secrets,  Elsevier,  second  edi:on,  2008,  p.369,  

375.  
 Other  pa.ent’s  compulsory  postures    
•  Meningi,s  –  on  the  side,  with  neck  extended,  thighs  
flexed  at  he  hips  and  legs  bent  at  the  knees;  
•  Large  pleural  effusions  –  lie  on  the  affected  side  to  
maximize  excursions  the  unaffected  side;  
•  Small  pleural  effusions  (dry  pleuri,s)  –  lies  on  
unaffected  side  (direct  pressure  worsen  the  pleuri.c  
pain);  
•  Large  pericardial  effusions  –  sit  up  in  bed  and  lean  
forward  (“praying  muslim  posture”,  neck  veins  are  
greatly  extended;  
•  Tetralogy  of  Fallot  –  children  assume  squa.ng  
posi.on,  especially  aSer  exercise,  oSen  cyanosis  is  
present;  
  S.  Mangione.  Physical  diagnosis  secrets,  Elsevier,  second  edi:on,  2008,  p.10.  
 Comatose  pa.ent’s  postures  
   
Dahl’s  sign  
 Apparent  age  (I)  
Older  than  stated  age:  
•  Cigareee  smoking;  
•  Chronic  exposure  to  sun  (especially  UV  band)  –  
ac:nic  face;  
•  Progeria  (Hutchinson-­‐Gilford  syndrome):  
–  affects  1  in  8  million  newborns;  
–  Accelera.ng  aging  by  6-­‐8  .mes;  
–  Symptoms  begin  around  18-­‐24  months  –  stunted  
growth,  alopecia,  small,  bizzare  face,  lives  by  their  late  
teens.      
 
S.  Mangione.  Physical  diagnosis  secrets,  2008,  p.22.  
Wiikipedia.org.  
 Apparent  age  (II)  
Younger  than  stated  age:  
•  Genes;  
•   Hypogonadism  and  other  endocrine  disorders  of  
developmental  arrest  or  retarda.on;  
•  Panhypopituitarism;  
•  Anorexia  nervosa  and  some  mental  illnesses;  
•  Imunosupressive  agents  (aSer  organ  
transplanta.on);  
•  Being  mildly  underweight.  

S.Mangione.  Physical  diagnosis  secrets,  2008,  p22.  

Mental  status  evalua4on  
Level  of  consciousness  
 Orienta.on  
1.  Person  (Does  the  pa.ent  know  who  he  and  
other  in  the  room  are?  Does  he  know  their  
names,  roles?);  
2.  Place  (Does  he  know  where  he  is  –  the  place,  
city,  state,  country?);  
3.  Time  (Does  he  know  the  year,  season,  day  
and  date?);  
4.  Situa,on.  
Glasgow  coma  scale  (GCS)  
 Demen.a  
Demen.a  -­‐  clinical  syndrome  characterized  by  
deteriora.ng  cogni.on,  behaviour  and  
autonomy.  
Affects  3-­‐11%  of  adults  older  than  65  years.  
 
 
 
 
 Delirium  
Delirium    -­‐  acute  and  reversible  confusional  state,  
affects  up  to  20%  of  elderly  pa.ents  hospitalised  
with  acute  medical  illness  (infec.on,  stroke  etc.):  
ü Change  in  mental  status  (compared  with  pa.ent  
baseline);  
ü Difficulty  focusing  aeen.on  or  trouble  keeping  
track  of  what  is  being  said;  
ü Disorganized  thinking  (rambling,  unpredictable  
switcing  between  subjects,  illogical  flow  of  ideas);  
ü Altered  level  of  consciousness  (lethargic,  
stuporous,  hyperalert).  
 Alcoholic  delirium  (delirium  tremens)  
•  Severe  form  of  alcohol  withdrawal;  
•  Usually  occurs  aSer  stoping  heavy  drinking  
(large  amounts  for  long  .me);  
•  OSen  starts  within  48-­‐96  hours  aSer  last  drink  
(some.mes  7-­‐10  days  aSer  last  drink);  
 Symptoms  -­‐    body  tremor,  changes  in  mental  
status,  agita.on,  confusion,  disorienta.on  
etc.).  
 Clock-­‐drawing  test  
Instruc.on  for  pa.ent:  
•  Draw  a  clock  by  hand  on  a  
large  piece  of  paper  (about  
10  cm  in  diameter).  
•  Draw  the  face  of  a  clock  and  
put  the  numbers  in  the  
correct  posi.ons.  
•  Then  draw  the  hands  to  
indicate  .me  (e.g.  3:40).  
 
Scoring  usually  0-­‐10.  
 
Mini  Mental  State  Examina.on  (MMSE)  
 MMSE  
•  The  maximum  score  –  30,  21-­‐24-­‐  mild  impairment,  
10-­‐20  –  moderate,  <10  -­‐severe;  
•  Target  popula.on  –  older,  community  dwelling,  
hospitalised  adults;  
•  Not  to  be  done  in  pa.ents  with  delirium  (high  false  
posi.ve  rates).          

 
 "MINI-­‐MENTAL  STATE."  A  PRACTICAL  METHOD  FOR  GRADING  THE  COGNITIVE  STATE  OF  PATIENTS  FOR  
THE  CLINICIAN.  Journal  of  Psychiatric  Research,  12(3):  189-­‐198,  1975.  
Evalua4on  of  nutri4on  
 Weight.  Body  Mass  Index  (BMI)  
Weight  (kg)/metres  (m2)=  
 
 The  waist-­‐hip  ra.o  (WHR)  
WHR  –  measurement    
of  obesity;  
Abdominal  obesity:  
ü >  0.85  –  females;  
ü >  0.90  –  males.  
Op.mal:  females  –  0.7,  males  –  0.9.  
 
 
 Comparison  of  abdominal  and  peripheral  obesity    

•  Abdominal  obesity  –  
visceral  fats  (omental,  
mesenteric  and  
retroperitoneal  fat).  
Metabolically  ac.ve  –  
constantly  releasing  free  
faey  acids  into  portal  
circula.on.    
•  Peripheral  obesity  –  
subcutaneous  fat.  
Metabolically  inac.ve,  
except  during  pregnancy  
and  postpartum  period.  

S.McGee.  Evidence  based  physical  diagnosis,  2007,  p.104-­‐105.  

 Obesity  associated  medical  condi.ons  

•  Gut – gastroesophageal reflux disease, non-alcoholic steatohepatitis.

Centers  for  Disease  Control  and  Preven:on    

 Metabolic  syndrome  

Metabolic  Syndromes  in  Endocrine  System.  J  Diabetes  Metab,  2011,  2:163.  

 Protein-­‐energy  malnutri.on  
The  supply  of  proteins,  calories  or  both  is  
inadequate.  
Causes:  
•  Decreased  oral  intake  (most  common  cause  
worldwide);  
•  Increased  nutrient  loss  –  malabsorb.on,  
diarrhea,  nephro.c  syndrome;  
•  Increased  nutrient  requirements  (fever,  
cancer,  infec.on  or  surgery).  
 Protein-­‐energy  malnutri.on  
Marasmus  –  severe  loss  of  
body  weight  (body  weight  
is  reduced  less  than  60%  
of  normal  body  weight  for  
the  age).  Reason  
inadequate  calorie  intake.  
Kwashiorkor    -­‐  severe  
protein  deficiency,  
characterized  by  ascites  
and  edema.    

Measurements  -­‐  arm  muscle  circumference  and  grip  strength  

 Severe  underweight  
BMI  <  18.5  kg/m2    -­‐  cachexia  (loss  of  weight,  muscle  atrophy,  fa.gue,  loss  of  
ape.te)due  to  decreased  caloric  intake,  increased  caloric  requirements  of  
malabsorb.on,  glucosuria,  hypermetabolic  state.    
Causes:  
ü  End  stage  malignancy  (especially  GI  cancers);  
ü  Conges.ve  heart  failure;  
65%  
ü  Chronic  obstruc.ve  pulmonary  disease;  
ü  Neurological  diseases  (e.g.  mul.ple  sclerosis);  
ü  AIDS;  
10%   ü  Psychiatric  diseases  (depression,  anorexia  nervosa,  schizophrenia);  
25%   ü  Unknown  cause.  

S.  McGee.  Evidence  based  physical  diagnosis,  2007,  p.99  

 Body  habitus  
Classifica.on  of  body  structures:  
•  Hypersthenic  (5%);  
•  Normosthenic  (50%);  
•  Hyposthenic  (35%);  
•  Asthenic  (10%).  
 Hypersthenic  type  
•  Body  of  massive  build;  
•  Broad  thorax,  ribs  go  
nearly  horizontal  upon  
inspira.on;  
•  Heart  short  and  wide.  
Diaphragm  is  high,  
resul.ng  in  long  
abdominal  cavity;  
•  Stomach  and  gallblader  
located  laterally  from  the  
midline.  
 Normosthenic  type  
•  Heart  is  moderately  
transverse;  
•  Lungs  are  moderate  
length;  
•  Diaphragm  is  
moderately  high;  
•  Stomach  high  upper  
leS,  gallblader  centered  
on  right  side  in  upper  
abdomen.  
 Asthenic  type  
•  Thin  and  slender;  
•  Narrow  and  shallow  ribs  
sloping  downward  sharply;  
•  Lungs  are  long  and  extending  
well  above  the  clavicals  with  
the  apex  of  the  lung  broader  
or  parallel;  
•  Heart  is  long  and  narrow,  
nearly  ver.cal  at  midline;  
•  Diaphragm  sits  naturally  low;  
•  Abdominal  cavity  is  very  short.  
Somach  is  ver.cal,  narrow.  
Gallblader  is  ver.cal  and  very  
close  to  the  midline;  
 Hyposthenic  type  
•  Intermediate  between  
the  average  
normosthenic  and  the  
asthenic  body  type;  
•  The  most  difficult  to  
classify.  
 Some  body  habitus  syndromes  (I)  

Cushing’s  syndrome   Rickets  

Some  body  habitus  syndromes  (II)  

Paget’s  disease  

Marfan  syndrome  
Some  body  habitus  syndromes  (III)  

         Klinefelter  syndrome          Turner’s  syndrome  

 Some  body  habitus  syndromes  (IV)  

Achondroplasia  
Inherited  ~20%  
Pa4ent’s  gait  
 Normal  gait  cycle  
Stance  –  begins  when  one  heel  strikes  the  ground  and  
lasts  for  the  en.re  period  during  which  thet  foot  
stays  grounded  (weight  bearing  phase).  
Swing  –  interval  between  the  liSing  of  that  foot’s  toes  
off  the  floor  and  the  .me  the  heel  of  the  same  foot  
strikes  the  ground  again.  
 
  
Gait  coordina.on  
Sensory  input  (visual,  propriocep.ve,  ves.bular);  
Motor  input  (muscls  and  joints).  
 
Basal  ganglia  –  for  automa.c  movements  (e.g.  swinging);  
Locomotor  region  of  midbrain  -­‐  for  ini.a.ng  walking;  
Cerebellum  –  for  mantaining  proper  posture  and  balance,  also  controls  
major  characteris.cs  of  movements  –  trajectory,  velocity  and  
accelara.on;  
Spinal  cord  –  for  coordina.ng  movements  and  relaying  propriocep.ve/
sensory  input  from  joints  and  muscles  to  higher  centres  of  CNS;  
Vision  –  for  feedback  on  head  and  body  movement  in  rela.on  to  the  
surrondings.  Vision  is  crucial  in  case  of  reduced  input  from  other  
sensory  systems  (e.g.  propriocep.ve,  ves.bular)  

S.  Mangione.  Physical  diagnosis  secrets,  2008,  p.  23  

Major  causes  and  types  of  gait  disturbance  
Mechanism     Gait  disturbance   Disease  
Pain     Antalgic  gait   Osteoarthri.s:  hip,  knee,  ankle  

Immobile  joint   Fixed  joint  gait   Osteoarthri.s:  prolonged  periods  of  

plaster  immobiliza.on  

Muscle  weakness   Trendelenburg  gait   Unilteral  weakness  of  hip  a  

    abductors  
Anserine  gait   Bilateral  weakness  of  hip  abductors  
   
High  steppage  gait   Foot  drop  (peroneal  paralysis)  
Weakness  of  hip  abductors  
Abnormal   Parkinsonian  gait   Parkinson’s  disease  
neurological  control   Hemiplegic  gait   Hemispheric  stroke  
Cerebellar  ataxia   Cerebellar  diseases  
Sensory  ataxia    
Scissor  gait   Spas.c  paraplegia  (  

S.  Mangione.  Physical  diagnosis  secrets,  2008,  p.  26  

 Antalgic  gait  
•  Gonarthrosis  –knee  s.ffness  and  
inability  to  flex  or  extend  leg  
during  gait;  
•  Coxarthrosis  –  causes  coxalgic  
gait  –  limited  range  of  hip  
extension  and  lateral  lurch  
(adduc.on).  This  is  excessive  
lateral  shiS  of  the  pa.ent’s  upper  
body  toward  the  affected  side  
when  standing  on  the  painful  limb  
(relocates  gravity  centre);  
•  Pain  in  foot  –  incomplete  and  
gentle  contact  with  the  ground.  

S.  Mangione.  Physical  diagnosis  secrets,  2008,  p.  27  

 Trendelenburg  gait  
•  Produced  by  weakness  of  the  hip  
abductors,  causing  the  pelvis  to  
fall  toward  the  unsupported  side.  
In  an  effort  to  rise  the  leg,  
pa.ents  lean  away  from  the  
unsupported  side,  with  a  
compensatory  lateral  lurch  
toward  the  side  of  weakened  
abductors;  
•  Causes  –  neuromuscular  
weakness  of  the  hip  abductors  
(nowadays  –  from  hip  
arthroplasty)  and  hip  diseases  
(congenital  disloca.on)  

S.  Mangione.  Physical  diagnosis  secrets,  2008,  p.  28  

  Foot  drop  gait    
•  “Foot  drop”  –  inability  to  dorsiflex  
ankle  while  walking  because  of  
weak  m.  .bialis  anterior  and  toes  
extensors:  
ü  High  steppage  -­‐  knee  is  raised  
unusually  high  to  allow  the  drooping    
foot  to  clear  the  ground;  
ü  “Foot  slap”  –  aSer  heel  touches  the  
ground,  the  forefoot  is  brought  down  
suddenly  and  in  slapping  manner.  
•  Causes  –lower  motor  neuron  
disease  (peripheral  neuropathy,  
peroneal  injury,  muscular  
atrophies).  If  the  prox  (girdle)  
muscles  affected  –  pa.ent  acquires    
anserine  (waddling)  gait      
S.  Mangione.  Physical  diagnosis  secrets,  2008,  p.  28  
 Sensory  ataxia  
•  Pa.ents  have  lost  sensory  and  
propriocep.v  sensa.on  in  the  lower  
extremi.es.  Pa.ents  are  unaware  of  
their  limb’s  posi.on  in  space;  

•   They  taking  steps  that  are  higher  

than  necessary,  while  at  the  same  
.me  carefully  monitoring  the  
ground.  Gait  is  wide,  feet  thrown  
forward  and  outward,  typically  slap  
the  foot  onto  the  ground,  first  on  
the  heels,  then  on  toes;  
 
•  Posi.ve  Romberg’s  sign  

S.  Mangione.  Physical  diagnosis  secrets,  2008,  p.  31  

 Cerebellar  ataxia  
•  Gait  is  unsteady,  staggering,  totally  
irregular  in  rate,  range,  direc.on.  
Accompanied  by  swaying  to  one  
side  or  the  other.  Pa.ents  looking  
for  smth  to  lean  on  (bed,  wall).  
Balance  typically  fails  when  
aeemp.ng  to  walk  heel  to  toe;  
•  Other  cerebellar  deficit  signs  
present  –  dysarthria,  nystagmus,  
inten.on  tremor.  

S.  Mangione.  Physical  diagnosis  secrets,  2008,  p.  31  

 Spas.c  hemiplegic  gait  
Affected  side:  
•  Upper  extremity  adduc.on  and  
flexion  at  all  levels;  
•  Lower  extremity  extension  at  all  
levels.  The  foot  is  internally  rotated;  
•  By  walking,  foot  is  swinging  in  a  half-­‐
circle  (circumduc:on)  with  foot  
scraping  the  ground  on  its  lateral  
edge;  
•  Upper  body  .lts  to  opposit  side  
(compensatory).  Walk  is  difficult  and  
slow.  
Causes  –  hemispheric  stroke.  

S.  Mangione.  Physical  diagnosis  secrets,  2008,  p.  31  

 Spas.c  paraplegic  gait  (“scissor  gait”)    
•  Hips  adducted  and  internally  rotated  (thighs  
rub  together),  legs  slightly  flexed  at  the  hips  
and  knees;  
 
•  Because  of  excessive  adduc.on  ,  legs  are  
unable  to  move  stright  forward,  instead  they  
swing  across  each  other  at  typical  criss-­‐cross  
mo.on  at  the  knees.  Since  ankles  are  
plantarflexed,  pt  walks  on  .ptoe,  with  feet  
scraping  the  floor.  To  compensate  for  the  
s.ff  movement  on  the  legs,  pts  may  move  
the  tunc  from  side  to  side;  
 
•  Causes  –  spinal  cord  diseases,  causing  lower  
motor  neuron  involvement  with  weakness  
and  spas.city  in  both  lower  extremi.es.  

S.  Mangione.  Physical  diagnosis  secrets,  2008,  p.  30  

 Parkisonian  gait  
•  Axial  rigidity,  trunc  bent  forward,  
arms  flexed,  immobile  at  the  side,  
never  swinging,  legs  bent  at  the  hips,  
knees,  ankles,  small,  narrow-­‐based  
steps;  
•  Difficult  to  ini.ate  gait;  
•  Freezing  episodes;  
•  Bradykinesia,  postural  instability;  
•  Fes:na:on  –  progressively  shorter  
and  accelerated  steps  aSer  the  walk  
has  finally  begun;  
•  Propulsion  –  a  tendency  to  fall  
forward  (the  reason  for  fes.na.on);  
•  Diminished  facial  expression,  
decreased  eye  blinking,  staring  gaze.    

S.  Mangione.  Physical  diagnosis  secrets,  2008,  p.  32  

 Video  with  gait  abnormali.es  
hep://stanfordmedicine25.stanford.edu/the25/gait.html  
The  skin  
 Facts  about  skin  
•  The  heaviest  single  organ  
of  the  body,  accounts  
approx.  16%  of  body  
weight  and  covering  an  
area  of  1.2-­‐2.3  m2;  
•  Contains  three  layers:  
–  The  epidermis;  
–  The  dermis;  
–  The  subcutaneous  .ssues.  
 
Bate’s    guide  to  physical  examina:on  and  history  taking,  2008.  
 Facts  about  skin  
•  Hair,  nails,  sebaceous  and  sweat  glands  are  
appendages  of  the  skin;  
•  The  color  of  normal  skin  depends  on  four  
pigments:  
–  Melanin  (brown);  
–  Carotene  (yellow);  
–  Oxyhemoglobin  (red);  
–  Deoxyhemoglobin  (bluish-­‐red).    
Skin  color  changes  
 Jaundice  (icterus)  
Jaundice  –  abnormal,  yellowish  
discolora.on  of  skin  and  
mucous  membranes,  caused  by  
accumula.on  of  bile  pigment.  
Reasons:  
1.  Hemoly,c  (pre-­‐hepa,c)  –2  %;  
2.  Hepatocellular  (hepa,c);  
3.  Obstruc,ve  (post-­‐hepa,c  or  
mechanical  obstruc,on  of  the  
biliary  ducts.  
Jaundice  types  
 Cyanosis  
 Cyanosis  –  abnormal  bluish  
discolora.on  of  the  skin  and  
mucous  membranes,  caused  by  
blue-­‐colored  blood  circula.ng  in  
the  superficial  capillaries  and  
venules.    
  Usually   represents   excessive  
a m o u n t s   o f   d e o x y g e n a t e d  
hemoglobin;  
  Best   appreciated   in   areas   of   body  
where   overlying   epidermis   is   thin  
and  subepidermal  vessels  abundant  
–   lips,   nose,   cheeks,   ,   ears,   hands,  
feet,   mucous   membranes   of   the  
oral  cavity.  
 
 Pathogenesis  
•  Blood  becomes  blue  when  an  absolute  amount  of  blue  
pigment  (deoxyhemoglobin)  accumulates  to  be  seen  through  
opaque  epidermis;  
•  The  color  of  the  skin  depends  on  the  color  of  blood  flowing  
through  the  dermal  capillaries  and  supapillary  venous  plexus,  
not  arteries  and  veins  (lie  too  deep  to  contribute  to  skin  color);  
•  Minimal  amount  of  arterial  deoxyhemoglobin  causing  cyanosis  
is  2.38  g/dL  (or  4.24  g/dL  in  the  capillaries  and  small  venules);  
•  Cyanosis  depends  on  absolute  quan.ty  of  deoxyhemoglobin  
(not  rela.ve):  
–  Pa.ents  with  high  Hb  (polycythemia)  become  cyano.c  with  mild  
hypoxemia;  
–  Pa.ents  with  low  Hb  (anemia)  become  cyano.c  with  severe  
hypoxemia.  
 
 Types  of  cyanosis  
Peripheral  cyanosis  (acrocyanosis)  
•  Increased    extrac.on  of  oxygen  by  peripheral  .ssues;  
•  Deoxyhemoglobin  accumulates  to  turn  blue  in  the  subepidermal  blood  
vessels  of  the  feet,  hands.  
•  Causes  –  low  cardiac  output,  artrerial  obstruc.on  (e.g.  Raynaud  disease)  
and  venous  disease  

Central  cyanosis  
•  Pa.ents  have  blue  discolora.on  of  the  lips,  tongue  and  sublingual  .ssues  
in  addi.on  to  the  hands  and  feet;  
•  Any  disorder,  causing  hypoxemia  –  pulmonary  edema,  pneumonia,  
intracardiac    right-­‐to-­‐leS  shunts  

Pseudocyanosis  
•  Mucous  membranes  of  the  mouth  are  pink  and  blanching  of  the  skin  by  
pressure  does  not  make  the  color  dissapear  
•  May  occur  aSer  exposure  to  metals  (gold  therapy,  topical  silver  
components)  or  drugs  (amiodarone,    minocycline,  cloroquine,  
phenothiazies)  

S.  McGee.  Evidence  based  physical  diagnosis,  2007,  p.85-­‐89  

 Pallor    
•  Deficiency  of  Hb  
(anaemia)  can  produce  
pallor  of  the  skin  and  
mucous  membranes  
(Hb<70  g/L);  
•  Shock  -­‐  facial  pallor,  
together  with  clammy  and  
cold  skin  (hypotension);  
•  Normal  variant  due  to  
deep-­‐lying  venous  sistem  
and  opaque  skin.  
 Hyperpigmenta.on  
Darkening  of  the  skin  or  nails  due  to  
increased  melanin  produc.on.  
Causes:    
•  Diffuse  
ü  Sun  damage;  
ü  Addison’s  disease;  
ü  Haemochromatosis;  
ü  Porphyria;  
 
•  Patchy  
ü  ASer  acne  healing;  
ü  Pregnancy  melanosis  (chloasma);  
 
Addison’s  disease