Last moment revision in Anatomy to Practice of Medicine

reading8Dr Sajeev V
Medical Officer, Department of Homoeopathy
Govt. of Kerala

Cranial Nerves

  • 12 pairs of Cranial Nerves
  • Part of Peripheral Nervous System
  • All cranial Nerves Except  1&2 arise from Brain Stem
  • All cranial nerves supply to same side except Trochlear
  • All CN have b/l upper control
  • Cranial Nerves carrying Parasympathetic Fibres 
  • Occulomotor, Facial, Glossopharyngeal,Vagus

 Parasympathetic ganglions

  • Ciliary ganglion associated with  3rd nerve
  • Sphenopalatine/pterygo palatine ganglion- 7th nerve
  • Submandibular ganglion– 7th nerve
  • Otic ganglion– 9th nerve

SURFACE ANATOMY
The horizontal plane passing through the disc that separates thoracic vertebrae T4 and T5 is one of the most significant planes in the body passes through the sternal angle anteriorly, marking the position of the anterior articulation of the costal cartilage of 2ndrib with the sternum. 

  • The sternal angle is used to find the position of rib II as a reference for counting ribs (because of the overlying clavicle, rib I is not palpable);
  • Separates the superior mediastinum from the inferior mediastinum and marks the position of the superior limit of the pericardium
  • Marks where the arch of the aorta begins and ends
  • Passes through the site where the superior vena cava penetrates the pericardium to enter the heart
  • Is the level at which the trachea bifurcates into right and left main bronchi
  • Marks the superior limit of the pulmonary trunk

Openings in diaphragm
Venacaval opening
-at T8 Vertebral level

Inferior venacava

Branches of rt phrenic nerve

Oesophageal opening- at T-10 level

  • Oesophagus
  • Rt &lt vagus nerve
  • Oesophageal branch of left gastric artery
  • Veins &lymphatics

Aortic opening  – at T 12 Level

  • Aorta
  • Azygous vein
  • Thoracic duct

The hilum of the right lung is arched by- Azygos vein

Bochdalek hernia occurs in –   Posterolateral part of diaphragm

Anteriorly, the costal cartilages of ribs 1 to 7 articulate with the sternum (true ribs)

The costal cartilages of ribs 8 to 10 articulate with the inferior margins of the costal cartilages above them.

Ribs 11and 12 are called floating ribs because they do not articulate

Centrally, the intercostal veins ultimately drain into theà azygos system of veins or into internal thoracic veins, which connect with the brachiocephalic veins in the neck.

The right costo-phrenic recess extends up to the 10th level of which rib in the mid-axillary line

The middle cardiac vein is located at the Posterior interventricular sulcus
The right coronary artery originates from the right aortic sinus of the ascending aorta

The left coronary artery originates from the left aortic sinus of the ascending aorta àbranches into LAD(anterior surface of the left ventricle) & LCx (courses toward the left )

Heart

  • Right border is formed by the right atrium
  • Left borderis formed by the left ventricle
  • Apex of heart is formed by left ventricle
  • Base of the heart is formed by the left atrium

Anterior surface is formed by right ventricle

The coronary sulcus circles the heart, separating the atria from the ventricles.

It  contains the right coronary artery, the small cardiac vein, the coronary sinus, and the LCx

The large majority of cardiac veins drain into the wide coronary sinus

The sinus opens into the right atrium between the opening of the inferior vena cava and the right atrioventricular orifice;

The opening is guarded by an endocardial fold semilunar valve (eustachian valve)

BREAST

Location: (female breast)
Superior border: 2nd rib
Inferior border: 6th rib
Medial border: Sternum
Lateral border: Midaxillary line

Location: (male nipple)
Fourth Intercostal Space, Midclavicular line
Underlying muscle
Pectoralis major and minor
Part of serratus anterior, external obliques

Arteries
Lateral Thoracic Artery, branches of Internal Thoracic A., Post. Intercostals

Veins
Intercostal, Internal Thoracic, Axillary Veins

Nerve
Branches of Intercostal Nerve

Spleen lies obliquely along the long axis of the 10th rib.
Directed downwards, forwards & laterally making an angle of about 45 degree with horizontal plane.

PHYSIOLOGY
Conduction velocity

Purkinje fibres     -4m/s

Internodal tracts   -1m/s

Vent muscle fibres -.5m/s

Atrial m.f          –     .3m/s

Bundle of His     -.12m/S

A.V Node –        .05m/s

Rythmicity

  • SA Node-70-80 beats/min
  • A.V Node-40-60 beats/min
  • Atrial m.f -40-60 beats/min
  • Purkinje fibres-30-40beats/min
  • Vent m.f           20-40 beats/min

Systolic  -cardiac output

Diastolic –total peripheral resistance

Blood will push into aorta –stretches aorta

More stroke volumeàMore stretchingà SBP increased

Diastolic BP

When diastole starts ventricular pressure drops- aortic valve closes

Elastic arteries recoil àblood tend to move forward&backwardàbackward movement is prevented by closed aortic valve

Blood flows out àflow regulated by the tone of arteries

BLOOD PRESSURE

          CO                           TPR

  • S /v-  heart  rate
  •  pre load  contractility
  •  EDV
  •  venous return
  •  venomotor tone — blood volume

Regulation  of BP

SHORT  TERM                               LONG TERM

 neurological                                      RAAA

NEUROLOGICAL

BP sensors in vessels

  • volume sensors in venous side
  • pressure sensors in arterial side

Pressure sensors

  • Carotid sinus
  • Aortic arch sinus

NTS (Nucleus Tractus Solitaris)

1)Stimulates cardio inhibitory  centre –  via rt  vagus ànd SA node

2)INHIBITS  cardio accelerator centre

3)vasomotor centre is inhibited

4)adrenal medulla is inhibited

5) JGA IS INHIBITED

Long term regulator :   RAAS

Lung volumes

  • IRV
  • TV
  • ERV
  • RV

FORENSIC  MEDICINE

Strong acids

  • Inorganic acids-sulphuric acid ,nitric acid,hydrochloric acid
  • Organic acids-carbolicacid ,oxalic acid,acetic acid,salycillic acid

Strong alkalies
Hydrates &carbonates of sodium,potassium &ammonia

MEDICAL ETHICS
Serious professional misconduct(infamous conduct)
P

  • Moral  principles which guide the members of medical profession
  • CENTRAL COUNCIL OF HOMOEOPATHY Act in 1973

Main cause of penal erasure(removal name from medical council   register)

Any conduct which is considered as disgraceful

Dichotomy –(fee splitting)  -receiving or giving commission to a professional colleague or trader,chemist etc

Adultery –voluntary sexual intercourse other than his or her spouse

Covering-assisting a person who has no medical qlfcn to attend, treat or perform an operation

Privileged communication – A statement made bonafied upon by a doctor to authority to protect the community

Professional negligence( malpraxis)- IPC 304 A,312

Absence of reasonable care and skill or willfull negligence of a doctor in tt of a patient which causes bodily injury or death

CIVIL NEGLIGENCE – If following conditions are present

Duty –existence of duty of care by the doctor

Dereliction-failure of the doctor to maintain care &skill

Direct causation -the failure to duty lead to death or damage

Damage – the damage which results must be reasonably anticipated

A civil wrong is known as TORT

NOVUS ACTUS INTERVINIENS
Unrelated action intervening

The responsibility for death or disability may pass from original incident to the negligent action of doctor

Criminal negligence-304A-IPC

If  gross negligence leads to death of patient.

CONTRIBUTORY NEGLIGENCE
If absence of care on the part of personal attend or patient along with doctors’

Therapeutic misadventure

If patient injured or died due to unintentional act by the doctor/hospital

Vicarious liability

An employer is not only responsible for his own act but also for his employees negligence (respondant superior-let the master answer)

Euthanasia(MERCY KILLING) –   producing painless death of a patient who suffers from incurable d’s –    No legal sanction in India  

CONSENT

  1. Expressed
  2. Implied

Oral consent-should be obtained in the presence of a third party 

OBSTETRICS
a/c toxaemia  of pregnancy

Pre-eclampsia  may be mild or severe charecterised by oedema,albuminuria &hypertension

ECLAMPSIA  is the above symptoms with convulsion or coma

Abortion – Termination of pregnancy before the uterus become viable

Can be due to

Foetal factors

  • Intrinsic defects of fertilised ovum
  • Cystic degeneration of chorionic villi
  • Haemorrhage into deciduous
  • Low quality sperm

Maternal factors 

  • Infections
  • DM
  • Htn ,c/c nephritis
  • Trauma,stress 

Uterine causes

  • Congenital malformation of uterus
  • Fibroid tumours of uterus
  • Retroversion of uterus
  • Ovarian tumours

 Hormonal causes

  • Incompatibility of blood of husb & wife 

Pregnancy

Changes in uterus &cervix

Weight -50à900 gms (GENERAL BODY  WT gain-5-9 kg)

Size-7.5x5x2.5 cmà30x23x20

Endometrium &myometrim undergo hypertrophy

Endometrium of pregnant uterus is called Decidua

Cervix  become softer 7secrete tenacious mucus

Irregular ,painless contractions-Braxton—Hicks contractions

In Vagina
Blood  supply increaseswith bluish discoloration-Jacquemier’s sign/chadwick’s sign

Vaginal Ph  becomes acidic 3.8-4.4

In Breast

  • Oestrogen acts more on glands &ducts
  • Progesterone acts on the secretory functions of Breast
  • Prominent tubercles in the areola-Mont-Gomery tubercles 

IN SKIN – Main changes are due to MSH

General changes

  • Total blood volume increases by 30 %
  • A/G ratio decreases
  • Fibrinogen level increases
  • ESR increases
  • Cardiac Output RISES BY 40%   

Foetal heart beat can be heard from 16th week

Qty of amniotic fluid-

       At  12 weeks -50 ml

             20 weeks-400ml

             35 weeks -1L

 UMBILICAL CORD-  50 CM

            2 arteries 1 vein

Labour

Stages of labour

Stage 1

Onset of true labor pain to full dilatation of cervix

Stage 2

Dilation of cervix to expulsion of foetus

Stage 3

Expulsion of foetus to expulsion of expulsion of placenta and its membranes

Mechanism of labor

  • Engagement
  • Flexion of head
  • Internal rotation of head
  • Crowning
  • Delivery of head by extension
  • Restitution
  • External rotation
  • Delivery of shoulders by lateral rotation
  • Caulophyllum,arnica,puls,phos,ipecac,secale cor,sabina 

GYNAECOLOGY
Amenorrhoea –absence of menstruation

Kallman’s syndrome -hypogonadotropic hypogonadism-

Dec:GnRH+ dec LH&FSH

LH (N)&FSH Inc-PCOD

LH inc &FSH inc- Ovarian failure

Sheehans syndrome -ischemia due to venous thrombosis

Dysmenorrhoea –painful menstruation

Menorrhagia –excessive menstruation in excess of amount &duration

Metrorrhagia –acyclical intermenstrual bleeding

Polymenorrhoea-frquent menstruation at regular intervals

Uterine fibroids

  • Subserous
  • Intramural
  • Submucous
  • Symptoms depend on the size of tumour

SURGERY

Types  of fracture are:

Complete fracture: A fracture in which bone fragments separate completely.
Incomplete fracture: A fracture in which the bone fragments are still partially joined. In such cases, there is a crack in the osseous tissue that does not completely traverse the width of the bone.
Linear fracture: A fracture that is parallel to the bone’s long axis.
Transverse fracture: A fracture that is at a right angle to the bone’s long axis.

Oblique fracture: A fracture that is diagonal to a bone’s long axis.
Spiral fracture: A fracture where at least one part of the bone has been twisted.
Comminute fracture: A fracture in which the bone has broken into a number of pieces.
Impacted fracture: A fracture caused when bone fragments are driven into each other.
Avulsion fracture: A fracture where a fragment of bone is separated from the main mass.

RENAL STONES

  • Calcium oxalate         80%     when urine is acidic (low pH)
  • Calcium phosphate   _5-10 %           when urine is alkaline (high pH)
  • Uric acid              5-10%         when urine is persistently acidic       

Diets rich in animal proteins and purines: substances found naturally in all food but especially in organ meats, fish, and shellfish.
Struvite  10-15%  infections in the kidney( “infection stones“)  Preventing struvite stones depends on staying infection-free.  (ammonium magnesium phosphate, NH4MgPO4·6H2O
Cystine    1-2%     rare genetic disorder

PATHOLOGY
Inflammation  is part of the complex biological response of vascular  tissues to harmful stimuli, such as pathogens, damaged cells, or irritants

Vascular  changes : vasodilation, increased permeability and increased             blood flow,

Increased permeability -results  in  àallows leukocytes to marginate (move) along the endothelium(margination)àdiapedisis-the passage of blood cells through the unruptured wall of a blood vessel into the surrounding tissues.

Chemotaxis-Movement of leukocytes within the tissue via

Classical signs

  • Redness – Rubor
  • Swelling –Tumor
  • Heat –  Calor
  • Pain –   Dolor
  • Loss of function –Functio laesa

The first four (classical signs) were described by Celsus

While loss of function was added later by Galen   

Cells in inflammation

  • Macrophages
  • Mast cells
  • Neutrophils
  • Basophils

The plasma contains four interrelated systems of proteins—

  1. Complement ,
  2. Kinins,
  3. Coagulation   factors,
  4. Fibrinolytic  system—that generate various mediators of inflammation.

Complement proteins serve as chemotactic factors for neutrophils, increase vascular permeability, and stimulate the release of histamine from mast cells

The kinin system, which is activated by coagulation factor XII, produces substances that increase vascular permeability.

The most important of the kinins is bradykinin

The coagulation system converts the plasma protein fibrinogen into fibrin

The fibrinolytic system contributes to inflammation primarily through the formation of plasmin

Chemical mediators

Histamine, which triggers vasodilation and increases vascular permeability. Stored in granules of circulating basophils and mast cells,

Prostaglandins   are a group of fatty acids, increase the effects of other substances that promote vascular permeability ,aggregation of platelets,

Prostaglandins are associated with the pain and fever of inflammation.

Acute  phase  proteins – C-reactive protein, serum amyloid A, and serum amyloid P

Repair

  • Granulation  tissue
  • Endothelial  cells give rise to new blood vessels
  • Fibroblasts   grow to form a loose framework of connective tissue.
  • This delicate vascularized connective tissue is called granulation tissue

As repair progresses, new blood vessels establish blood circulation in the healing area, and fibroblasts produce collagen  that imparts mechanical strength to the growing tissue

Eventually a scar consisting almost completely of densely packed collagen is formed.

Necrosis
A form of cell injury that results in the premature death  of cells in living tissue

1. Coagulative necrosis – characterized by the formation of a gelatinous substance in dead tissues

  • Seen in hypoxic (low-oxygen) environments, such as infarction.
  • Coagulative necrosis occurs primarily in tissues such the kidney, heart and adrenal glands

2)Liquefactive necrosis (or colliquative necrosis)-characterized by the digestion of dead cells to form a viscous liquid mass.

Hypoxic infarcts in the brain

3) . Caseous necrosis -a combination of coagulative and liquefactive necroses,  typically caused by mycobacteria (e.g. tuberculosis), fungi and some foreign substance

4) Fat necrosis is specialized necrosis of fat tissue- acute pancreatitis

Two  pathways

1) Oncosis  (swelling of the cells)àblebbing,  àpyknosis (nuclear shrinkage).In the final step of this pathway  karyorrhexis   (nucleus is dissolved into the cytoplasm)

2) Karyolysis  .Nucleusbreaks into fragments 

Infarction
Tissue  death (necrosis) caused by an obstruction of the tissue’s blood supply

divided  into 2 types according to the amount of blood present:
White infarctions (anemic infarcts) affect solid organs such as the spleen and kidneys
Red infarctions (hemorrhagic infarcts), generally affect the lungs or other loose organs (testis, ovary, small intestines). 

Neoplasia
Abnormal  proliferation of cells.

Anaplasia        – Lack of differentiation
Aplasia             – when an entire organ or a part of an organ is missing
Hypoplasia     – inadequate or below-normal number of cells
Hyperplasia    – physiological proliferative increase in  number of cells
Neoplasia       – abnormal proliferation
Dysplasia        – change of phenotype (size,shape and organization   of tissue)
Metaplasia      –conversion of cell type
Prosoplasia     – cell type develops new function
Desmoplasia  – connective tissue growth

Neoplasms may be benign, pre-malignant (carcinoma in situ) or malignant .

Adeno  – Epithelial glands-Adenoma-Adenoscarcinoma
Fibro-   Connective tissue- Fibroma- Fibrosarcoma

BACTERIOLOGY
Staphylococcus + + + + + + + + + + + +

  • Gram + bacteria, round (cocci), and form in grape-like clusters
  • Staphylococcus spp. are facultative anaerobes (capable of growth both aerobically and anaerobically).

Streptococcus ++++++++++++++

  • Spherical Gram-positive bacteria
  • The most common of these infections include streptococcal pharyngitis (strep throat) and impetigo,scarlet fever ,rheumatic fever and acute glomerulonephritis

Mycobacterium

  • The genus includes pathogens  known to cause  tuberculosis  (Mycobacterium tuberculosis) and leprosy  (Mycobacterium leprae)
    Mycobacteria are aerobic and nonmotile bacteria  that are characteristically acid-alcohol-fast.
  • Mycobacteria do not contain endospores or capsules and are gram-positive
  • Ziehl-Neelsen stain

M. tuberculosis
First discovered in 1882 by Robert Koch,
M. tuberculosis is highly aerobic and requires high levels of oxygen.

Mycobacterium leprae
(Hansen’s coccus )

  • Bacterium  that causes leprosy (Hansen’s disease).
  • It is an intracellular, pleomorphic, acid-fast  bacterium.
  • M. leprae is an aerobic bacillus (rod-shaped)
  • Has been grown in mouse foot pads and more recently in nine-banded armadillos  because they, like humans, are susceptible to leprosy

Virus
Human immunodeficiency virus (HIV)

  • Lentivirus   (a member of the retrovirus family) that causes acquired immunodeficiency syndrome (AIDS)
  • Enveloped  RNA viruses
  • HIV infects vital cells in the human immune system such as helper T cells (specifically CD4+ T cells), macrophages, and dendritic cells

Viral RNA  genome  is converted (reverse transcribed) into double-stranded DNA by a virally encoded reverse transcriptase that is transported along with the viral genome in the virus particle.

HIV-1 and HIV-2.

 HIV-1  is more virulent

Malaria
Develops via two phases:

1) Involves the liver (exoerythrocytic phase), that 2) Involves red blood cells, (erythrocytic phase).

An  infected mosquito pierces a person’s skin

Sporozoites in the mosquito’s saliva enter the bloodstream and migrate to the liver where they infect hepatocytes,àmultiplying asexually and asymptomatically for a period of 8–30 days

HELMINTHS

  • Cestodes (tapeworms)
  • Trematodes (flukes)
  • Nematodes (roundworms)

A. lumbricoides-causes ascariasis.

Is the largest intestinal roundworm and is the most common helminth infection of humans worldwide.

SPM

Water
Purest form of water –rain water

CHEMICAL IMPURITIES :dissolved gases(oxygen nitrogen etc),dissolved salt(chloride carbonate bicarbonate etc)
PHYSICAL IMPURITIES :suspended impurities, colloidal impurities
MICRO ORGANISMS :algae, fungi, bacteria etc

Water purification

  • Physical  processes -filtration, sedimentation, and distillation,
  • Biological  processes -slow sand filters or biologically active carbon
  • Chemical  processes -flocculation  and chlorination and the use of ultraviolet light.

Rapid  sand filter
The most common type of filter is a rapid sand filter.

Water moves vertically through sand which often has a layer of activated carbon or anthracite coal above the sand.

The top layer removes organic compounds

NUTRITION

  • FORTOFICATION –increase nutrient value by adding small qty  of nutrients to improve the qlty of food
  • Adulteration –prevented by PFA Act of 1954
  • Macronutrients-vitamins &minerals
  • Net protein utilization -wt gain per unit volume of protein consumed
  • Most common deficiency in india is IRON def anemia
  • Pastorization donot kill anthrax but kill TB bacilli

Family planning

Population
World more than 700 cr

India 122 cr

Most effective method of spacing between pregnancy is IUCD

Opinion of 2 doctors is necessary FOR mtp BEYOND 12 WEEKS OF GESTATION

MTP ACT ON 1971-alow MTP nly up to 20 weeks of gestation

Couple protection rate indicates prevalence of contraceptive use in the community

Pearl index-failure rate /100 woman yrs of exposure of contraception 

Immunization schedule

Live attenuated vaccines

  • BCG,
  • Typhoid oral (Ty21A), Plague,
  • Oral Polio,
  • Yellow fever(17 D), Measles, Mumps, Rubella, Influenza,  

Inactivated or Killed Vaccines

  • Typhoid(TAB),
  • Cholera,
  • Pertussis,
  • Rabies,   ,
  • hepatitis B,
  • JE,
  • Diphtheria and Tetanus are Non- human antisera (immunoglobulins)
  • While hepatitis A & B,measles, rabies,mumps varicella are human immunoglobulins

Most effective vaccine is yellow fever vaccine

PRACTICE OF MEDICINE

JOINT DISEASES

Osteo Arthrosis
Most common form of arthritis

Kashin –beck disease is endemic OA

No acute phase response

Nodal OA

Heberden’s nodes -terminal interphalangial joint

Bouchards nodes -proximal inter phalangeal joint 

X-Ray

  • Focal narrowing &osteophyte formation
  • Bone density is normal or increased 

Rheumatoid Arthritis

  • Most  common form of inflammatory arthritis in India
  • Most  common form of arthritis below the age of 50

HLA DRW 4 &HLA DR 4 are ass with RA

HLA DR 4 is correlated with the severity of the disease

Anti globuln  antibodies —acts on synovial membrane –

More  in females 

Symmetrical arthritis ,early morning stiffness

Duration of symptoms for diagnosis-6 months

F:M-3:1

c/c symmetrical polyarthritisof distal joints

Morning stiffnes

Extra  articular

  • Skin –subcutaneous nodules,  raynaud’s phenmenon
  • Eye  -scleritis ,blue colour
  • Resp -;caplans syndrome, interstitial fibrosis
  • Rh nodules &cavitation
  • CVS -percarditis
  • AR ,conduction defects

Variants of RA                                            

Stills  disease

  • c/c juvenile polyarthritis
  • before 16 yrs
  • pauciarticular
  • rash ,fever, lymhadenopathy&splenomegaly 

Felty’s syndrome : RA +SPLENOMEGALY+NEUTROPENIA 

Sjogren ‘s syndrome

  • Keratoconjunctivitis scca+xerostomia+RA
  • Schrimmer’s test -blotting paper to eye -no wetting 

SLE

  • INFLAMATORY DISEASE OF AUTO IMMUNE NATURE
  • M:F-1:18
  • Suppression of T cells with over activity of B cells
  • Auto antibodies of IgG &IgM class
  • Circulating immune complexes deposited in the tissues leading to inflammation

Type II( brain damage, abortion)& Type III (renal ,vascular) Immune reactions

  • Arthralgia/itis in 70-90 %
  • Large joints
  • Juccouds arthropathy of hand
  • Skin-65%
  • Erythromatous photosensitive butter fly rash of cheeks and nose
  • Frontal baldness,alopacea
  • Discoid lupus-form of SLE  in which manifestation is only in skin for few years
  • CVS-25-40%
  • Pericarditis,pericardial effusion myocarditis
  • Libmann-sacks endocarditis-non bacterial verrucous endocarditisof miteral valve
  • Raynaud’s phenomenon

Respiratory system-30%dry pleurisy ,pleural effusion

Shrinking lung syndrome

Kidney -60%

  • Most important lesion deciding the prognosis
  • Nephritic ,nephritic syndrome,RF
  • Wire loop lesions produced by thickening of glomerular walls 

Blood

  • Coomb’s positive ,autoimmune haemolytic anaemia
  • LE cells (PMNL )
  • ESR increased
  • Moderate anaemia,leukopaenia,thrombocytopaenia
  • ANA in 95% 

Polymyositis/dermatomyositis
Muscles show non suppurative inflammatory lesions ass:weakness atrophy &later calcification

5 clinical types

Type 1 –typical polymyositis

Type 2–      ,,   dermatomyositis

Type 3- dermatomyositis  ass:with malignancy

Type 4-childhood dermatomyositis

Type 5 – D/P ass;with other collagen d’s

Muscles show loss of fragmentation ,loss of cross striations

Dermatomyositis more common in females

Proximal muscles are more affected in early stage

Tenderness prominent

Muscles are hyper reflexic

Ocular muscles spared

Muscle enzyme increased

Heliotrope eruption on face with periorbitaal oedema

Cutaneous lesions may ulcerate and leave behind deep scars

Sero –negative Spondarthropathies

HLA-B  27   common association

Ankylosing spondylitis

  • Marie stumpell disease,pocker back
  • Predominantly affects Axial Skelton
  • M:F  -7:3
  • K .pneumonia is the triggering infection
  • LBA more in morning aggravated by rest
  • Sacroiliac &vertebral joints more affected
  • Obliteration of lumbar lordosis &limitation of mvmnt due to muscle spasm
  • Ankylosis of spinal joint –whole spine rigid coloumn
  • X-ray shows bamboo spine 

Psoriatic arthropathy

4 types

  1. predominantly distal arthritis involving interphalangeal joints
  2. classic arthritis mutilans
  3. closely resembling RA
  4. Spondylitis with or without peripheral arthritis 

Rieter’s arthritis

  • One among reactive arthritis
  • Non –specific urethritis ,conjunctivitis, urethritis &arthritis
  • Usually follows an attack of dysentery or urethritis
  • R/A  of tenosynovitis ,plantar fasciitis,enteropathy &frank arthritis
  • Keratoderma blennorhagica
  • Oral & cutaneous lesions painless 

Gout

  • Due to disorder of purine metabolism resulting in hyperurecemia & deposition of urate crystals in synovium
  • Primary gout /genetic  -95 %
  • Almost excusive in males 

From over production/diminished excretion

  • 1) Asymptomatic urecaemia
  • 2) Acute gout – 1st metatarso phalangeal joint is commonly affected (podagra)
  • 3) Chronic gout

Tophi –deposition of mono sodium urate crystals

At ankle,tendoachiles,helix of ear

  • Initially soft later hard
  • Discharges chalky material
  • Punched out erosions with overhanging cortical bone
  • Hips &shoulders are generally spared 

Saturine gout

  • Chronic lead poisoning resulting in attacks of gouty arthritis
  • Chronic urate nephropathy is imp complication
  • Synovial fluid is turbid due to increased cell count
  • Renal failure is the major cause of death
  • Chondrocalcinosis –  CPPD,

PSEUDO GOUT

  • Deposition of calcium pyrophosphate crystal (CPPD)
  • MOST COMMON JOINT AFFECTED IS KNEE JOINT
  • Calciumpyrophophate ,rhomboid shaped crystal
  • Normal serum urate levels 

Respiratory Infections

PNEUMONIA

  • Inflammation of lung parenchyma
  • Organisms
  • Most common in community acquired- streptococcus pneumonia
  • In hospital acquired      -pseudomonas

Pneumococcal pneumoni-

Commonest type

  • causes lobar consolidation
  • productive cough with Rusty sputum

High pitched bronchial breathing

Homogenous dense opacity

Klebsiella –(FRIEDLANDERS pneumonia)

  • common in alcoholic &diabetics
  • massive consolidation of one or more lobe

Currant jelly sputum -viscid blood stained sputum

Bulging interlobar fissure is characteristic finding 

Staphylococcus pneumonia

  • common in IV drug users,leukemia,lymphoma
  • pyopneumothorax &abcess formation is common

Legionella pneumonia

  • humidifiers,cooling towers &shower heads
  • GI symptoms &mental confusion,heameturia
  • hyponatremia ‘proteinuria

Pnemocystis carni  pneumonia

  • Most common cause of death in AIDS
  • Bibasal creps
  • Peripheral shadowing

Influenza virus- most common viral cause of pneumonia

Hemophilus influenza –produces green sputum

Actinomycosis    b/l empyma with chest wall sinuses ,  sulphur granules in chest discharge

CXR in pneumonia

  • Lobar consolidation-Pneumococci,H .influenza,klebsiella,
  • Staphylococcus aureus-patchy infiltration
  • E.coli- patchy infiltrates, pleural effussion
  • Pseudomonas- patchy infiltrates &consolidation
  • Chlamidiye-subsegmental infiltrates

Broncho  pneomonia

  • More common during infancy &old age
  • Occurs as complication of measles ,whooping cough,viral d’s,etc
  • Wide spread patchy consolidation in both lungs 

Tuberculosis

  • Caused by m.tuberculosis
  • Primary –organisms in alveolià lymphatics àhilar nodes enlarge
  •  Parenchymal lesion(gohn lesion) +lymphatics+hilar nodeàgohn complex/ (ranke complex)
  • USUALLY SEEN IN CHILDHOOD 

Fate  …

  1. completely heal with /without calcification
  2. prim focus walled off by collagen, but organism remain inside:   can reawaken
  3. actively progressing from beginning
  4. healing incomplete in lymph node
  •  bacilli enters the blood stream
  •  a)a/c-in infants &children  àmiliary TB
  •  b)c/c-tb in kidneys ,lungs ,bones etc 

Post prim PT

FROM

  1. direct progression of prim lesion
  2. reactivation of dormant lesion
  3. heamatogenous spread into lungs
  4. exogenous superinfection
  • Lymph node involved less ,more parenchymal lesion
  • Apical lobes more affected
  • Tuberculous cavity main feature
  • The liquefied centre is discharged into the bronchus
  • Post-tussive creps is characteristic
  • Puhl’s lesion -chronic PT of apex of lung
  • Simon’s focus -sec PT in apex &post part of upper segment
  • Asman’s focus -chronic intraclavicular lesion
  • Riche’s focus -dormant intracranial focus
  • Rasmussen’s  aneurysm-Dilated vessel in tuberculous cavity
  • Poncet’s polyarthritis-extra pulmonary complication of PT

Asthma

  • Episodic or chronic symptoms of airflow obstruction: breathlessness, cough, wheezing, and chest tightness.
  • Due to increased responsiveness of tracheo bronchial tree
  • Muscle spasm, mucosal oedema,viscid bronchial secretion

Cells

  • Mast cellsMacrophages eosnophils T-lymphocytes 

Mediators

  • Cytokine,Histamin,e Bradykinin, Prostaglandins,Thromboxane ,PAF
  • FREQUENT BRETH ATTACKS,
  • Bronchomotor tone &bronchial reactivity reaches max at 3-4 am
  • Morning dipping of PEFR  is charecteristic
  • Dimension that is not altered in asthma is FVC
  • Sputum contains cruschmann’s spirals &charcot layden crystals 

Acute severe astma

  • Silent chest
  • Pulsus paradoxus
  • Central cyanosis
  • Pigeon chest
  • Nervous System

Meningitis

Inflam’n of leptomeninges &SA space

Most common organisms

Whole age together –streptococcal pneumonia

In neonates                –E .coli

In infants /child     –HEMOPHILUS INFLUENZA

2-20 yrs                   –meningio cocci

In immunocompromised ,alcoholics&diabatics-listeria monocytogens

  • VASCULAR TERRITORY
  • CERBRAL CORTEX-ACA,MCA,PCA
  • MIDBRAIN-post CA
  • PONS-PONTINE BRANCH OF BA
  • Medulla-Br of VA,Br of PICA
  • Cerebellum-sup cerebellar,AICA,PICA
  • INT CAPS-MCA,ACA,ANT choroidal

CVA

ISCHAEMIC stroke-

  • throbotic
  • embolic

Heammorhagic-

Intracranial aneurysm

AV malformation

  • MC artery involved in stroke is –MCA
  • MC site intracranial hyper tensive bleeding -PUTAMEN

LACUNAR INFARCTS –infarcts of less than 5 mm ,

Lesion is in the artarioles

Classical/dense hemiplegia –lesion in internal capsule

 Monoplegia in c/l side -Motor area &corona radiata

i/l Cr n palsies +c/l hemiplegia –brainstem lesions

CSF  (Normal)

  • Colour-clear &transparent
  • Pressure-60-150 mm of CSF
  • Qty -150 ml
  • Prd’n-550ml/day
  • Cells-0-5 WBC
  • PROTIENS-20-40mg%
  • Sugar-40-70 %
  • Chlorides -720-750 mEq /l

FACIAL NERVE

  • Ramsay hunt syndrome
  • Herpes zoster of geniculate ganglion
  • Pain in ears with vesicles I pinna,along with LMN palsy 

Bell’s palsy

  • Idiopathic facial palsy of LMN type
  • Pain about the ear,taste disturbanceon ant 2/3 rd of tongue
  • Brainstem stroke syndromes
  • Webers syndrome-  i/l 3rd N palsy +c/l  hemiplegia
  • Claud’s syndrome’-i/l  3rd N palsy +c/l cerebellar signs
  • Millard –gubler syndrome -6th n palsy +c/l hemiplegia
  • Wallenberg syndrome/LMS –I/L 9,10,11 PALSY+C/L SPINOTHALAMIC SENSORY LOSS+I/L

ISCHEMIC HEART Diseases
Risk factors

Fixed

  • Male >25 ,Female >45 ,f/h of premature CAD

Modifiable

  • Hypertension ,smoking ,DM ,BMI >22 , LDL:HDL >5 

ORGANISMS ASS: CAD-

  • Chlamidiye  pneumonia,
  • Cyto Megalo Virus,
  • H Pylori

Biochemical markers-

CK,LDH,TOPONIN –T, myoglobin, SGOT

MOST SPECIFIC-        CK (MB)

EARLIEST  ecg change is ST elevation

LARGER INFARCT MAY UNDERGO SOFTENING –myomalaciacordis

MC site is LV

MCC of death is Ventricular fibrillation

  • Creatine phosphokinase(MB)   2-4 hrs    24 hr     72 hr
  • LDH                             24 hrs      4-5 days  after 10 days
  • AST/SGOT             With in 12 hr   48 hr    4-5 days
  • TOPONIN I/T        As early as 4 hr-
  • myoglibin            with in a few hr 

Dressler’s syndrome –post MI syndrome

  • Few weeks (1-12) MI

PRESENTS AS PERICARDITIS

Hypertension

Malignant  hypertension

  • With papilledema,nephropathy,&encephalopathy
  • Fibrinod necrosis-on the walls of arteries

Most  common cause of sec htn-renal parencymal d’s

Keiyh  wagne classification -Grades

  • silver wiring-grade 1
  • sun sign-2
  • salu’s sign -2
  • flame shapd h’ges&cotton wool patches-3
  • papilloedema-4

Download the anatomy & FMT table  

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