Presentation on Shock (Pathology). A brief explanation of types of shock with flow charts and diagrams.

1. SHOCK

3.  Definition of shock
 What exactly happens in shock?
 Classification
 Pathogenesis
 Pathophysiology – Stages of shock
 Morphologic features
 Clinical features
 Complications

4. Shock is a life threatening clinical syndrome,
of cardiovascular collapse, characterised by-
Hypotension
Hypoperfusion

5. What is Hypotension?
Acute reduction of
circulatory blood volume.
Decreased blood pressure.

6. What is Hypoperfusion?
It is the inadequate amount
of blood that flows
through the capillaries,
which leads to
decreased supply of
oxygen and nutrients to
the cells.

9. Hypovolaemic
Shock
Cardiogenic
Shock
Septic
Shock
Other
Types
Inadequate
circulatory
blood volume
Sudden fall in
cardiac output
from acute
diseases of
the heart
Severe
bacterial
infection
Anaphylactic
Shock
Severe
reaction in
response to
an allergen

10. Other types of Shock
Traumatic
Shock
Neurogenic
Shock
Hypoadrenal
Shock
Spinal cord injury
Anesthetic Accidents
Peripheral
Vasodilatation
Pooling of blood

11. What exactly does the word pathogenesis
mean?
The pathogenesis is the mechanism by which a disease is caused.

13. Effective circulating blood
volume
Venous return to heart
Cardiac output
Blood flow
Supply of oxygen at cellular level
Anoxia
Inflammatory mediators
Heart Failure

14. Occurs from -
Inadequate circulating blood volume
due to various causes.
Major effects of hypovolaemic shock are due to -
Cardiac Output
C.O.
Low Intracardiac
pressue

15. Inadequate circulatory blood volume
BLOOD LOSS DEHYDRATION
Burns
Excessive
use of
diureticsVomiting
Excessive Perspiration
Bleeding
from
cuts,
injuries
Internal
bleeding
Increased
Heart Rate
Low
Blood
Pressure
Low
Urinary
Output
Alteration in
mental state
Diarrhoea

16. Compensatory
MechanismsHYPOVOLAEMIA HYPOTENSION REDISTRIBUTION OF
BLOOD SUPPLY
Fluid
conservation
1. ADH
2. Aldosterone
3. Renin -
Angiotensin
Blood Pressure
1. Sympatheic
Vasoconstriction
2. Peripheral
resistance
Coronary and
Cerebral vessels
are spared due to
sympathetic
vasoconstriction

18. Inadequate circulation of blood
due to primary failure of the ventricles

19. Decreased Cardiac Output
Decreased Tissue Perfusion
Decreased movement of fluid from Pulmonary vascular bed into
pulmonary interstitial space
Pulmonary interstial odema followed by
Alveolar Pulmonary odema
Myocardial Infarction
Arrhythmia
Cardiac Tamponade
Pulmonary Embolism
Failure of Myocardial Pump

20. Compensatory mechanisms
1. Frank – Starling mechanism :
Increased preload of dilatation enhancing cardiac contractility.
2. Myocardial structural change : Hypertrophy
3. Activation of neurohumoral system:
a) Release of neurotransmitter :
Nor epinephrine by adrenergic cardiac nerves which increases the
heart rate & augments myocardial contractility
b) Activation of renin-angiotensin-aldosteron system

21. Compensatory mechanisms to maintain
 Arterial pressure
 Perfusion of vital organs

22. Ana - against Phylaxis - protection

23. Anaphylaxis is an allergic reaction condition in
which the C.O. and B.P. often decrease
drastically.
It results primarily from an Ag-Ab reaction
that takes place immediately after an antigen to
which the person is sensitive enters the
circulation.

24. HISTAMINE CAUSES :
Venous
Dilatation
Decreased
V.R.
Dilatation of
Arterioles
Decreased
B.P.
Increased Capillary
Permeability
Great Loss of fluid and
protein into tissue
spaces.

25. Anaphylaxis can occur in response to
any allergen.
Animal Dander : Material shed from the
body of animals – Hair, Dry skin, Feathers

27. Hives or Urticaria are dark red, raised icthy bumps.

29. Septic shock is a serious medical condition caused by
decreased tissue perfusion and oxygen delivery as a result of
infection and sepsis,
though the microbe may be systemic or localized to a
particular site.
Septic shock results from spread & expansion of initially
localized infection to blood stream
The mortality rate from septic shock is approximately 50%

30. In septic shock,
there is immune system activation
and
severe systemic inflammatory response to infection as follows:
1. Activation of macrophage - monocytes.
2. Activation of other inflammatory responses:
Ulitimately – the net result of these mechanisms is
vasodilation and increased vascular permeability.

31. Gram-negative bacteria enter the body from -

32. LYSIS OF GRAM –VE
BACTERIA
RELEASE OF ENDOTOXIN LPS
LPS BINDS TO LBP
LPS-LBP BINDS TO CD14 RECEPTOR ON MACROPHAGE
THIS STIMULATES RELEASE OF CYTOKINES MOST IMPORTANT BEING TNF AND IL1

33. What are these cytokines?
Cytokines : cyto - cell kinos - movement)
are small cell-signaling protein molecules
used extensively in intercellular communication.

34. Shock
Hypoperfusi
on
Hypoxic Cell
Injury
Activation of innate
immunity
Stimulation of Macrophages
Release of inflammatory
mediators
Tumor Necrotic
Factor - alpha
Interleukin 1 Other
cytokines

36. Toxic Shock
Syndrome

37. Pathophysiology is the study of the changes of
normal mechanical,
physical,
and biochemical functions, caused by a disease.

38. Stages of Shock
Progressive StageNon Progressive Stage Irreversible Stage
Reflex
Compensatory
Mechanisms
Activated
Perfusion of
Vital Organs
Maintained
Tissue
Hypoperfusion
Onset of
Worsening
circulatory BV
and metabolic
imbalances-
acidosis
Severe cell and
tissue injury
Even if
Haemodynamic
effects are
corrected
Survival not
possible

39.  Brain - Hypoxic Encephalopathy
 Heart in shock - Focal Myocardial Necrosis
 Shock Lung – Acute Respiratory Distress Syndrome ARDS
 Shock Kidney – Acute Tubular Necrosis ATN
 Adrenals in Shock – Necrosis
 Liver in Shock – Necrosis
 Blood – Disseminated Intravascular Coagulation

40. Shock Kidney – Acute Tubular
Necrosis ATN

41. Norm
al
Pathology
KIDNEY
Proteinaceous casts in tubu

42. Ischemic encephalopaNormal
Swollen brain,
distended gyri,
narrow sulci

43. Very low BP
Shallow and Sighing
Respiration
Subnormal Temperature Feeble and irregular pulse

44.  ARDS – Acute Respiratory Distress
Syndrome
 DIC – Disseminated Intravascular
Coagulation
 ARF – Acute Renal Failure
 Multiple Organ failure
are due to hypoxic cell injury resulting in immuno-inflammatory
responses and activation of various cascades

45. SOURCE
1. Textbook of Pathology –
Harsh Mohan
2. Pathologic Basis of Disease –
Robbins & Cotran
3. Internet