Mind Map by melian.yates, updated more than 1 year ago
Created by melian.yates over 6 years ago


Doctorate Pathology Mind Map on Shock, created by melian.yates on 23/10/2013.

Resource summary

1 Types
1.1 Cardiogenic
1.1.1 Failure of the heart to pump properly Causes: Death of Cardiac muscle Ex. Disease of blood vessels Thrombosis Arrhythmia Obstruction of blood flow leaving heart Ex. PTE (Pulmonary thromboembolism) Primary Cardiac Disease Ex. DCM, HCM DCM: Dogs HCM: Cats Cardiomegaly Tricuspid valve dysplasia Myocardial fibrosis Decrease in SV & CO
1.2 Hypovolemic
1.2.1 Shock due to reduced circulating blood volume Causes: Blood Loss Haemorrhage Blood volume = 7% of BW Ex. 5kg Cat: 5 *.07 = 0.35L = 350mL blood Fluid loss Vomiting, Diarrhea, Burns Hypotension & Hypoperfusion Recovery possible under certain circumstances If caught early => Fluid Therapy Can lose 10% of fluid volume
1.3 Blood Maldistribution
1.3.1 Blood pools in peripheral tissues due to a decrease in peripheral resistance in blood vessels Blood volume is unchanged, but the VASCULAR SPACE increases so that effective circulating blood volume decreases Types: Neurogenic Shock Damage to CNS (usually spinal cord) Loss of autonomic signals to smooth muscle in blood vessel walls Vasodilation Blood pooling in veins Need resistance to keep blood flowing Anaphylactic Shock Food Pollen Bee stings Mast cell degranulation Histamine Leaky dilated blood vessels Drop in BP & Reduced perfusion Hypovolemia & Hypoperfusion Oedema Septic Shock Most common form of maldistributive shock Mediated by vascular & inflammatory mediators in response to bacterial & fungal infection Trigger: Gram -ve Bacteria => LPS (Endotoxin) Binds TLR4 & CD14 (Monocyte derived cells: Dendritic cells & Macrophages) Cytokine release: IL-1 & IL -6 Factor XII Coagulation Thrombosis + Low Dose: Activation of Macrophages, Endothelial cells & Complement Medium Dose: Raised TNF & IL-1 => Pyrexia High Dose: Vasodilation, Hypotension, Reduced myocardial contractility (Reduced CO) & Hypoperfusion BV injury (release of too many cytokines) => DIC
1.3.2 Pooling, stagnation, Hypoxia
2 Stages
2.1 1) Compensated
2.1.1 Increase in CO & Vasoconstriction to maintain BP & tissue oxygenation Tachycardia Via Stimulation of SNS Adrenaline
2.1.2 Control of H2O balance GRF drops => Increase H2O absorption RAAS ADH
2.2 2) Progressive
2.2.1 Compensatory Mechanisms cannot cope with prolonged or severe drop in blood volume Hypoperfusion & Cell injury Low O2 => Cell metabolism shifts to Anaerobic respiration Lactic Acid production & reduced ATP Cell membrane damage, Lysosomal enzyme release => Tissue Necrosis ATP needed to maintain cellular membranes
2.3 3) Irreversible
2.3.1 Mechanisms aimed at Vasoconstriction are overwhemled Widespread Vasodilation & Organ failure
3 Clincal Features
3.1 Hypotension
3.2 Weak pulse & Tachycardia
3.3 Hyperventilation
3.4 Decreased urine production
3.5 Peripheral vasoconstriction (During compensation)
3.6 Lesions
3.6.1 Congestion & pooling of blood
3.6.2 Oedema & Haemorrhage Petechial Ecchymotic
3.6.3 Thromobosis (Microscopic) Coagulation cascade
3.6.4 Cellular Necrosis (Microscopic) Ex. Myocardial cells, Neurons, Hepatocytes, Renal Tubules

Media attachments

Show full summary Hide full summary


Fluid and Electrolyte Imbalances
Infectious diseases
Clare Yu
Mark George
General Pathoanatomy Final MCQs (401-519)- 3rd Year- PMU
Med Student
General Pathoanatomy Final MCQs (301-400)- 3rd Year- PMU
Med Student
General Pathoanatomy Final MCQs (201-300)- 3rd Year- PMU
Med Student
General Pathoanatomy Final MCQs (401-519)- 3rd Year- PMU
Mohammad Khan
patho. practical slides
Clinical Pathology (301-400) MCQs- Year 4 PMU
Med Student
Pathology of Alimentary Tract 2 (Ruminant Forestomachs/ Glandular stomach)
patho. jars.. formative