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Phase 2a Medicine > ICS > Flashcards

ICS Flashcards

1
Q

What are the types of autopsy?

A

Hospital Autopsy (10%)
Medico-Legal Autopsy (90%)

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2
Q

Types of medico-legal autopsies?

A

Coronial : death not due to unlawful action
Forensic : unlawful death eg murder

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3
Q

Coronial Autopsy role:

A

Who , when, where, how

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4
Q

3 reasons why deaths are referred to coroner

A
  1. Presumed Natural - No known cause. Pt hasn’t seen doctor 14 days prior.
  2. Presumed Iatrogenic - peri/post operative death. Anaesthesia, illegal abortion.
  3. Presumed Unnatural : Accidents, suicide, neglect, murder, industrial death: coal mine/asbestos
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5
Q

Where do referrals come from?

A
  1. doctors - don’t have a statutory duty to refer. common law duty.
  2. registrar of BDM: Stat duty to refer
  3. relatives/police
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6
Q

Who performs autopsies?

A
  1. Histopathologist: Hospital Autopsy. Coronial: Natural death, drowning, suicide, accident, road traffic, fire , industrial, peri/postoperative
  2. Forensic Pathologist : homicide, death in custody, neglect.
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7
Q

Autopsy steps?

A
  1. External Exam: Identify, Disease/treatment, injuries, Evisceration
  2. Internal Exam : Avoid lower GI tract (infection risk). GU tract is common for cancer.
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8
Q

What is evisceration?

A

Y shaped incision - behind ears down clavicles down midline. examine organs in situ. remove thoracic, Abdo organs and brain.

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9
Q

What is acute inflammation?

A

The initial and often transient series of tissue reactions to injury - might last few hrs to few days

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10
Q

What is inflammation?

A

the local physiological response to tissue injury

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11
Q

2 benefits of acute inflammation?

A
  1. destruct invading microorganisms.
  2. wall of abscess cavity= prevent infection spread
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12
Q

2 limitations of acute inflammation?

A
  1. abscess in the brain = space occupying lesion compressing vital surrounding structures.
  2. fibrosis due to chronic inflammation = distorted tissues and permanently altered function.
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13
Q

Steps of Acute Inflammation

A
  1. initial reaction of tissue to injury
  2. vascular component : dilation
  3. exudative component: vascular leakage of protein rich fluid.
  4. neutrophil polymorph (wbc) - characteristic cell recruited to the tissue.
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14
Q

Outcomes of Acute Inflammation

A
  1. Resolution - goes away
  2. Suppuration - pus forms
  3. Organisation - fibrosis healing.
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15
Q

What is suppuration?

A

pus formation eg abscess

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16
Q

What is organisation (Acute inflammation) ? (STEPS)

A
  1. healing by fibrosis (scar formation) - where tissue lacks ability to regenerate specialised cells. substantial damage to connective tissue.
  2. dead tissue + acute inflammatory exudate removed by macrophages from damaged areas.
  3. defect becomes filled with granulation tissue.
    4.granulation tissue gradually produces collagen to form fibrous (collagenous) scar constituting the process of repair.
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17
Q

6 causes of acute inflammation

A
  1. Microbial infections - pyogenic (pus causing), bacteria, viruses
  2. hypersensitivity reactions - parasites, tubercle bacilli
  3. Physical agents - trauma, ionising radiation, heat, cold (frost bite)
  4. Chemicals - eg: corrosives, acids, alkalis, reducing agents (gross tissue damage)
  5. Bacterial toxins
  6. Tissue Necrosis - ischaemic infarction
18
Q

How do microbial infections cause acute inflammation?

A
  1. Most common cause
  2. viruses kill cells by intracellular multiplication.
  3. bacterial release of exotoxins causing inflammation and endotoxins associated with there cell walls.

some organisms cause immunologically mediated inflammation through hypersensitivity reactions

19
Q

How do hypersensitivity reactions cause acute inflammation?

A

when an altered state of immunological responsiveness causes inappropriate or excessive immune reaction that damages tissues.
They have cellular or chemical mediators.

20
Q

What are hospital autopsies used for?

A
  1. teaching
  2. research
  3. governance
21
Q

5 macroscopic appearances of acute inflammation

A
  1. redness - rubor - due to dilation of small blood vessels
  2. heat - calor - only in peripheries - increased blood flow (hyperaemia) = vascular dilation and delivery of warm blood to area
  3. swelling - tumor - due to oedema - fluid in extravascular space. minor reason is inflammatory cells migrating into area. as inflammation progresses new connective tissue forms.
  4. pain - dolor - stretching and distoring tissue due to oedema. chemical mediators like bradykinin, prostaglandins, seratonin induce pain.
  5. loss of function - inflamed area consciously and reflex inhibited
22
Q

What happens in early stages of acute inflammation?

A
  1. oedema fluid, fibrin , neutrophil polymorphs accumulate in extracellular spaces of damaged tissue.
23
Q

3 Steps of acute inflammatory response

A
  1. changes in vessel calibre (gets wider) = increased vessel flow
  2. increased vascular permeability and formation of fluid exudate
  3. formation of cellular exudate = emigration of neutrophil polymorphs into extravascular space.
24
Q

Which cellular component is essential for histological diagnosis of acute inflammation?

A

Neutrophil Polymorph

25
Q

What is granulation tissue?

A

specialised vascular connective tissue

26
Q

Explain tissue necrosis

A

death of tissues from lack of oxygen/nutrients = inadequate blood flow (infarction) - this is a potent inflammatory stimulus.

27
Q

Name an indication of a recent infarction

A

acute inflammatory response due to peptide release from dead tissue

28
Q

Explain the vascular changes in acute inflammation

A
  1. capillaries have no smooth muscle and are very narrow.
  2. smooth muscle of arteriolar walls form precapillary sphincters which relax in inflammation and increase blood flow. = red and heat
  3. increased capillary hydrostatic pressure.
  4. escape of plasma proteins into extravascular space
  5. increased osmotic pressure.
  6. more fluid leaves vessels than returned = increased vascular permeability.
29
Q

Normally how does vascular exchange work?

A
  1. high hydrostatic pressure at the arteriolar end of capillaries forces fluid out into extravascular space.
    2.. fluid returns into capillaries at venous end (hydrostatic pressure is low here)
30
Q

Name 3 causes of increased vascular permeability

A
  1. Immediate transient - chemical mediators (histamine, bradykinin, nitric oxide, c5a , leukotriene b4, platelet activating factor
  2. immediate sustained - severe direct vascular injury like trauma
  3. delayed prolonged - endothelial cell injury eg x ray or bacterial toxins
31
Q

What is the net escape of protein-rich fluid in vascular permeability called?

A

exudation and the fluid is fluid exudate.

32
Q

What are the 4 steps for neutrophil polymorph emigration?

A
  1. Margination of neutrophils - normally cells are in axial stream not peripheral (plasmatic) zone near the endothelium. Due to loss of intravascular fluid and increase in plasma viscosity.
  2. Adhesion - adhesion of neutrophils to vascular endothelium at site of acute inflammation is called pavementing only in venules. increased leucocyte adhesion results from interaction between paired adhesion molecules.
  3. Neutrophil Emigration : leucocytes migrate through walls of venules and small veins but dont exit from capillaries. neutrophils, eosinophil polymorphs and macrophages all insert PSEUDOPODIA between endothelial cells, and then on through the basal lamina into the vessel wall.
  4. Diapedesis - RBC escape from vessels passively. depends on hydrostatic pressure. presence of large number of RBC in extracellular space = severe vascular injury like a tear in vessel wall.
33
Q

Which chemical mediators cause the upregulation of adhesion molecules on the surface of endothelial cells in acute inflammation?

A

histamine and thrombin

34
Q

name 5 things which endogenous chemical mediators cause

A
  1. vasodilation
  2. emigration of neutrophils
  3. chemotaxis
  4. increased vascular permeability
  5. itching and pain
35
Q

why is histamine able to have immediate effect in acute inflammation?

A

its stored in preformed granules and so is instantly able to be released.

36
Q

What does histamine cause during acute inflammation?

A

vascular dilation and immediate transient phase of increased vascular permeability.

37
Q

most important source of histamine is?

A

mast cells

38
Q

name 4 enzymatic cascade systems contained in plasma

A
  1. complement system
  2. kinin system
  3. coagulation factors
  4. Fibrinolytic system
39
Q

explain the complement system

A
  1. complex series of interacting plasma proteins which form a major effector system for antibody mediated immune system reactions.
40
Q

5 essential macroscopic appearances of acute inflammation

A
  1. Redness - rubor
  2. Heat - Calor
  3. Swelling - tumor
  4. Pain - dolor
  5. Loss of function

Phase 2a Medicine (22 decks)

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