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Smmlws > Patho Semi Until Midterm > Flashcards

Patho Semi Until Midterm Flashcards

1
Q

Amyloidosis diagnose

A

Congo red apple green birefringence and electron microscope

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2
Q

Amyloidosis classification

A 
A)systemic:
Immunocyte dyscrasis
Reactive systemic amyloidosis
Hemodialysis associated
Hereditary familial

B)Localized:
Senile cerebral – Alzheimer’s disease
Atrial
Endocrine Amyloid -medullary carcinoma and type 2 dm

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3
Q

Hyalinization

A

Tissue degenerates into translucent glass like substance hyaline

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4
Q

Transudate

A

Protein content less than 3 mg over milliliters

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5
Q

Exudate

A

Protein content more than 3 mg are in milliliters

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6
Q

Edema causes

A 
Inflammation,lymphangitis , tumor 
nephrosis syndrome 
liver failure 
malnutrition 
decreased album in concentration 
locally define thrombosis 
generalized heart failure plus renin angiotensin fluid retention 
and acute renal failure /salt and water retention
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7
Q

Lung edema cause

A

Cardiogenic Left heart failure hydrostatic pressure increase
Noncardiogenic vascular permeability increase;
Toxic damage
renal failure
hypoxia
fluid and electrolyte management disorder (iatrogenic infusion mis management)

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8
Q

Congestion = passive hyperthermia

A

Systemic heart failure
local venous occlusion
acute
chronic leads to parenchymatous degeneration and necrosis

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9
Q

Acute lung congestion

A

Longs are heavy firm elastic

Alveolar capillaries engorged with blood

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10
Q

Chronic lung congestion

A

Induratio brunea pulmonis (firm and brownish)
Fibrotic septa
Hemosiderin laden macrophage (heart failure cells)

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11
Q

Lung congestion is caused by

A

Left heart failure

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12
Q

Chronic liver congestion look

A

Nutmeg liver (hepar moschatum)
Dilation of central veins
Fatty degeneration

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13
Q

Hepar moschatum

A

Centralobular stasis and sinusoidal dilation

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14
Q

Liver fibrosis

A

Chronic complication
Dilation of central vein
Fatty degeneration
Periportal/septal fibrosis

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15
Q

Disseminated intravascular coagulopathy. DIC

A 
Endothelial damage
Thrombi in microcirculatory system
Coagul. Factors, thrombocytes are consumed
Fibrinolysis is active
SEVERE BLEEDING
PTAH STAIN
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16
Q

Thrombus cause (virchows triad)

A

Decrease blood flow (stasis)/ turbulence
endothelial injury
hypercoagulability of the blood

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17
Q

Localisation of thrombus

A

Arterial: white thrombus
Veneous: red thrombus
Heart chamber: embolus

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18
Q

Fate of thrombus

A

Propagation
embolization
dissolution
organization and recanalization

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19
Q

Forms of embolism

A 
Thromboembolism 
Air embolism 
fat embolism 
amniotic fluid embolism 
bacterial embolism 
tumor embolism 
foreign body embolism
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20
Q

Shock

A

Collapse of circulation characterized by hypotension and failure of microcirculation

Cardiogenic, Hypovolemic, Septic, Neurogenic, Anaphylactic, Endocrine
(Trauma)

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21
Q

Consequences of shock

A

Hypotension (systemic vasodilation )
decreased myocardial contractility
Endothelial damage and activation >ARDS
activation of coagulation cascade>DIC

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22
Q

Morphology of shock

A

Kidney-ischemia, acute tubular necrosis,,shock kidney,,
Lung-diffuse alveolar damage>ARDS
Liver-microthrombus formation>centrilobular necrosis
GI tract-erosions
Endocrine Organs-hemorrhage in adrenal gland,pancreas,hypophysis

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23
Q

Fat embolism

A 
Stain=Sudan 3
Neutral fatty acids(red)
Cause=
Mechanical-bone fraction
Biochemical-sepsis/trauma >systemic release of fatty acids
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24
Q

Hemodynamic disorders

A 
Hyperemia( active and passive )
edema 
hemorrhage 
thrombosis 
embolism 
infarction 
shock
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25
Q

Hyperemia meaning

A

LOCALLY increased blood volume

Can be active or passive(congestion)

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26
Q

Active hyperemia

A

Active dilation of arteriae, arterioles, capillaries
Erythema (oxygenated blood accumulation)
Forms ; physiological and pathological

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27
Q

Passive hyperemia

A 
Congestion
Dilation of veneous side due to decreased outflow
Cyanosis Hypoxia
Causes:
Local:thrombosis, obstruction
Systemic:congestive heart failure
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28
Q

Left sided heart failure

A

Lungs =heavy firm (ct accumulation)

Hf cells on microscopy Induratio Brunea Pulmonum

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29
Q

Right sided heart failure
Right ventricle function comprimised
LIVER :

A 
nutmeg liver (hepar moschatum)
 centrulobular necrosis
 cardiac fibrosis(cirrhosis-misnomer)
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30
Q

Right sided heart failure

KIDNEY

A

stellate veins accentuated
cortex widened
sharp separation of medulla and cortex

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31
Q

Right Sided Heart Failure

SPLEEN

A

enlarged, livid
fibrosis with time (Induratio
cyanotica lienis)

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32
Q

Right Sided Heart Failure

SKIN

A

cyanosis, anasarca

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33
Q

Right sided heart failure

BODY CAVITIES

A

Ascites, hydrothrox

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34
Q

Hemosiderin

A

iron-storage complex that is composed of partially digested ferritin and lysosomes
The breakdown of heme

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35
Q

Local chronic congestion

A

May occur in every organ

Vena cava superior syndrome
Budd Chiary syndr (hepatic vein thrombosis)
Extremities etc

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36
Q

Superior vena cava syndrome

A

Lung cancer, cancer in mediastinum compresses sup. Vena cava
Head and neck cyanosis

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37
Q

Edema

A

-INCREASED INTRAVASCULAR HYDROSTATIC PRESSURE (arteriolar dilation or impaired venous return)
(LOCAL- eg. Deep venous thrombosis of the legs, SYSTEMIC- eg. Congestive heart failure)

– DECREASED PLASMA COLLOID OSMOTIC PRESSURE (eg. nephrosis sy, cirrhosis, protein
malnutrition)

– LYMPHATIC OBSTRUCTION
(lymphedema, elephantiasis)

– SALT AND WATER RETENTION (GN, Acute renal failure)

– INFLAMMATION (EXUDATE)

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38
Q

Normal hemostasis sequence of events

A 
Arteriolar vasoconstriction
 (major regulator: endothelin)
Platelet adherence, activation and aggregation
 Primary hemostasis (major regulator: ECM)
Fibrin meshwork creation, additional platelet recruitment   
Secondary hemostasis (major regulator:Tissue factor)
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39
Q

haemorrhagia per rhexim

A

Rupture of vessel wall

40
Q

haemorrhagia per arrosionem

A

Erosion of vessel wal

41
Q

haemorrhagia per diapedesim

A

Vascular wall disturbances and other hemorrhagic diathese

Platelet disturbances or disturbances in coagulation cascade

42
Q

Thrombocytopenia

A

Low platelet count

43
Q

Thrombasthenia

A

Defective platelet function

Primary and secondary ,aspirin,

44
Q

Hemorrhage Categories by extent

A 
By extent:
Exsanguination
Hematoma
Suffusion
Ecchymosis 
Purpura
Petechia
45
Q

Hemorrhage by localisation

A 
Hemothorax
Hemopericardium
Hemascos
Hemarthrosis
Epistaxis
Hematemesis
Melena
Hematochesia
46
Q

Hemorrhagia per rhexim

A

By rupture - cerebral
Hypertension
Blood can fill the ventricles or stay in sub arachnoidal space

47
Q

Haemorrhagia per arrosionem

A

By erosion

Hypopharynx tumor

48
Q

Hemorrhagia per diapedesim

A

Diapedesim -by diffusium

Retechia-Pericardium hemorrhage
Thrombocytopenia

Petechia-fat embolism due to trauma

49
Q

Hematoma

A

blood suffusion is a localized bleeding outside of blood vessels, due to either disease or trauma including injury or surgery

50
Q

Hemopericardium

A

Due to aortic dissection
Usually due to myocardial infarction
Interfere with heart moving

51
Q

Arterial thrombosis pathogenesis

A

Endothelial injury
Turbulent flow

Can be due to athero sclerosis or vasculitis

52
Q

Arterial thrombosis complications

A

Ischemia (non occlusive thrombosis)
Infarction (occlusive thrombosis)

Art coronary - Acute MI, angina pectoris
Cerebral arteries- Transient Ischemic Attack, stroke, status lacunaris
Art Mesenterica Sup or Inf- bowel infarction

53
Q

Veneous thrombosis (phlebothrombosis) pathogenesis

A

Stasis (varicose, immobilisation)

Thrombophlebitis (inflammatory condition)

54
Q

Veneous thrombosis localisation

A 
90% legs 
Parametrial plexus
Dura sinus
V.portae
V.hepatica
Trousseau phenomenon(migratory thrombophlebitis)
55
Q

Venous thrombus (phlebothrombosis ) complications

A

Ulcus cruris
Postthrombotic synd
Vena cava superior synd
Vena cava inf syndrome (comgestion in lower extremities and pelvis)

56
Q

Thrombosis in heart chambers pathogenesis

A 
Endothelial injury (ami)
Turbulent blood flow (ami)
57
Q

Thrombosis in heart chambs complications

A

Atrial, ventricular, valvular (endocardiatis maranthica) thrombi maybe source of EMBOLISM

58
Q

Fibrin (hyalin) thrombi

A

In arterioles, capillaries, venules (disordered microcirculation)
composed of platelets , fibrin
Disseminated intravascular coagulation

59
Q

Secondary hypercoagulable states

High risk of thrombosis

A 
Prolonged bedrest or immobilization
 myocardial infarction 
atrial fibrillation
tissue damage 
prosthetic cardiac valves 
disseminated intravascular coagulation 
heparin induced thrombocytopenia 
cancer 
antiphospholipid antibody syndrome
60
Q

Secondary hypercoagulable states

Low risk of thrombosis

A 
Cardiomyopathy 
nephrotic syndrome 
Hyperestrogenic syndrome 
oral contraceptives 
hyperlipidemia 
sickle cell anemia 
smoking
61
Q

Possible complications of pulmonary thromboembolism

A

Sudden death (saddle thrombus)
Pulmonary hypertension cor pulmonale (small)
Hemorrhage, hemorrhagic infarction

62
Q

Systemic thrombo embolism

A

80% mural thrombi within heart chambers (ami, left atrial thrombi)

Other aortic atherosclerosis, aortic aneurysm, vegetation, paradoxical embolism

63
Q

Paradoxical embolism

A

Because of open foramen ovale , deep leg thrombus that usually would go to pulmonary circulation gets into systemic circulation by by passing to left side through the opening.

64
Q

Systemic thrombo embolism complications

A

Arterial Embolisation
In lower extrem (75%)
In brain (10%)
In arteries of bowel, kidney, spleen , upper extrm

INFARCTION

65
Q

Most common systemic arterial embolisations

A 
Lower extremities
Brain
Retina 
Heart
Spleen
Kidney
Small bowel
66
Q

Fat embolism

A

After fracture of long bones (bone marrow embolism)
• Clinical signs: respiratory distress, neurologic symptoms (restlessness irritability, delirium, coma), anemia,
thrombocytopenia
• Mechanic and toxic injury

67
Q

Air embolism causes

A

Trauma(chest wall injury)
Obstetric complications
Decompression disease (scuba divers) (hydrogen usually in liquid phase, become gaseous, physicsl bubble formed in vessels) (Caissons Disease (bends ) )

68
Q

Air embolism complications

A

Neurological symptoms
Pulmonary hemorrhage and edema
Atelectasis
Epiphyseal necrosis of long bones

69
Q

What is thrombi

A

Platelets mixed with fibrin, red blood cells, leukocytes

70
Q

Hemorrhagic infartion seen in

A

Dual or collateral arterial system organs or veneous occlusions
Like bowels or lungs

71
Q

Inflammation meaning

A

The reaction of vascularized living tissue to local injury

72
Q

Causes of inflammation

A 
Mikroorganisms (bacteria, fungus, viruses) 
Zoonosis (worms, protozoa, insects) 
Toxic agents 
Mechanic agents (car accidents, trauma)
Termic agents(physical agents)
Radioactivity (uv radiation)
Endogenous toxins (uraemia) 
Tumours (malignants , NOT benigns)
Necrosis
73
Q

Phases of inflammation

A

Acute
Subacute
Chronic

74
Q

Main Symptoms Of Inflammation (Galenus)

A 
Rubor (color)
Calor (temp.)
Dolor (pain)
Tumor 
Functio laesa (functional disturbance)
75
Q

Inflammatory mediators

A

Vasoactive- Increase permeability-Edema

Chemotactic- Chemotaxis and Activation of Inflammatory Cells

76
Q

What cells are in acute inflammation

A

Neutrophils and platelets

77
Q

Cells of chronic inflammation

A

Macrophages
Lymphocytes
Plasma cells

(Neutrophils disappear )

78
Q

Vasoactive mediators

A 
Histamin 
Serotonin
Bradykinin
Anaphylatoxin
Lt, pg,paf
79
Q

Chemotactic mediators

A 
C5a
Ltb
Peptides
Lymphokines
Monokines
80
Q

Function of endothelial cells in inflammation

A

(Regulate intensity and type)

Regulation of permeability
Metabolic activity
Uptake and degredation

81
Q

Neutrophil granulocyte induced necrosis

A 
Primary granules: to digest and breakdown inflammed tissue
Phospholipase A
Myeloperoxidase
Lysosyme
Cationic proteins
Acid hydrolases
Elastase
Catneosins
82
Q

Mast cell basophil granulocyte function ininflammation

A

Primary inflammatory mediators

Histamins ,Leukotriens, Platelet Activation Factors, Eosinophil Chemotactic Factors

83
Q

Types of ACUTE inflammation

A

Serous inflammation – inflammatio serosa
Fibrinous inflammation – inflammatio fibrinosa
Purulent inflammation – inflammatio purulenta
Hemorrhagic inflammation – inflammatio haemorrhagica
Gangrenous inflammation – inflammatio ichorosa seu gangraenosa

84
Q

Serous inflammation – inflammatio serosa

A

Rich in fluid , low protein content

Viral infections
Endocarditis serosa, Meningitis serosa

85
Q

Fibrinous inflammation – inflammatio fibrinosa

A

Exudate rich in fibrin

Surgeries can induce
Pericarditis fibrinosa
Lobar pneumonia

86
Q

Purulent inflammation – inflammatio purulenta

A 
Pleuritis purulenta
Meningitis purulenta
Metastatic brain abcesses
Liver abcesses
Purulent bronchopneumonia

Pus in spaces
Empyema vesicae fellae(gall bladder stone initiates, bacteria from duodenum)
Nephritis apostematosa (e.coli)
Pyelonephritis acute

87
Q

Hemorrhagic inflammation – inflammatio haemorrhagica

A

Trachae acuta heamorrhagica
Pneumonia heam. (Influenza/covid)
Enteritis hemorrhagica
Anthrax hemorrhagic inflammation

88
Q

Gangrenous inflammation – inflammatio ichorosa seu gangraenosa

A

Gangrene pulmonum

89
Q

Acute inflammation, exsudate, cause

A

Bacterial: purulent, neutrophyl predominance
Viral: serous/hemorrhagic, lymphocytic/MPH (or macrophage)
Fungi: purulent, neutro+ eosinophyl

90
Q

Sepsis

A

circulating infectious agents + clinical symptoms of systemic acute infections

91
Q

Content of abcesses

A

Neutrophil granulocyte

92
Q

Waterhause friderichsen synd

A

Hemorrhage of adrenal gland in meningococcus sepsis

93
Q

Subacute inflammation

A

Few weeks or 1-2 months in progress
Decreasing exsudate
Decreasing edema
Eosinophiles, lymphocytes

NOXIOUS AGENT + INFLAMMATION + REPARATION

94
Q

Primary healing of wound

A 
► 0-24h: blood clot + neutrophiles
► Few days: granulation tissue,
mitosis in epithelium
► Few weeks: scar tissue
SURGICAL WOUNDS MOSTLY
95
Q

Secondary healing of wound

A

► 0-24h: Necrotic tissue, inflammatory cells, more fibrin
► Few days: granulation tissue
► Few weeks: scar, contraction of the wound

Smmlws (4 decks)

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